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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of hydralazine (3 mg/kg) and the angiotensin I-converting enzyme (ACE) inhibitor captopril (SQ 14,225) (100 mg/kg) on mean arterial blood pressure, plasma renin activity, urinary volume and urinary Na+,K+, and aldosterone concentrations were examined in spontaneously hypertensive rats of the Okamoto and Aoki strain (SHR) after oral daily dosing for 2 weeks, 3 or 6 months. Captopril caused progressive cumulative reductions in blood pressure resulting in normalization of pressure after 6 months of dosing. Hydralazine also significantly reduced blood pressure but not to the level of normotensive rats of the Wistar-Kyoto strain (WKY). Reductions in heart size paralleled the changes in blood pressure, normalization of cardiac hypertrophy occurring after captopril but not hydralazine. Plasma renin activity increased approximately 2-3 fold after hydralazine and 15-fold after captopril. Neither hydralazine nor captopril had any consistent effects on 24-hr urine volume, urinary Na+,K+ or aldosterone excretion. These results indicate that chronic inhibition of ACE with captopril induces normalization of blood pressure in SHR, a normal-renin model of hypertension.
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PMID:Effects of chronic treatment with captopril (SQ 14,225), an orally active inhibitor of angiotensin I-converting enzyme, in spontaneously hypertensive rats. 23

To evaluate the relationship between urinary albumin excretion and left ventricular hypertrophy in essential hypertension, we studied, cross-sectionally, 64 subjects with essential hypertension and no diabetes. Urinary albumin excretion and Sokolow index correlated significantly (r = 0.483; P = 0.0001). Five subjects were positive for microalbuminuria (> 30 mg/24 h) and Sokolow index (> 35 mm); 43 were negative for both, with a concordance rate of 77 percent (chi-squared test 11.1; P = 0.0009). Stepwise multivariate regression analysis indicated two independent determinants for urinary albumin excretion: Sokolow index (F = 18.29), and diastolic blood pressure (F = 12.23). The relationships between urinary albumin excretion, Sokolow index, and blood pressure were not different in the 18 subjects taking angiotensin I-converting enzyme inhibitors and in the 46 others. The close relationship between urinary albumin excretion and Sokolow index observed in this study suggests that left ventricular hypertrophy due to hypertension may account for the increased cardiovascular mortality observed in non diabetic subjects with microalbuminuria.
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PMID:[Microalbuminuria and left ventricular hypertrophy in essential arterial hypertension. A study in non-diabetic patients]. 143 89

To test the effect of converting enzyme inhibition (CEI) on diabetes, with or without renal insufficiency, we studied streptozotocin-induced diabetic rats, with or without reduced renal mass, which were treated with insulin in sufficient amounts to maintain glucose values in the mild to moderately hyperglycemic range. We found that diabetes increased glomerular filtration rate (GFR) (inulin clearance, 2.3 +/- 0.5 ml/min vs 1.9 +/- 0.1 ml/min; p < 0.05) and blood pressure (137 +/- 15 mm Hg vs 116 +/- 6 mm Hg; p < 0.05) but did not increase plasma atrial natriuretic peptide (ANP) values, when compared with control rats (72 +/- 38 vs 68 +/- 24 pg/ml). CEI decreased GFR and blood pressure to control values. In rats with diabetes and concomitantly reduced renal mass, hypertension, elevated ANP values, proteinuria, and glomerulosclerosis were prominent features. CEI was associated with reduced blood pressure (172 +/- 17 mm Hg vs 138 +/- 15 mm Hg; p < 0.05), without a concomitant decrease in GFR (1.1 +/- 0.1 ml/min vs 1.1 +/- 0.1 ml/min). Further, CEI reduced the elevated ANP values (140 +/- 34 pg/ml vs 66 +/- 19 pg/ml; p < 0.05) to those of control rats. CEI reduced proteinuria by 50% and ameliorated the histopathologic changes. In separate experiments, rats with 5/6th nephrectomy and hypertension but without diabetes were also found to have elevated ANP levels that decreased to control values with CEI. The data speak for a renal protective effect of angiotensin I-converting enzyme inhibition in this model but do not support a specific role for ANP in the model of diabetes with concomitantly reduced renal mass.
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PMID:Effects of angiotensin-converting enzyme inhibition in diabetic rats with reduced renal function. 145 98

