Endothelial dysfunction and improvement of the angiotensin II-reactivity in hypercholesterolemic rabbits: role of cyclooxygenase metabolites.

The aim of this paper was to study the effect of high cholesterol diet on endothelial function and vascular reactivity to angiotensin II and to test the role of vasoconstrictor cyclooxygenase metabolites in this experimental condition. Rabbits were fed with either normal chow or a diet containing 1% cholesterol for 6-7-week. Isometric contractions were measured in rubbed or unrubbed aortic rings. Arteries were contracted with noradrenaline and then exposed to one cumulative dose-response curve to acetylcholine in absence (control) or in presence of indomethacin, (N-[2-cyvlohexyloxy)-4-nitrophenyl]-methanesulfonamide) (NS 398) or 4-hydroxy-2,2,6,6-tetraethylpiperidine-N-oxyl (tempol). After washing the arteries, one cumulative dose-response curve to angiotensin II was constructed in absence or presence of indomethacin, NS 398, [1S-[1 alpha,2 beta (5Z),3 beta,4 alpha]-7-[3-[[2-[(phenylamino) carbonyl]hydrazino]methyl]-7-oxabicyclo[2.2.1] hept-2-yl]-5-heptenoic acid (SQ29548) or 17-octadecynoic acid (17-ODYA). In other group, resting potential was recorded in basal and angiotensin II-stimulated conditions. Indomethacin, NS 398 or 17-ODYA were added to the bath before angiotensin II-stimulation. Rabbits fed on a diet enriched with cholesterol showed higher plasma levels of total cholesterol and LDL. Hypercholesterolemic diet impaired acetylcholine relaxation. Indomethacin normalized endothelium-dependent relaxation whereas NS 398 and tempol had no effect on this phenomenon. Angiotensin II-reactivity was increased in endothelium intact hypercholesterolemic aortic rings and indomethacin, SQ29548 or 17-ODYA blocked this effect. The resting potential of unrubbed hypercholesterolemic arteries was significantly less negative to control after angiotensin II-stimulation. 17-ODYA but not indomethacin prevented angiotensin II-depolarization. High cholesterol diet caused endothelial dysfunction and increased the angiotensin II-reactivity. Both effects were cyclooxygenase1-dependent. Deficit in the NO-production might improve 20-hydroxyeicosatrienoic acid availability, which induces depolarization and angiotensin II-sensitization. In addition, 20-hydroxyeicosatrienoic acid would be metabolized by cyclooxygenase1 to 20-endoperoxides which act through thromboxane A(2)/prostaglandin H(2) receptors contributing to angiotensin II-reactivity increase.

Increased NADPH oxidase activity mediates spontaneous aortic tone in genetically hypertensive rats.

NADPH oxidase is critically involved in increased blood pressure, vascular hypertrophy, inflammation and endothelial dysfunction in experimental and clinical hypertension. We hypothesized that NADPH oxidase might also play a role in the development of spontaneous aortic tone in spontaneously hypertensive rats (SHR). Wistar Kyoto rats (WKY) were used as normotensive controls. Tone was recorded under isometric conditions. NADPH oxidase activity was measured by both lucigenin luminescence and dihydroethidium fluorescence. p47phox protein was localized by immunohistochemistry. SHR (but not WKY rat) aortae showed spontaneous tone in the absence of exogenous vasoconstrictors as evidenced by a stronger relaxant effect of Ca2+-free sodium nitroprusside solution. This tone was enhanced in endothelium-denuded arteries and was inhibited by superoxide dismutase, apocynin, diphenylene iodonium and quercetin. Aortic NADPH oxidase activity, measured by both lucigenin luminescence and dihydroethidium fluorescence, was increased in SHR compared with WKY rats. Immunohistochemical analysis revealed a strong increase in p47phox expression in the medial layer in SHR. Taken together, the present results indicate that enhanced NADPH oxidase activity and, hence, NADPH driven O2- production, is involved in the spontaneous aortic tone in SHR. This was associated with an increased expression of p47phox in the medial layer of the aorta.

