Endothelial function in normotensive and high-normal hypertensive subjects.

To evaluate the impact of a mild increment in blood pressure level on endothelial function, we evaluated 61 healthy volunteers (24 women, 37 men, and aged 35-50 years). All subjects underwent a blood chemistry panel to exclude any metabolic abnormalities and were submitted to a Doppler ultrasound of the brachial artery to assess endothelial function. We assessed the endothelial response to reactive hyperaemia and exogenous nitric oxide administration considering an increase in systolic blood pressure (SBP) at each 10-mm Hg interval. Our study population was divided as follows: SBP <115 mm Hg (SG1, n=13), SBP > or =115 mm Hg and <125 mm Hg (SG2, n=20), SBP > or = 125 mm Hg and <135 mm Hg (SG3, n=13) and SBP > or = 135 mm Hg and < 140 mm Hg (SG4, n=15). We found a significant difference in flow-mediated dilation among SG2, SG3 and SG4, 16.2+/-5.6, 13.4+/-5.2 and 11.5+/-3.6%, P<0.05, respectively). After nitrate administration, we observed a nonsignificant decrease in brachial artery dilation among groups, P=0.217. Our data showed in a healthy normotensive population, without any risk factor for atherosclerotic disease that small increases in SBP but not in diastolic blood pressure may impair endothelial function even in subjects considered as high-normal, meaning that this population deserves more attention than usually ascribed to intervene and prevent complications, as endothelial dysfunction may represent an early change in those who develop hypertension later in life.

Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system.

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Central and peripheral indices of sympathetic activity after blood pressure lowering with enalapril (MK-421) or hydralazine in normotensive rats.

Various antihypertensive drugs have different effects on vasoactive mechanisms. In normotensive Wistar rats, we investigated the effects on plasma and tissue catecholamines of chronic treatment with two agents: MK-421, an angiotensin converting-enzyme inhibitor (CEI), and hydralazine, a vascular smooth muscle relaxant. Both agents lowered blood pressure via arteriolar dilation, to the same final level. However, hydralazine stimulated the renin-angiotensin system and elevated the plasma norepinephrine (NE) and epinephrine (E) levels, whereas MK-421 did not. In MK-421-treated animals, NE, E, and the ratio of E/NE were decreased in the brain stem, and this ratio was increased in the heart. In hydralazine-treated rats, the catecholamine levels were unchanged in the brain stem and heart. The turnover rate of NE was significantly reduced in the brain stem and heart of MK-421-treated rats, whereas, after hydralazine, the turnover rate in the heart was increased (decreasing the half-life of NE by about 50%), indicating increased sympathetic activity. Thus, elimination of angiotensin II (AII) by CEI is associated with decreased sympathetic activity in both the brain stem and heart, whereas an equipotent antihypertensive action by smooth muscle relaxation leads to stimulation of both the renin-angiotensin and the sympathetic systems. These differences are more readily apparent by measurement of catecholamine turnover rates in tissues than of catecholamine levels, and they may account for the different hemodynamic effects of the two agents, even though both drugs act through arteriolar dilation.

Effects of a specific inhibitor of the vascular action of vasopressin in humans.

Experimental evidence indicates that arginine vasopressin (AVP) may contribute to the rise of blood pressure (BP) in hypertension induced by renal failure and sodium overload. We studied the AVP inhibitor [1-(B-mercapto-B,B-cyclopentamethylenepropionic acid)-2-(O-methyl)tyrosine] AVP in 12 normal and seven hypertensive subjects with end-stage renal disease. To test the agent's capacity to block the pressor action of exogenous AVP In humans, we constructed a dose-response curve with AVP doses of 1 to 20 mU/kg, raising BP by up to 30 mm Hg. Subsequently, five volunteers receive intravenous (i.v.) doses of 0.1 mg, and five volunteers received 0.5 mg of the inhibitor. The dose-response curve was then repeated with AVP doses up to 200 mU/kg. Both doses of the inhibitor shifted the curve to the right and downward, with the BP response to 20 mU/kg AVP being inhibited by 23% and 80% respectively. The duration of action of the compound was tested in two additional subjects, and was found to be over 3 hours. We then tested the compound in seven hypertensive patients with end-stage renal failure. Two days before dialysis, patients received a 150 mEq/day Na diet. After an additional Na load of 180 mEq via i.v. saline over 3 hours under constant BP and ECG monitoring, they received an i.v. bolus of 0.5 mg AVP inhibitor. A moderate BP fall occurred in five patients; it was maximal at 45 to 60 minutes and returned to baseline by 70 to 90 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Methylprednisolone-induced hypertension. Role for the autonomic and renin angiotensin systems.