The spontaneously hypertensive rat and the stroke-prone spontaneously hypertensive rat are useful models for human hypertension. In these strains hypertension is a polygenic trait, in which both autosomal and sex-linked genes can influence blood pressure. Linkage studies in crosses between the stroke-prone spontaneously hypertensive rat and the normotensive control strain Wistar-Kyoto have led to the localization of two genes, BP/SP-1 and BP/SP-2, that contribute significantly to blood pressure variation in the F2 population. BP/SP-1 and BP/SP-2 were assigned to rat chromosomes 10 and X, respectively. Comparison of the human and rat genetic maps indicates that BP/SP-1 could reside on human chromosome 17q in a region that also contains the angiotensin I-converting enzyme gene (ACE). This encodes a key enzyme of the renin-angiotensin system, and is therefore a candidate gene in primary hypertension. A rat microsatellite marker of ACE was mapped to rat chromosome 10 within the region containing BP/SP-1.
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PMID:Chromosomal mapping of two genetic loci associated with blood-pressure regulation in hereditary hypertensive rats. 165 69

The effects of a new angiotensin I-converting enzyme inhibitor (ACEI), enalapril via sublingual was studied in 16 patients (median age 60.5 +/- 8.7 years). 10 were female and 6 male with hypertension crisis defined as systolic pressure (SP) greater than or equal to 220 mmHg and/or diastolic pressure greater than or equal to 120 mmHg (DP). We observed a significant decrease of SP and DP 20 min after the enalapril administration, without affecting the cardiac rate (p less than 0.001). This decrease was maintained during 30 and 60 min (p less than 0.001). Secondary effects were not observed. We concluded that sublingual enalapril can be a useful drug in hypertension crisis when not an urgent life compromising situation in elderly patients, because of its gradual hypotensive and maintained effect, allowing the commencement of an oral treatment.
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PMID:[Sublingual enalapril in hypertensive crisis. A preliminary study]. 256 44

The occurrence of neurologic abnormalities is described in a series of nine infants with chronic hypertension, in whom antihypertensive therapy decreased BP markedly and for a prolonged period, although to levels often within the normal range. All infants had mean systolic BPs greater than 113 mm Hg and elevated renin values to a mean of 134 +/- 128 ng/mL/h. Antihypertensive therapy, such as captopril, an inhibitor of angiotensin I-converting enzyme, consistently lowered the systolic BP by 20% from baseline per dose. However, the nine infants exhibited a total of 17 episodes of striking decreases in systolic BP of greater than 40% from baseline; the markedly decreased systolic BP values were usually within the normal range for corrected age. Seven of the 17 episodes were characterized by marked decrease in systolic BP, ie, decreased by 57% +/- 10%, and were prolonged, ie, remained at the lower values for 17 +/- 6 hours despite therapeutic interventions. These seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/h) and neurologic abnormalities (ie, seizures). In the remaining ten episodes, the systolic BP decreased by 50% +/- 8%, but the decreases were relatively brief, ie, remained at the lower values for 2.8 +/- 2 hours. These briefer episodes were not accompanied by renal or neurologic signs. These data indicate a particular vulnerability of the cerebral and renal circulation in premature infants with chronic hypertension to decreases in systolic BP to levels that would otherwise be considered in the normal range. The findings suggest that adaptive responses in both cerebral and renal blood flow are altered by chronic hypertension in such infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurologic complications of captopril treatment of neonatal hypertension. 264 19

Capillary hypertension is suggested to be the underlying cause of microvascular disease affecting the kidney, the retina, and other organs and tissues in diabetic patients and animals. Hyperglycemia causes an expansion of extracellular volume, which induces a vasodilatory response. Hemodynamic adaptation to vasodilation leads to an increase in intracapillary hydraulic pressure, which subsequently causes vascular damage. In experimental animals, restoration of capillary pressure to normal levels by ingestion of a low-protein diet or administration of an angiotensin I-converting enzyme inhibitor has been shown to prevent microvascular damage in the kidney, and dietary protein restriction limits injury in the retina as well. Atrial natriuretic peptide, which is secreted by atrial myocytes in response to volume expansion, may be involved in mediation of the hemodynamic adaptation (vasodilatory response) that results in diabetic microvascular disease.
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PMID:Influence of antihypertensive therapy on development and progression of diabetic glomerulopathy. 297 86

