Mesenteritis retráctil asociada a linfoma difuso en una paciente de 74 años / Mesenteritis retractile associated to lymphoma diffuse in a 74 years old patient

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Factores genéticos en la hipertensión arterial / Genetic factors in arterial hypertension

La hipertensión arterial (HTA) resulta de la interacción entre factores genéticos y ambientales. Aunque las bases genéticas de la enfermedad están firmemente establecidas y el desarrollo en el campo de la biología molecular y genética ha sido muy importante en los últimos años, el avance en el conocimiento de las alteraciones genéticas causantes de la HTA no ha sido muy satisfactorio. Se han identificado las mutaciones genéticas responsables de algunas formas raras de hipertensión de origen mendeliano, pero el estudio de los genes posiblemente implicados en la herencia de la HTA (genes candidatos) ha dado en general resultados contradictorios. En esta revisión resumimos los estudios más recientes y significativos realizados sobre los genes candidatos en la HTA (AU)

Renin-angiotensin-aldosterone system and G-protein beta-3 subunit gene polymorphisms in salt-sensitive essential hypertension.

Approximately 50% of hypertensive patients are salt sensitive (they increase their Blood Pressure in response to sodium intake or volume expansion). Mechanisms underlying salt sensitivity are not completely elucidated although there is evidence that they may be genetically determined. The aim of this study is to establish the relation among some genetic polymorphisms of the renin-angiotensin system (RAAS) and the beta-3 subunit of the protein G and salt sensitivity. We studied 102 essential hypertensive patients, stage 1-2 and without target organ damage. Salt sensitivity was assessed by the rapid protocol of Weinberger. We determined by polymerase Chain reaction techniques the following polymorphisms: insertion/deletion (I/D) of the angiotensin-converting enzyme (ACE), A1166C of the angiotensin II type 1 receptor (AT1R), -344C/T and intron 2 conversion (IC) of the aldosterone synthase (CYP11B2), and C825T of the beta-3 subunit of the protein G (GNB3). 41 patients (40.19%) were salt sensitive. The distribution of the different polymorphisms was similar in both groups of patients, but subjects carriers of the W allele of the CYP11B2 IC polymorphism had a greater risk for salt sensitivity as compared with no carriers (37 of 41, 90.2% vs 4 of 41, 9.8%, OR 3.02, P<0.05). Although there is no association between salt sensitivity and the different studied genotypes of the RAAS and of the GNB3, our data show a greater risk for salt sensitivity among carriers of the W allele of the CYP11B2 1C polymorphism.

Hematoma en psoas / Psoas hematoma

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Genetic variation in the beta-3-adrenergic receptor in essential hypertension.

We investigated the role of the beta-3-adrenergic receptor polymorphism in membrane lipid composition and erythrocyte membrane sodium transport in essential hypertensive patients. We studied 87 essential hypertensive patients determining: The Trp64Arg mutation of the beta-3-adrenergic receptor by PCR, lipoprotein profile by standard laboratory methods, membrane lipid composition by IATROSCAN and erythrocyte sodium lithium countertransport by Canessa technique. Patients with the mutation as compared with those without it showed lower membrane cholesterol, membrane cholesterol phospholipids ratio and erythrocyte sodium lithium countertransport, however blood pressure and the other studied variables were similar in both groups of patients. After adjusting by sex sodium lithium countertransport activity remained significant. These data suggest that although the Trp64Arg mutation of the beta-3-adrenergic receptor is related with a different membrane lipid composition and erythrocyte sodium lithium countertransport values it does not contribute to blood pressure levels in essential hypertensive patients.

[The effect of the angiotensinogen M235T and the angiotensin-converting enzyme I/D polymorphisms on arterial hypertension and other cardiovascular risk factors]. / Influencia de los polimorfismos M235T del angiotensinógeno e I/D de la enzima conversiva de la angiotensina sobre la hipertensión arterial y otros factores de riesgo cardiovascular.

BACKGROUND: It has been reported the association between M235T angiotensinogen (AGT) and I/D angiotensin converting enzyme (ACE) gene polymorphisms and hypertension and other cardiovascular risk factors. However there are few data about Spanish population. So that we have studied the relationship among the aforementioned polymorphisms and hypertension and the possibility of association between any polymorphism and a worse cardiovascular risk profile. PATIENTS AND METHODS: 251 hypertensive and 245 control normotensive subjects were studied. The M235T AGT and the I/D ACE gene polymorphisms were determined by polymerase chain reaction (PCR). Family and personal history of cardiovascular disease, lipoprotein profile, microalbuminuria and left ventricular hypertrophy (LVH) by Sokolow index were analyzed in hypertensive patients. RESULTS: The distribution of the different polymorphisms was similar among hypertensive and normotensive subjects. There was not any relationship among AGT nor ACE genotypes and target organ damage. The II ACE genotype was associated with higher lipoprotein (a) (Lp[a]) levels and greater cerebrovascular disease family history and the MT AGT genotype with lower total cholesterol (TC) and triglycerides (TG) levels. CONCLUSIONS: In our study there was not any relationship between arterial hypertension and M235T AGT or I/D ACE gene polymorphisms. None specific genotype was associated with worse cardiovascular risk profile. The II ACE genotype was a predictor of cerebrovascular disease risk through higher levels of Lp(a) and the MT AGT genotype was associated with a better lipid profile.

Modifications induced by -10 degrees Trendelenburg's posture in sodium tubular handling in patients with essential hypertension.