The role of the autonomic nervous system (ANS) in the pathogenesis of hypertension induced by methylprednisolone (20 mg/kg/week subcutaneously) was studied in rats before and during chronic renin angiotensin system (RAS) blockade with captopril (20 mg/kg/every 8 hrs by mouth). Sympathetic nervous system (SNS) blockade was accomplished by the intravenous (i.v.) administration of propranolol (0.20 mg/100g) plus phentolamine (1.25 mg/100g/i.v.) and ganglionic (G) blockade by the use of pentolinium tartarate (0.5 mg/100g/i.v.). After 4 weeks, methylprednisolone-treated animals showed significant decreases in mean arterial pressure (MAP) with both SNS (-34 +/- 2 mm Hg) and G (-56 +/- 3 mm Hg) blockades; during chronic RAS blockade, even greater falls in MAP were observed (SNS = -43 +/- 2 mm Hg and G = -75 +/- 3 mm Hg). Nevertheless, for both groups the levels of MAP obtained during SNS and G blockades were higher than those observed in their control groups. At the end of second week, however, in captopril-treated hypertensive rats the values of MAP obtained during ANS blockade were lower than those observed in the control group. An increased responsiveness to exogenous administration of norepinephrine (NE) was observed in animals receiving methylprednisolone and captopril. It is concluded that methylprednisolone hypertension in the rat may be initially explained by activation of RAS and ANS. At later phases, a third mechanism has to be postulated to explain the hypertensive state.

Role of substance P in blood pressure regulation in salt-dependent experimental hypertension.

The participation of substance P in the pathogenesis of five models of experimental hypertension, ie, DOCA-salt, subtotal nephrectomy, one-kidney-one clip renovascular, two-kidney-one clip renovascular, and spontaneous hypertension, was evaluated via an acute infusion of a newly synthesized potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt, subtotal nephrectomy, and one-kidney-one clip renovascular hypertensive rats but only small and nonsignificant changes in blood pressure of two-kidney-one clip renovascular and spontaneously hypertensive rats. CP 96,345 had no effect on the blood pressure of sham-treated controls and Wistar-Kyoto rats. This NK-1 receptor antagonist did not significantly affect the heart rate of any experimental model studied. The data suggest that endogenous substance P may act as a partial counterregulatory mechanism against vasoconstriction in models of salt-dependent hypertension.

Cardiovascular effects of a specific nonpeptide antagonist of substance P (NK-1) receptor in DOCA-salt hypertension.

The neurotransmitter substance P acts also as a potent vasodilator. Its participation in the pathogenesis of deoxycorticosterone acetate (DOCA)-salt hypertension was evaluated by an acute infusion of a newly synthesized, potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt rats but only small, transient, and nonsignificant rises in blood pressure of sham-treated control rats. The rise in blood pressure was not accompanied by changes in heart rate. Maximal blood pressure increase in DOCA-salt rats was 31.7 +/- 14.8 mm Hg. In a second series of experiments, the hemodynamic effects of this antagonist were evaluated under anesthesia in both DOCA-salt and sham-treated control rats by the thermodilution method. During CP 96,345 infusion, sustained increases in cardiac index and stroke volume and decreases in total peripheral resistance were observed in both DOCA-salt and control rats. In DOCA-salt rats, cardiac index rose by 79.4%, while total peripheral resistance fell by 27.9% of the baseline values. In control rats, the changes were smaller (+27.2% and -22.5%, respectively). Stroke volume changed in parallel to cardiac output in both groups. The data suggest that acute blockade of NK-1 receptors increases blood pressure in DOCA-salt rats mainly by an increase in cardiac output. We conclude that endogenous substance P tends to counteract the DOCA-salt-induced elevation of blood pressure by modulating both cardiac output and peripheral resistance.