Nitric oxide modulates angiotensin II-induced endothelial vasoconstrictor prostanoid release.

UNLABELLED: This study investigated the modulation of angiotensin II-induced endothelial prostanoid release in rabbit aortic rings. Two cumulative dose response curves with 90-min washing interval were performed. Incubation with L-N(G)-nitroarginine methyl ester (L-NAME) 10(-4) M increased angiotensin II maximal contractile response (E(max)). This effect was reversed by indomethacin 10(-5) M, diphenyliodinum 10(-5) M, Tempol 10(-5) M or ascorbic acid 10(-4) M in both cumulative dose response curves and by SQ 29548 10(-6) M in the second cumulative dose response curve. When segments were treated with tetraethylamonium 10(-3) M but not with glibenclamide 10(-5) M during the washing period, L-NAME recovered its ability to enhance the E(max) in arteries incubated with SQ 29548. CONCLUSIONS: nitric oxide modulates angiotensin II-induced endothelial release of cyclooxygenase-dependent eicosanoids, one of which acts through thromboxane A(2)/prostaglandin H(2) receptors and would decrease K(Ca) channel activity. An increase in free radical production may account for the enhancement of such prostanoid release. Furthermore, it was found that in the present conditions, the release of the hyperpolarizing factor would improve in order to maintain the vascular tone.

Structural changes in the renal vasculature in streptozotocin-induced diabetic rats without hypertension.

BACKGROUND/AIM: We evaluated in diabetic-streptozotocin rats (STZR) the structural changes of glomeruli, preglomerular vessels, glomerular tuft and renal parenchyma in order to determine the degree of renal injury and the presence of remodeling in afferent arterioles developed by diabetes without overimposed hypertension. METHODS: Renal mass index and histological score (glomerular number, density, tubular lesions and degree of arteriosclerosis) were estimated. In afferent arterioles the ratio of wall thickness/lumen was obtained by stereological methods. RESULTS: STZR developed diabetes without hypertension; renal mass index increased and matched changes in glomeruli (decrease of capillary number and enlargement of mesangium and basement capillary membrane). Both glomerular number and density as well as afferent arteriole number were diminished. Degenerative changes in both proximal (glycogenic and hyaline degeneration) and distal tubules (hyaline casts) were also observed. At variance with preglomerular vessels, the efferent arterioles only presented initial arteriosclerosis. Finally, the stereological study of afferent arterioles showed a significantly lower arteriolar lumen area and arteriolar wall thickness in STZR, resulting in a remodeling without modification of wall/lumen ratio. CONCLUSION: Diabetes, uncomplicated by hypertension, is associated with (1) a reduction in glomerular number; (2) degeneration in parenchyma and renal tubules, and (3) a specific pattern of remodeling in preglomerular vessels different from that induced by hypertension. Although this work demonstrated that these changes are not triggered by hypertension, further investigations are required in order to determine which mediators are involved in diabetic-vascular renal dysfunction.

[The prothrombotic state in early stages of chronic chagas' disease]. / Estado protrombótico en estadios tempranos de la enfermedad de Chagas crónica.