In essential hypertensive patients "exaggerated natriuresis" is a response to acute volume expansion. However, the underlying mechanisms for this remain to be determined. We studied 19 patients with essential hypertension (HP) and 9 normotensive subjects (NS). In all examined subjects the response to acute central volume expansion, without the plasma compositional change that Trendelenburg's position involves, was evaluated during 90 min (period T) after a similar period of deambulation (period D). Mean blood pressure (MBP), tubular sodium handling by the lithium clearance technique, plasma renin activity (PRA), plasma aldosterone (PA), plasma catecholamines and urine prostaglandine E2 and kallikrein were assessed after D and T. MBP was significantly higher in HP than in NS (p = 0.00001). HP showed "exaggerated natriuresis" after T (fractional excretion of sodium increased from 0.55 +/- 0.1% after D to 1.20 +/- 0.2% after T, p < 0.01). This was because of a decrease in their proximal fractional reabsorption of sodium (from 74.96 +/- 1.8% after D to 62.50 +/- 2.8% after T, p < 0.01). Plasma epinephrine and plasma dopamine after T were significantly lower than in standing position in HP (p < 0.01) but no in NS. The decrease in plasma renin activity after T in HP was 53%, and 32% in NS. There were not any significant differences between groups in the other neurohormonal systems studied. We conclude that the major determinant of "exaggerated natriuresis" in hypertensive patients is a higher stimulation of the cardiopulmonary receptors following Trendelenburg's position and consequently stronger reflex inhibition of sympathetic system activity and renin-angiotensin II activity. The "exaggerated natriuresis" after Trendelenburg's position in HP was an expression of abnormal pressure natriuresis.

High-fructose feeding elicits insulin resistance without hypertension in normal mongrel dogs.

This study was undertaken to characterize blood pressure (by continuous blood pressure recording), renal hemodynamics, and excretory function in high-fructose-fed insulin-resistant dogs. We fed 10 mongrel dogs for 28 days with a normal sodium diet containing 60% of the calories either as fructose (n = 6) or dextrose (n = 4). Fructose-fed dogs developed insulin resistance by the 21st day of the experimental diet, as estimated by the mean glucose concentrations (in arbitrary units, AU) during the final hour of the insulin suppression test (640.3 +/- 57 AU fructose-fed dogs upsilon 397.5 +/- 24.7 AU dextrose fed dogs; P < .05). Neither of the groups showed any change in body weight, or in fasting plasma levels of glucose or insulin. There was no difference in mean arterial pressure between the groups before or during either diet, nor did we find any important alterations in renal function in these animals. We conclude that insulin resistance can be induced by a high-fructose diet in the dog. However, it is not accompanied by either hypertension or alteration in renal function. These findings emphasize the importance of continuously recording blood pressure under resting conditions and suggests that in the fructose-fed dog, insulin resistance does not appear to lead directly to hypertension.

Renal response to amino acid infusion in essential hypertension.

In the present study, we evaluated the renal response to a 4-hour infusion of amino acids in essential hypertensive patients, as well as the effects that dietary sodium restriction and enalapril (a converting enzyme inhibitor) had on this renal response. During normal sodium intake, amino acid infusion significantly increased renal plasma flow from 383 +/- 58 to 478 +/- 51 mL/min and glomerular filtration rate from 82 +/- 8 to 100 +/- 13 mL/min. All these effects were abolished when the patients received a low sodium diet (40 mmol/d) for 3 days before the amino acid infusion. The administration of enalapril to the patients during sodium restriction restored the amino acid-induced increment in renal plasma flow (from 388 +/- 35 to 573 +/- 48 mL/min) and glomerular filtration rate (from 88 +/- 9 to 103 +/- 10 mL/min). Mean arterial pressure remained unaltered under all experimental conditions. The results show that in patients with essential hypertension dietary sodium restriction prevents amino acid-induced increments in glomerular filtration rate and renal plasma flow and that this effect is restored during the simultaneous administration of enalapril.

[Influence of arterial pressure and plasma renin activity on tubular reabsorption of sodium]. / Influencia de la presión arterial y de la actividad de renina plasmática sobre la reabsorción tubular de sodio.

BACKGROUND: With the aim of confirming the possible existence of an increase in the fractional proximal reabsorption of sodium in the development of essential hypertension, the tubular dynamics of sodium were compared by the lithium clearance technique in a group of hypertensive patients and controls. METHODS: Following a week of drug suspension 186 patients with slight or moderate essential hypertension and 37 normal subjects with homogeneous sodium ingestion were studied. A clearing period of 90 minutes prior to the administration of a tracing doses of lithium was considered to calculate the fractional proximal and distal reabsorption of sodium in terms of glomerular filtration. In addition to global comparison of the measurements, the hypertensives were classified and compared according to mean arterial pressure (MAP) and percentages of plasma renin activity (PRA). RESULTS: No differences were found in tubular dynamics of sodium between hypertensive and normotensive patients. Neither did the degree of hypertension induce differences. However, upon classifying the patients according to PRA, it was found that those with PRA higher than 0.5 ng/ml-1/h-1 had less secondary natriuresis to a greater fractional distal reabsorption of sodium (p < 0.05). CONCLUSIONS: The findings of the this study do not support the possible existence of a primary defect of the transport of sodium in the proximal tubule in the origin and/or maintenance of essential arterial hypertension.

[Renovascular hypertension and Takayasu disease]. / Hipertensión vasculorrenal y enfermedad de Takayasu.

We present three cases of Takayasu disease which were peculiar because all three of them first manifested as vasculorenal hypertension. The pathogenic mechanisms of hypertension in this disease are reviewed, being renal arteries stenosis the most important mechanism. The great prognostic and therapeutic implications of hypertension in these patients made us suggest the performance of arteriographies of supraaortic trunks in all cases of vasculorenal arterial hypertension associated to certain clinical, analytical and/or arteriographic criteria which are mentioned.