Rapid eye movement sleep deprivation and hypertension. Genetic influence.

We studied the importance of genetic predisposition in the development of stress-induced hypertension in the spontaneously hypertensive rat (SHR), Wistar-Kyoto (WKY) rat, and borderline hypertensive rat (BHR; first-generation offspring of SHR and WKY). Rats were submitted to seven 72-hour sessions of rapid eye movement sleep deprivation (REM-sd) every other week during 13 weeks. Tail arterial pressure was determined throughout the experiment. At the end of the study, mean arterial pressure (direct measurement), sympathetic activity (acute blockade with propranolol and phentolamine), and ventricular weight were determined. Results showed that REM-sd induced sustained hypertension only in rats with a partial predisposition to developing hypertension (BHRs). Values of tail arterial pressure at the end of the study were BHR REM-sd, 175 +/- 1.6 mm Hg and control BHR, 155.9 +/- 0.9 mm Hg, p less than 0.05; SHR REM-sd, 219 +/- 2.6 mm Hg and control SHR, 211.9 +/- 3.4 mm Hg, NS; WKY REM-sd, 123.9 +/- 2 mm Hg and control WKY, 125.4 +/- 2.2 mm Hg, NS. Stressed groups showed higher reduction of mean arterial pressure than their controls when submitted to sympathetic blockade (SHR REM-sd, -75.7 +/- 13.2 mm Hg and control SHR, -60 +/- 4.5 mm Hg, p less than 0.05; BHR REM-sd, -38.4 +/- 3.6 mm Hg and control BHR, -24.3 +/- 2.1 mm Hg, NS; WKY REM-sd, -34.4 +/- 2.5 mm Hg and control WKY, -25.6 +/- 3.3 mm Hg, NS). REM-sd increased ventricular weight in all strains. These increments showed no correlation with blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension and economic activities in São Paulo, Brazil.

A study of the prevalence of hypertension was undertaken among workers in 10 subsectors of the economy in São Paulo, a major urban-industrial area of Brazil. Included in the study were 5500 subjects 15-65 years of age, employed in 57 randomly selected firms. Hypertension rates (DBP greater than or equal to 90 mm Hg) were higher among males up to 44 years of age. There was a decreasing gradient from mild to moderate and severe forms in all groups. Severity tended to increase with age in all groups. Black males showed higher rates than whites (29.2% vs 16.7%, p less than 0.05), the excess being partially accounted for by moderate and severe forms (40% vs 20%). Subjects who overworked showed a trend toward higher hypertension rates. Higher rates in four subsectors (metallurgy, finance, transport, and journalism), aside from the distribution of known risk factors and job selection, may reflect a variety of work-related stressors.

Sodium chloride-induced partial inhibition in vivo of alpha 2-adrenoceptor agonist function.

Recent research has demonstrated that sodium diminishes the affinity of alpha 2-adrenoceptors for agonists in vitro. Clonidine, a highly specific agonist for alpha 2-receptors, has a transient hypertensive effect when administered parenterally. We studied in conscious anephric Wistar rats the effect of equimolar saline or mannitol solutions on the hypertensive response to clonidine administered subcutaneously in doses of 10, 100 and 1000 micrograms/kg body weight. Prior saline infusion reduced the hypertensive response to the two higher doses of clonidine by 65 and 70%, and displaced the slope of the dose-response curve downwards, but mannitol had no such effect. Pre-treatment with the alpha 2-antagonist yohimbine abolished the differences in clonidine-induced pressor response between saline-treated, mannitol-treated and control rats. On the contrary, after pre-treatment with the alpha 1-antagonist prazosin, the pressor action of clonidine was significantly reduced in the saline-infused rats compared to the other two groups. Thus the saline-induced blunting of the pressor response elicited by clonidine could be negated by prior alpha 2- but not alpha 1-blockade, indicating that sodium interfered with the stimulation of post-synaptic vascular alpha 2-adrenoceptors. These findings indicate that loading with sodium chloride attenuates the alpha 2-adrenoceptor function in vivo. Based on this, we suggest that the mechanism by which sodium excess causes a rise in blood pressure involves modification of the alpha 2-adrenoceptors.