OBJECTIVE: This study was designed to explore the presence of a prothrombotic state in the early stages of chronic Chagas' disease by evaluating serum markers of thrombosis and fibrinolysis. PATIENTS AND METHOD: Forty-two patients with chronic Chagas' disease (12 men and 30 women, 32.5 6.7 years) were compared with 21 healthy volunteers (10 men and 11 women, 24.2 5.6 years). The markers of thrombotic activation used were fragment 1 + 2, ATM complex, PDF/pdf, D-dimer, and beta-thromboglobulin. Fibrinolysis was evaluated before and after venous occlusion, together with euglobulin lysis time, t-PA, and PAI-1 titers. RESULTS: The markers of thrombotic state were significantly higher in patients with chronic Chagas' disease than in controls: F1 + 2 (p < 0.0001), ATM (p < 0.0001), PDF/pdf (p < 0.05), and D dimer (p < 0.05). There was no significant difference in beta-thromboglobulin (p = 0.06). Euglobulin lysis time, a global fibrinolytic marker, differed significantly (p < 0.0001) between patients with Chagas' disease and healthy volunteers. However, the more specific fibrinolytic markers t-PA and PAI-1 did not differ significantly between the two study groups. CONCLUSIONS: Although there were no significant differences in fibrinolytic markers between patients with chronic Chagas' disease and healthy volunteers, the significant increase in thrombosis markers (F1 + 2, ATM complex, PDF/pdf, and D dimer) suggests the presence of a prothrombotic state in the early stages of chronic Chagas' disease.

Inflammatory and prothrombotic activation with conserved endothelial function in patients with chronic, asymptomatic Chagas disease.

UNLABELLED: Previously, our group showed a prothrombotic state in asymptomatic patients with chronic Chagas disease. The current paper studies the inflammatory status and endothelial function in these patients. METHODS: In 40 patients and 40 healthy volunteers, we evaluated prothrombotic state, blood parasitemia (molecular biology: polymerized chain reaction [PCR]-amplification), tissue factor pathway inhibitor antibodies (aTFPI), interleukin 6 (IL-6), and vascular cell adhesion molecule-1 (VCAM-1). Endothelial function was determined by reactive hyperemia (pulse plethysmography). RESULTS: In patients, prothrombin fragment 1 + 2, d-dimer, PAI-1, and fibrinogen were higher. Amplification of 121/122 primers (Trypanosoma cruzi) was positive in 45% of the patients. Patients presented higher values of aTFPI- immunoglobulin G (IgG; P < .05), aTFPI-IgM (P < .001), IL-6 (P = .004), and VCAM-1 (P = .00001). In both groups, endothelial function was preserved. CONCLUSIONS: We found that asymptomatic patients with chronic Chagas disease presented a prothrombotic/inflammatory status. The fact that endothelial function is still preserved suggests that prothrombosis and inflammation are primarily implicated in the beginning of cardiovascular damage.

Reactivity of isolated toad aortic rings to angiotension II: the role of nitric oxide.

Little is known about the vascular actions of angiotensin II (Ang II) and nitric oxide (NO) in Amphibia. This study investigated (1) Ang II contractility, (2) NO concentrations, and (3) correlations between Ang II contractility, NO concentration and mean arterial pressure (MAP) in isolated Bufo arenarum toad aortic rings. Contractility was measured in isometric conditions, NO concentrations were determined by the Griess reaction, and MAP was determined by a direct method. In isolated toad aortic rings, Ang II produced a contractile response (292.7 +/- 89.2 mg; n = 20). Furthermore, a contractile response to norepinephrine (NE) was also obtained. A significant correlation between both the Ang II and NE contractile responses was found (r = 0.89; n = 11; P < 0.01). Administration of Ang II increased MAP values (Basal 16.8 +/- 1.7; n = 19 vs. Ang II 28.4 +/- 1.8 mmHg; n = 19; P < 0.001), and the increase of MAP by Ang II was positively correlated with the Ang II contractile response (P < 0.01). Administration of L-NAME also increased MAP values, and this effect was higher in those toads that presented a lower pressure response to Ang II (Pearson r = -0.68; P < 0.05). NO was present in all aortic rings, and its concentrations were negatively related to the Ang II contractile response (P < 0.036) and pressure response (Pearson r = -7.08; P < 0.001). These findings suggest that, in the B. arenarum toad, the NO system contra-regulates both the contractile and pressure Ang II responses, although its action could be different in each specimen.

Internal mammary artery grafts reactivity in hypertensive patients: role of stretching in extraendothelial nitric oxide.