The acute antihypertensive effect of a new long-acting oral angiotensin I-converting enzyme (ACE) inhibitor, enalapril maleate, was assessed in 20 hypertensive patients, of whom 14 had essential hypertension, 4 had renovascular hypertension, one had hypertension associated with chronic renal failure, and one had primary aldosteronism. Enalapril maleate significantly lowered the blood pressure in either low-renin or normal- and high-renin hypertensives. There was a significant correlation for all patients as a group between the pretreatment levels of serum ACE activity and the reduction in mean blood pressure (r = -0.454, p less than 0.05, n = 20) 2 h after drug administration. The serum ACE activity decreased maximally 3 to 4 hours after drug administration and did not return to baseline levels within 24 h. There was a significant correlation between the reduction in mean blood pressure and changes in ACE activity 90 min and 2 h after drug administration, respectively, for all patients as a group (r = 0.495, p less than 0.05, n = 20, at 90 min; r = 0.508, p less than 0.05, n = 20, at 2 h). The plasma renin activity (PRA) significantly increased in normal- and high-renin hypertensives but not in low-renin hypertensives. There was a close correlation between the reduction in mean blood pressure and the PRA 8 h after drug administration in normal- and high-renin patients (r = -0.623, p less than 0.05, n = 13), while no such relationship was observed in low-renin patients. The plasma aldosterone concentration (PAC) significantly decreased within 3 h, the lowest values occurring at 8 h after drug administration, and it returned to baseline levels within 24 h in all patients. No relationship was found between the reduction in mean blood pressure and changes in PAC after drug administration in either low-renin or normal- and high-renin hypertensives. The plasma bradykinin concentration (PBC) increased within 1 h, the highest values occurring at 3 h after drug administration, and returned to baseline levels within 24 h in low-renin hypertensives, while the PBC was significantly increased at 4 h and had not returned to baseline levels within 24 h in normal- and high-renin hypertensives. There was a significant correlation between percentage changes in mean blood pressure and those in PBC 90 min after drug administration in normal- and high-renin hypertensives (r = -0.556, p less than 0.05, n = 13), while no relationship was observed between them in low-renin hypertensives.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The acute effects of the new angiotensin I-converting enzyme inhibitor, enalapril maleate, on blood pressure, plasma renin, aldosterone and kinins in hypertensive patients]. 299 Oct 35

Enalapril (MK-421) was administered orally as a single dose of 2.5, 5.0, 10 and 20 mg to 13 patients with either essential or renovascular hypertension. At these doses, enalapril produced a moderate reduction in both supine and standing blood pressure as well as a significant reduction in angiotensin I-converting enzyme activity, an increase in peripheral plasma renin activity and a decrease in plasma aldosterone concentration 4 to 8 hours after administration of the drug. Plasma levels of prostaglandins E1 and E2 were unchanged. The calculated ratio of urinary Na/K was increased in the patients with renal artery stenosis after enalapril. Creatinine clearance was increased in the patients with essential hypertension and reduced in the patients with renal artery stenosis. No adverse effects occurred in these patients treated with single doses of enalapril.
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PMID:Effect of enalapril on renin, angiotensin converting enzyme activity, aldosterone and prostaglandins in patients with hypertension. 299 32

The present study was designed to clarify the role of serum angiotensin I-converting enzyme (ACE) in the occurrence and maintenance of hypertension in essential hypertension (EH). For this purpose, following experiments were carried out: 1) Correlations between serum ACE activity and renin activity (PRA), aldosterone concentration (PAC) and bradykinin concentration (PBC) in plasma, and blood pressure (BP) as well as serum creatinine levels. 2) Circadian rhythm of serum ACE activity. and 3) Effect of furosemide, upright posture, both furosemide and upright posture, propranolol, indomethacin, 9 alpha-fluorocortisol or angiotensin II (A-II) on the serum ACE activity, PRA, PAC and circulating plasma volume (CPV). The following results were obtained: The serum ACE activity was 30.2 +/- 5.0 U/ml (means +/- SD) in EH as a group, which was significantly higher than that (27.3 +/- 3.9 U/ml) in age matched normotensive subjects (NT) (p less than 0.001). While there was no significant difference in the enzyme activity between low-renin EH (LREH) and NT, a significant difference was found between normal- (NREH) or high-renin EH (NREH) and NT (p less than 0.05 for NREH, p less than 0.01 for HREH). A negative correlation was observed between enzyme activity and age in EH (r = -0.221, 0.05 less than p less than 0.10) as well as in NT (r = -0.306, p less than 0.05). No significant relationships were observed between enzyme activity and BP in either EH or NT. There was a significant positive correlation between enzyme activity and PRA in NT. (r = 0.501, p less than 0.001), NREH (r = 0.658, p less than 0.001) and HREH (r = 0.695, p less than 0.001). However, no significant relationship was found between them in LREH. The enzyme activity was significantly correlated to PAC in NT (r = 0.368, p less than 0.01), NREH (r = 0.567, p less than 0.001) and HREH (r = 0.529, p less than 0.01), but not in LREH. Although no significant correlation was observed between enzyme activity and PBC in NT, NREH and HREH, a significant relationship was found in LREH (r = -0.460, 0.05 less than p less than 0.10). The enzyme activity was not related to serum creatinine levels in EH as well as in NT. In NT, the serum levels of ACE activity reached a maximum values at 6:00 a.m. or 9:00 a.m., and gradually decreased between 6:00 p.m. and 3:00 a.m. An almost similar circadian rhythm of enzyme activity was found in EH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical significance of serum angiotensin I-converting enzyme in essential hypertension]. 300 63


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