Evidence for dopaminergic regulation of vasopressin release in the anephric rat.

Arginine vasopressin (AVP) release elicited by osmotic stimuli induces variable hypertensive responses. In normotensive anephric rats, a significantly greater blood pressure response was elicited by hypertonic saline than by mannitol infusion, and was further enhanced by previous dopaminergic receptor blockade. Plasma levels of AVP were significantly more elevated after saline than after mannitol despite more pronounced elevation of plasma osmolality in the latter animals, and were the highest in dopaminergically blocked animals. These findings indicate that dopamine exerts an inhibitory effect on the release of AVP.

Angiotensin-converting enzyme (ACE) inhibition. Therapeutic option for diabetic hypertensive patients.

When choosing antihypertensive agents for the treatment of diabetic patients with hypertension, it is necessary to consider the individual characteristics of these patients. In this respect, angiotensin-converting enzyme (ACE) inhibitors constitute an attractive option for diabetic patients. The effects of enalapril alone for 16 weeks in 23 non-insulin-dependent diabetic (NIDD) patients and in 10 non-diabetic patients with mild to moderate essential hypertension (EH) [diastolic blood pressure greater than 95 mm Hg and less than 115 mm Hg] were evaluated. Similar reductions in both systolic and diastolic blood pressure were observed in 17 NIDD patients (from 155 +/- 18/100 +/-11 mm Hg to 128 +/- 12/82 +/- 8 mm Hg, respectively) and in 6 EH patients (from 155 +/- 21/100 +/- 6 mm Hg to 125 +/- 20/84 +/- 8 mm Hg, respectively) who achieved and maintained blood pressure control (diastolic blood pressure less than 90 mm Hg) for 16 weeks. In 4 NIDD and 4 EH patients blood pressure was not controlled. Two NIDD patients discontinued the medication, one because of symptomatic postural hypotension and the other, who had a plasma creatinine level of 1.8 mg/dl, because of hyperkalaemia (K = 6.1 mEq/L). In the responders, enalapril did not alter glucose tolerance, plasma or urinary excretion of creatinine, potassium, sodium and aldosterone. Plasma renin activity increased in the NIDD group only. In 11 patients (6 NIDD and 5 EH), the elevated protein or albumin excretions decreased. It is concluded that enalapril is a good therapeutic option for NIDD patients with hypertension.

The renin-angiotensin system in the control of systemic arterial pressure.

The renin-angiotensin system through its active octapeptide, angiotensin II, has an important role in systemic arterial pressure control. Angiotensin II is a potent direct vasoconstrictor and is also the main regulator of aldosterone secretion. The complete analysis of the role of angiotensin II has to take into account the prevailing sodium balance for a given level of angiotensin II and also its indirect action upon the sympathetic nervous system as well as other hormonal systems. A number of studies have provided evidence for an important role for the renin-angiotensin system in renovascular hypertension, malignant and severe hypertension, as well as in mild to moderate forms of essential hypertension.

Altered blood pressure profile, autonomic neuropathy and nephropathy in insulin-dependent diabetic patients.

To evaluate the relationship between autonomic neuropathy (AN) and nephropathy we measured 24-h blood pressure (BP) and overnight urinary albumin excretion (UAE) in 38 patients with insulin dependent diabetes mellitus (IDDM). Autonomic function was evaluated by the heart rate response to deep breathing. Valsalva maneuver, heart rate at rest and BP variation with posture. Sympathetic cutaneous reflex was also tested in both inferior and superior limbs. Patients with mean day diastolic BP (DDBP) < or = 90 mmHg without AN (N = 15) compared to 12 normal controls had similar BP values, but compared to those with DDBP < or = 90 mmHg and AN (N = 12) they had lower night diastolic BP (NDBP) (66 +/- 4.8 vs 72 +/- 8.8 mmHg: p < 0.05) and UAE (9.8 +/- 2.3 vs 107.2 +/- 3.5 micrograms/min; p < 0.001). No difference in DDBP was observed between these two diabetic groups (80 +/- 3.9 vs 83 +/- 6.1 mmHg). Of the 11 patients with DDBP > 90 mmHg, only three were free of AN and only two of the eight with AN where free of diabetic nephropathy. The percentage day/night changes in systolic BP were lower in patients with AN (13 vs 7.9%; p < 0.05) and were inversely related to autonomic score, used as an index of the degree of autonomic dysfunction (r = -0.48; p < 0.01) and to UAE (r = -0.39; p < 0.05). Furthermore, UAE correlated with autonomic score (r = 0.69; p < 0.0001) and with NDBP (r = 0.44; p < 0.01). Our results show that AN in IDDM patients is associated with a reduced nocturnal fall in BP and suggest a pathogenic role of autonomic dysfunction in the development of diabetic nephropathy, possibly favoring both BP elevation during the night and increases in intraglomerular pressure.