BACKGROUND: The internal mammary artery (IMA) used in bypass coronary surgery remains efficient for a longer time than other grafts, such as saphenous veins; however, its biological characteristics are incompletely defined. OBJECTIVE: To compare in IMA grafts from hypertensive (HT) and normotensive (NT) patients the presence of endothelium and their functionability, the response to passive stretching and basal tone, the reactivity to exogenous vasoconstrictors, the role of stretching in NO release, and the possible extraendothelial NO source. METHODS AND RESULTS: IMA rings contractility, presence of endothelium, and nitrite release were studied. An endothelial dysfunction associated with hypertension was found. IMA rings from HT had an impaired response to passive stretching, resulting in a decreased relaxation. All IMA grafts had an increased basal tone demonstrated by relaxation to SNP; however, a lesser response was found in HT. Interestingly, it was demonstrated that NO release was present in IMA grafts, despite an endothelial dysfunction and that stretching increased NO release. This effect was inhibited by Ca2+ -free media, L-NAME and a specific neuronal NO synthase (nNOS) inhibitor. Furthermore, the demonstration of the presence of nNOS in smooth muscle cells by immunohistochemistry supports a role of extraendothelial NO. CONCLUSION: We demonstrate the impact of hypertension in IMA grafts producing increased endothelial dysfunction, reduced response to passive stretching, increased basal tone, and impaired responsiveness to exogenous vasoconstrictors and NO release. A specific role of stretching in extraendothelial NO release was demonstrated, which may have an important role in the outcome of IMA grafts due to the protective actions of NO, even in the absence of the endothelium.

Cross talk between angiotensin II and alpha 1 adrenergic receptors in rabbit aorta: role of endothelium.

Interaction between the renin-angiotensin system and the sympathetic nervous system has been proposed to be like a physiological regulation mechanism. The present work was designed to study the cross talk between angiotensin II and adrenergic receptors on the smooth muscle contractile response and the endothelium influence in this phenomenon. Homologous and endothelium independent desensitization of angiotensin II-contractile response was observed. Treatment with noradrenaline between two cumulative doses response curves (CDRC) to angiotensin II caused a rightward shift of the second CDRC in unrubbed arteries and increased the maximal response in rubbed arteries. Prazosin blocked these effects. No homologous desensitization of noradrenaline contractile response was found. Treatment with angiotensin II between two CDRC to noradrenaline caused a loss of affinity in the second CDRC in unrubbed arteries. Losartan was able to avoid this phenomenon. Maximal response was enhanced both in arteries with and without endothelium treated or not with angiotensin II. Results demonstrate homologous and endothelium-independent desensitization of the contractile response to angiotensin II but not to noradrenaline. In addition, heterologous and endothelium-dependent desensitization induced by noradrenaline and angiotensin II on the contractile response to each other was found. Furthermore, results provided the first evidence that there is an endothelium-dependent cross talk between alpha1-adrenergic and angiotensin II receptors in smooth muscle of rabbit aorta.

Role of nitric oxide on the vasorelaxant effect of atrial natriuretic peptide on rabbit aorta basal tone.

The role of nitric oxide (NO) on the vasorelaxant effect of atrial natriuretic peptide (ANP) on the basal tone of rabbit aortic rings conditioned to angiotensin II (Ang II) was studied. ANP aortic relaxation and nitrite release were measured in the presence and absence of endothelium and a NO-synthase inhibitor. Ang II at 10(-8) M triggered a contractile response, conditioning the vessel to a vasorelaxant effect of ANP (10(-8) M). This effect was significantly enhanced by endothelium removal, NG-nitro-L-arginine methyl ester (L-NAME, 10(-4) M), and methylene blue (10(-5) M). ANP decrease of basal tone in Ang-II-sensitized aortic rings was improved when a higher concentration of Ang II was used (l0(-6) M). Basal and Ang-II-stimulated nitrite release were measured in stretched (S) and nonstretched (NS) aortic rings. Nitrite release was significantly increased in S rings (p < 0.001). L-NAME (10(-4) M) partially inhibited nitrite release in both basal and Ang-II-stimulated S aortic rings. In NS aortic rings, the NO inhibitor did not inhibit basal nitrite release but blunted the Ang-II-stimulated nitrite level. A significant negative correlation between nitrite release and the ANP vasorelaxant effect on basal tone was dependent on the Ang-II-sensitizing dose. The present results demonstrate that ANP relaxant effects on aortic basal tone are related to NO levels, which are regulated by S- and Ang-II-concentration-dependent NO generation and quenching.