Effect of blood glucose on left ventricular mass in patients with hypertension and type 2 diabetes mellitus.

The aim of our prospective study was to evaluate the influence of blood glucose (BG) on left ventricular mass and diastolic function in patients with hypertension and type 2 diabetes mellitus (DM). Fifty-six hypertensive patients with type 2 DM and 26 healthy controls were investigated. They were submitted to echocardiography (ECHO) with Doppler and we calculated the mean of their fasting BG values, office blood pressure (OBP), cholesterol and fractions, and triglycerides during the previous 4 years. The diabetic patients were then followed-up for 1 year with OBP, fasting BG, and lipids measured every 2 months. After this period, the patients were again submitted to ECHO and in 22 patients (group I [GI]), reductions greater than 10% in left ventricular mass index (LVMI) were observed (122 +/- 35 v 89 +/- 23 g/m2, P < .01), whereas increases greater than 10% (group II [GII], n = 17) (94 +/- 18 v 115 +/- 27 g/m2, P < .01) or no changes (group III [GIII], n = 17) (98 +/- 16 v 99 +/- 18 g/m2, NS) in LVMI were detected in the remaining patients. The OBP values did not change during the follow-up. In GI the reduction of LVMI was associated with a BG fall from 178 +/- 36 to 147 +/- 30 mg/dL (P < .01) and a correlation was observed between BG and LVMI percent variations (delta) (r = 0.48, P < .01). No important changes in left ventricular diastolic function were observed during the follow-up. We concluded that the improvement in glycemic control may contribute to LVH regression in hypertensive patients with type 2 DM.

Contribution of vasopressin to orthostatic blood pressure maintenance in essential hypertension.

Arginine vasopressin (AVP) has been found to participate in blood pressure maintenance especially when other pressor systems are endogenously or pharmacologically impaired. The purpose of this study was to assess the pressor contribution of AVP to orthostatic blood pressure maintenance in otherwise healthy patients with essential hypertension. Twenty-seven patients were grouped according to age (young n = 13, elderly n = 14) and race (white n = 13, black n = 14). Integrity of autonomic nervous system (ANS) was assessed by Valsalva's maneuver, cold pressor test and head-up tilt. AVP contribution to blood pressure was estimated by the fall in mean arterial pressure in response to IV injection of 0.5 mg of a V1 AVP inhibitor (AVPi). Elderly subjects were found to have a mild (subclinical) ANS impairment as indicated by absence of bradycardia in phase 4 of Valsalva's maneuver and hypotension without concurrent tachycardia during head up tilt. Depressor responses to AVPi while subjects were in the upright position, were greater in elderly and blacks (-15 +/- 11 mm Hg and -15 +/- 12 mm Hg, respectively, P < .05) than young and whites (-8 +/- 6 and -7 +/- 6 mm Hg, respectively, ns). The greater importance of the AVP component in the elderly may be at least partially explained by a mild ANS impairement, whereas hormonal characteristics of hypertension in blacks may explain greater AVPi induced fall in mean arterial pressure. Our data show that both age and race influence the response to AVPi.

Diffusion-broadened velocity spectra of convection in variable-temperature BP-LED experiments.