The novel serine protease PreR-Co promotes endothelium-independent vasorelaxation in rabbit aortic rings.

The effect of a novel enzyme (PreR-Co) that activates renal prorenin was studied on rabbit aortas with and without endothelium. It was tested 1) in the basal tone of nonstimulated or ANG II-sensitized rings or rings precontracted with norepinephrine (NE), PGF(2alpha), high KCl concentration, and 2) in rings pretreated with enalaprilat, losartan, PD-123319, N(omega)-nitro-l-arginine methyl ester, HOE-140, indomethacin, or serine protease inhibitors (PMSF, aprotinin, or soybean trypsin inhibitor); kallilkrein and bradykinin were also tested in ANG II-sensitized rings. PreR-Co produced a vasorelaxant effect in the basal tone and in the precontracted rabbit aorta. The effect was endothelium independent, potentiated by endothelium removal or nitric oxide (NO) synthase inhibition, and abolished by boiling the enzyme. In addition, the effect improved when basal tone was increased in ANG II-sensitized aortic rings or in precontracted vessels. No activation of the ANG II, bradykinin, prostaglandin, or NO pathway mediating the PreR-Co response could be obtained, suggesting a direct action of the enzyme. This action seems to be dependent on esterasic activity because serine protease inhibitors like PMSF and aprotinin were able to block the vasorelaxant effect of PreR-Co.

Probables mecanismos involucrados en la etiopatogenia del estado protrombótico en la enfermedad de Chagas crónica. ¿Activación inflamatoria con función endotelial conservada? / Possible mechanisms involved in the pathogenesis of prothrombotic state Chronic Chagas disease. Inflammatory activation with preserved endothelial function?

Introducción: En el estadio indeterminado de la enfermedad de Chagas crónica, se comprobó un estado protrombótico asociado con factores de riesgo trombofílicos. La etiopatogenia de la enfermedad de Chagas es multifactorial sin que ninguno de los mecanismos involucrados explique por sí mismo el inicio y progresión de las lesiones. Objetivo: Evaluar probables mecanismos involucrados en la etiopatogenia del estado protrombótico en el estadio indeterminado de la enfermedad de Chagas crónica. Material y Métodos: Desde marzo de 2004 hasta diciembre de 2006 se evaluaron 40 pacientes chagásicos crónicos, 14 varones y 26 mujeres, (33.5 ± 4.9 años); en clase funcional I, de la clasificación clínica de la miocardiopatía chagásica crónica, comparándolos con un muestreo accidental de 40 voluntarios sanos, 19 varones y 21 mujeres (28.8 ± 6.3 años). Se evaluó la presencia del parásito por técnica de amplificación de las cadenas de polimerasa (PCR) y se determinó anticuerpo inhibidor de la vía extrínseca de la coagulación (aTFPI) por un método de ELISA optimizado, con valor de corte para aTFPI IgG >18 Uml-1 y para aTFPI IgM >15 Uml-1. Valores altos de aTFPI (IgG e IgM) se consideraron los >50 Uml-1. Se tomaron también muestras de sangre para la determinación por ELISA de dos marcadores de inflamación; Interleuquina 6 (IL-6) y de la molécula de adhesión a célula vascular (VCAM-1). La función endotelial se evaluó por pletismografía de onda de pulso digital para determinar hiperemia reactiva, la que discrimina sujetos con y sin disfunción endotelial. Resultados: En los pacientes chagásicos estudiados se detectó presencia del parásito por la técnica de amplificación de PCR utilizada en el 45 por ciento (n=18) de los casos. Los pacientes chagásicos presentaron valores de aTFPI mayores que los controles, con una p<0.05 para aTFPI IgG y p<0.001 para aTFPI IgM; superando en muy pocos casos los valores de corte establecidos para el método...

Oxido nítrico en vasos usados para bypass: arteria mamaria vs. venas safena, rol de la tensión de estiramiento / Nitric oxide on bypass glasses: mammary artery vs safena vein, lift strain role

Una estimación de la función endotelial de arterias mamarias (art mam) y venas safenas (vena saf) usadas parabypass coronario sería medir la liberación de oxido nítrico (NO). En nuestro laboratorio observamos, en arterias de conejos, que el estiramiento (stretching) incrementa el NO. Objetivos: Determinar la presencia de endotelio en art mam y vena saf en pacientes (p) de bypass coronario y dosar el contenido de NO. Evaluar el rol del estiramiento. Métodos: Se usaron restos (1-4 anillos) de art mam y vena saf de 44 p del CMC con o sin factores de riesgo (FR) asociados. Se efectuaron dos protocolos in vitro: NT) anillos no tensados (precarga de 0g) y T) anillos tensados (precarga de 2g:art mam o 3g:vena saf). La presencia de endotelio se determinó por relajación (con endotelio) o no (sin endotelio) a acetilcolina 10-6M o bradiquinina 10-7M sobre precontractura con noradrenalina en baño de órgano aislado. El NO se dosó por método de Griess a los 15 min y en una curva de tiempo (90 min) con y sin tratamiento con L-Name 10-3M o Ang II (10-9 a -6M). Resultados: 7 p presentaron endotelio sin asociación con los FR. En T el NO basal fue mayor en vasos con endotelio en art mam (1829±259 vs 3699±65 pmol/mg n=19; p<0,05) y vena saf (694±103 vs 1290±216 pmol/mg, n=18; p<0,01). T estimuló laliberación de NO, este efecto es mayor en art mam con endotelio que en vena saf (p<0,001) y se mantiene aúnen anillos sin endotelio a los 90 min. En NT no hubo diferencias entre art mam y vena saf. Ang II mostródiferencias entre T y NT. L-Name solo inhibió el NO en vena saf con endotelio. Conclusiones: Los vasospresentaron disfunción endotelial generalizada sin asociación con ningún FR. Sin embargo, hubo liberación deNO incluso en anillos sin endotelio. Demostramos mayores niveles de NO en art mam. Sin embargo art mam yvena saf aumentan su liberación si se someten a T y este aumento se mantiene en la disfunción endotelial. Suorigen involucraría activación de la enzima NO Sintetasa neuronal(nNOS). La T activaría la nNOS, situaciónhomologable in vivo a la T que sufriere el vaso injertado en el circuito arterial coronario. Este mecanismocompensador de NO ayudaría a explicar la buena perfomance, aun en vena saf, de los puentes coronarios, más allá del FR asociado.

Monitoreo ambulatorio de la presión arterial / Ambulatory blood pressure monitoring

El propósito de este artículo es dar una síntesis del desarrollo del monitoreo ambulatorio de presión arterial: un método auxiliar en el diagnóstico y tratamiento de la hipertensión arterial. El perfeccionamiento de estos equipos permite obtener lecturas de la presión arterial durante la actividad diaria del paciente y durante el sueño con un mínimo de molestias. Los datos son analizados por un programa adecuado y procesados en una computadora, obteniéndose medias, sus desvíos y gráficos de las variaciones de la presión arterial. El método tiene sus indicaciones precisas en pacientes con hipertensión limítrofe; refractarios al tratamiento; hipertensión del "guardapolvo blanco" y otras circunstancias. No reemplaza a los métodos de determinación clínica, correctamente aplicados, en los pacientes con hipertensión arterial definida.