When NMR diffusion experiments are performed at temperatures different from ambient temperature, temperature gradients due to probe design can cause thermal convection and therefore significantly affect the signal amplitude. Fourier transformation of the signal amplitude gives rise to a diffusion-broadened velocity spectrum, which contains information about the convection velocity. It is shown that when the diffusion broadening factor is smaller than the maximum velocity, the broadening has little effect on the determination of the maximum velocity. Thus, convection velocity can be determined in the presence of diffusion.

Toroid cavity detectors for high-resolution NMR spectroscopy and rotating frame imaging: capabilities and limitations.

The capabilities of toroid cavity detectors for simultaneous rotating frame imaging and NMR spectroscopy have been investigated by means of experiments and computer simulations. The following problems are described: (a) magnetic field inhomogeneity and subsequent loss of chemical shift resolution resulting from bulk magnetic susceptibility effects, (b) image distortions resulting from off-resonance excitation and saturation effects, and (c) distortion of lineshapes and images resulting from radiation damping. Also, special features of signal analysis including truncation effects and the propagation of noise are discussed. B(0) inhomogeneity resulting from susceptibility mismatch is a serious problem for applications requiring high spectral resolution. Image distortions resulting from off-resonance excitation are not serious within the rather narrow spectral range permitted by the RF pulse lengths required to read out the image. Incomplete relaxation effects are easily recognized and can be avoided. Also, radiation damping produces unexpectedly small effects because of self-cancellation of magnetization and short free induction decay times. The results are encouraging, but with present designs only modest spectral resolution can be achieved.

Influence of autonomic neuropathy upon left ventricular dysfunction in insulin-dependent diabetic patients.

BACKGROUND: Diabetic cardiomyopathy is a well-defined complication of diabetes that occurs in the absence of ischemic, vascular, and hypertensive disease. HYPOTHESIS: The study was undertaken to test the relationship among autonomic neuropathy (AN), 24-h blood pressure (BP) profile, and left ventricular function. METHODS: Nineteen type-1 diabetic patients underwent autonomic tests and echocardiographic examination. Patients were divided according to the presence (AN+) or absence (AN-) of AN. RESULTS: In the AN+ group (n = 8), the E/A ratio at echo was lower than in the AN- group (n = 11) (1.1 +/- 0.3 vs. 1.6 +/- 0.3; p < 0.005). Systolic and diastolic BP reductions during sleep were smaller in the AN+ than in the AN- group (6.6 +/- 6.6 vs. 13.0 +/- 4.3%; p < 0.03 for systolic and 12.8 +/- 6.8 vs. 20.0 +/- 4.0% for diastolic BP reduction; p < 0.03, respectively). Considering all patients, the E/A ratio correlated inversely with awake diastolic BP (r - 0.63; p = 0.005); sleep systolic BP (r - 0.48; p = 0.04), and sleep diastolic BP (r - 0.67; p = 0.002). The AN correlated with diastolic interventricular septum thickness (r 0.57; p = 0.01), sleep systolic BP (r 0.45; p = 0.05), sleep diastolic BP (r 0.54; p = 0.02), and correlated inversely with systolic and diastolic sleep BP reduction (r - 0.49; p = 0.03 and r - 0.67; p = 0.002, respectively). Finally, E/A ratio and AN score correlated between themselves (r - 0.6; p = 0.005). CONCLUSION: Our results suggest that left ventricular diastolic dysfunction may be detected very early in type-1 diabetic patients with AN. Parasympathetic lesion and nocturnal elevations in BP could be the link between AN and diastolic ventricular dysfunction.

Inhibition of central angiotensin I conversion by oral captopril.

1. The central action of captopril (D-3-mercapto-methylpropanoyl-L-proline, SQ 14225) in the rat was evaluated by measuring the effect of the orally administered drug on responses to angiotensin I given intracerebroventricularly. 2. The pressor and dipsogenic effects of angiotensin I (20 ng) injected into the third ventricle were reduced by about 50% for 4 h following the oral administration of captopril, 20mg/kg. Both responses returned to pretreatment control values 8 h after captopril administration. 3. Orally administered captopril affects the action of angiotensin I on the central nervous system thus providing an alternative explanation for the hypotensive effect of captopril. This effect if probably due to the direct passage of captopril through the blood brain barrier.