Efecto de antagonistas de los receptores de angiotensina II y alfa2 adrenérgicos sobre la liberación de óxido nítrico inducida por angiotensina II / Effect of angiotensin II and alpha2 adrenergic receptor antagonists on angiotensin II-stimulated nitric oxide release

El objetivo del presente trabajo fue caracterizar la interacción entre el sistema adrenérgico y la liberación de óxido nítrico (ON) estimulada por angiotensina II en aorta de conejo. Anillos de aorta torácica se colocaron en un baño de órgano aislado. Se equilibró durante 30 min, se lavó y se agregó angiotensina II a diferentes dosis, dejándose actuar 20 min. En otro grupo se efectuaron dos estimulaciones con un intervalo de 60 min. Los antagonistas de angiotensina II: losartan, PD 123319 y Sar1-Leu8-angiotensina II; y el antagonista a2 adrenérgico (yohimbina), todos 10-5 M, y L-NAME o D-NAME 10-2 M, se agregaron antes de estimular con angiotensina II 10-6 M o 5.10-6 M. A otro grupo, además de losartan o PD 123319, se agregó yohimbina. La determinación de nitritos se realizó con el reactivo de Griess. La angiotensina II 10-8 M hasta 10-6 M, incrementó la producción de metabolitos de ON medidos como nitritos con respecto al control. A dosis mayores hubo una disminución con respecto a 10-6 M La liberación de nitritos inducida por angiotensina II cayó en la segunda estimulación con la hormona en todos los casos, mientras el L-NAME la bloqueó. Los antagonistas de angiotensina II la incrementaron sólo a dosis máxima de la hormona, efecto anulado por yohimbina. Asimismo, yohimbina disminuyó la producción de nitritos a dosis de angiotensina II 5.10-6 M pero no 10-6 M. Estos resultados permiten postular que la liberación de ON inducida por angiotensina II sería en parte mediada por estimulación de receptores a2. Los antagonistas de angiotensina II desenmascararían este efecto a dosis máxima de la hormona, mientras que a dosis supramáximas prevalecerían mecanismos inhibitorios que serían compensados por activación a2

Modificaciones de la pressión arterial ante una situación de estres experimental / Modificaciones of blood pressure in a stress situation experimental

Una situación estresante produce en el individuo, como reacción, una valoración cognitiva del evento asociada con activación emocional. Esta reacción, a través de mecanismo neuroendócrinos, activa numerosos sistemas siendo uno de ellos el cardiocirculatorio. Esta respuesta ciruclatoria, puede ser valorada en laboratorio. Nuestro propósito es presentar un instrumento: DEXTERIMETRO, creado en nuestro laboratorio para producir estrés psicológico de corta duración, y valaorar su efectividad, utilizando como variable la PA (PAS y PAD). Para este fin, adminsitramos la prueba a 76 estudiantes voluntarios de 3§ año de Medicina, con edad promedio de 21 años. En cada caso registramos dos medidas de PA: una antes de la ejecución y otra al finalizar la misma. El incremento promedio de PAS fue de 11,15 mmHg, y de PAD: 8,88 mmHg. Además, se observó, en el 14% de los sujetos, una marcada reactividad vascular (incremento mayor al incremento medio más una desviación estándar). Se discute el valor del dexterímetro para detectar futuros hipertensos a partir de la valoración de reactividad de PA

El Losartan inhibe el efecto de la hormona antidiurética en un modelo funcional de nefrón distal / Losartan inhibits the effect of antidiuretic hormone in a functional model of distal nephron

ANTECEDENTES: En un trabajo previo se demostró que un antagonista peptídico de la hormona antidiurética era capaz de bloquear el efecto de la angiotensina II en la permeabilidad al agua en presencia de un gradiente osmótico en la piel aislada del sapo, tejido con propiedades funcionales similares a las del nefrón de los mamíferos. En el presente trabajo se estudió el efecto de un antagonista de los receptores AT1 de la angiotensina II (Losartan) en la respuesta de la piel y vejiga aislada del sapo a la hormona antidiurética. MATERIAL Y METODO: La permeabilidad al agua en presencia de un gradiente osmótico fue medida por un método gravimétrico usando mitades simétricas de la piel ventral pélvica del sapo (Bufo arenarum). Después de mediciones controles se agregó Losartan al lado dérmico de una mitad, 10 minutos antes de una dosis de arginina vasotocina, la hormona antidiurética normalmente existente en los anfibios. Experimentos similares fueron realizados con vejigas urinarias usando una mitad como control y la otra como experimental. RESULTADOS: El Losartan no modificó la permeabilidad al agua en presencia de un gradiente osmótico basal en piel aislada de sapo pero inhibió significativamente la respuesta a la arginina vasotocina (10 menos 9M) en un 70,1 por ciento en concentraciones de 10 menos 5M, en 42,9 por ciento (10 menos 6M) y en 63,7 por ciento (10 menos 7M). El Losartan (10 menos 5M) no modificó en cambio la respuesta a la arginina vasotocina (10 menos 10M) en vejiga aislada de sapo. CONCLUSIONES: En la piel del sapo existiría un nuevo tipo de receptor común para la angiotensina II y la hormona antidiurética que difiere del receptor existente en la vejiga urinaria (V2), el cual sería exclusivo para la hormona antidiurética

Edad y reactividad cardiovascular a pruebas presoras de laboratorio / Age and cardiovascular reactivity to a laboratory presor test

El presente trabajo buscó valorar las respuestas a dos pruebas presoras de laboratorio en sujetos de edades diferentes. Se tomaron dos muestras de sujetos sanos de diferente edad: Grupo 1 (n=17), edad promedio 23 ñ 1 años y Grupo 2 (n=18), edad promedio 53 ñ 2 años. Ambos grupos fueron sometidos a dos pruebas presoras de laboratorio, esfuerzo muscular isométrico y dexterímetro. El grupo 2 presentó mayores valores basales de presión arterial sistólica (PAS) y diastólica (PAD) (p<0,05) y también mayores incrementos de PAS y PAD frente ambas pruebas (p<0,01). No se encontraron diferencias en los valores basales de frecuencia cardíaca (FC). El grupo 1 presentó mayores incrementos FC ante ambas pruebas (p<0,05). Estos resultados indicarían que según la edad se responde con patrones hemodinámicos diferentes frente a estímulos presores. Diversos autores sugieren la asociación de una serie de factores, la declinación de los barorreceptores, el incremento de las resistencias periféricas y el endurecimiento de las arterias, como explicación a este fenómeno

Factores psicológicos y respuesta cardiovascular a una prueba presora / Psychologic factors and cardiovascular response to a pressing essay

En los últimos años se han encontrado relaciones entre diversos factores psicosociales y la ractividad cardiovascular al estrés. El objeto de presente trabajo fue buscar correlación entre factores psicológicos y los incrementos de la presión arterial provocados por esfuerzo muscular isométrico (prueba de hand-grip). Para ello, 15 estudiantes de medicina (edad promedio 23 años) fueron sometidos a una prueba de hand-grip. Posteriormente y en forma individual, los sujetos complementaron el inventario Multifásico de Personalidad de Minnesota (MMPI). Se encontraron correlaciones (r de Pearson) significativas entre las reactividades de presión arterial sistólica y 3 escalas de MMPI: F, 7 y 8. Estas correlaciones podrían interpretarse como una actitud más defensiva de estos sujetos que los llevaría a ocultar la información sobre si mismo. Estos resultados coinciden con lo hallado por diversos autores