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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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 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

In order to investigate the role and origin of serum angiotensin I-converting enzyme activity (ACEA) in hypertension, the correlation between serum ACEA and the renin-angiotensin-aldosterone system was evaluated in hypertensive patients of whom 36 had essential hypertension, five had hypertension associated with chronic renal failure, three had renovascular hypertension, and one had primary aldosteronism. Serum ACEA was 17.0 +/- 3.3 U (mean +/- sd) in the normotensive control, 20.1 +/- 7.1 U in patients with essential hypertension, 11.6 +/- 3.4 U in patients with chronic renal failure, 31.7 +/- 1.1 U in patients with renovascular hypertension, and 9.7 U in primary aldosteronism in a recumbent state. There was a significant correlation between serum ACEA and plasma renin activity (PRA) (r = 0.615, p less than 0.001, n = 45) and plasma aldosterone concentration (PAC) (r = 0.599, p less than 0.001, n = 34) in a recumbent state. However, there was no significant correlation between serum ACEA and mean blood pressure. Serum ACEA elevated with furosemide and an upright posture significantly correlated with elevation in PRA (r = 0.369, p less than 0.05, n = 32) but did not significantly correlate with elevation in PAC. It is suggested, therefore, that the kidney is the suspected source of the plasma activity of the enzyme and that serum ACEA plays a possible role in the regulations of blood pressure and electrolyte metabolism modulating the renin-angiotensin-aldosterone system.
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PMID:[The correlation between serum angiotensin I-converting enzyme activity and the renin-angiotensin-aldosterone system in hypertensive patients (author's transl)]. 627 8

Bradykinin (BK) and [des-Arg9]-bradykinin (-9BK) concentrations in blood and urine samples from 18 normotensive subjects and 23 patients with low-renin essential hypertension were determined by radioimmunoassay. BK and -9BK levels in venous blood from normotensive subjects were 67.1 +/- 60.8 pg/ml and 204.1 +/- 44.5 (mean +/- S.D.), respectively, and levels in urine from normotensive subjects were 5.3 +/- 5.3 ng/ml and 1.6 +/- 1.2, respectively. The blood and urinary levels of BK and -9BK in low-renin essential hypertensives were not significantly different from those of normotensives and did not change when the hypertensives were treated with the new orally active angiotensin I-converting enzyme (ACE) inhibitor, enalapril (MK421). It has been proposed that BK levels do not change with ACE inhibition because under these conditions BK might be metabolized to -9BK by kininase I. Since -9BK levels did not increase with MK421 treatment, this possibility can be excluded. The absence of elevations in blood and urine BK and -9BK after administration of MK421 does not support an involvement of kinins in the mechanism of antihypertensive action of MK421 in these patients. On the basis of the data, it is not possible to exclude such an involvement, however, because local changes in kinin concentrations could occur that are not reflected by changes in circulating or urinary kinin levels.
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PMID:Immunoreactive bradykinin and [des-Arg9]-bradykinin in low-renin essential hypertension--before and after treatment with enalapril (MK 421). 631 33

The angiotensin I-converting enzyme inhibitor, captopril (SQ 14225) was proposed as first treatment in 12 cases of uncomplicated essential hypertension maintained on unrestricted sodium intake (group I). Arterial pressure was normalized in 7 patients (subgroup Ia) whilst hydrochlorothiazide was added to captopril in 5 patients (subgroup Ib). A significant dose-response curve between the dose of captopril (range 75 to 450 mg/day) and the antihypertensive effect was obtained with a maximum at 300 mg/day. In 8 patients (group II) hydrochlorothiazide was proposed first and the addition of captopril was necessary in 4 cases. No relationship between pretreatment PRA and the maximum effect of captopril was observed (r = -0.34, NS). No disturbance of upright blood pressure regulation was noted. Adverse reaction consisted of 4 cases of benign and spontaneously regressive skin rash or pruritus.
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PMID:[Effect of captopril in essential hypertension (author's transl)]. 702 49

Antihypertensive effect of an orally active angiotensin I-Converting enzyme inhibitor, SQ 14225 (Captopril) was assessed in 18 hypertensive patients, of whom 13 had essential hypertension, 2 had malignant hypertension, 2 had hypertension associated with chronic renal failure, and 1 had renovascular hypertension. Blood pressure decreased markedly not only in patients with high renin levels but also in those with low renin levels. Nevertheless, the magnitude of blood pressure reduction was correlated with the pre-treatment plasma renin activity (r =-0.64, p less than 0.01 systolic, r =- 0.60, p less than 0.05 diastolic). There was a significant correlation between the fall in mean blood pressure and the decrease in plasma aldosterone concentration 3 weeks after treatment (r = 0.64, p less than 0.05). The serum potassium elevated from 4.2 +/- 0.4 to 4.8 +/-0.9 mEq/L (p less than 0.05), and the change correlated inversely with the reduction of plasma aldosterone concentration (r = 0.71, p less than 0.02), while serum sodium slightly decreased from 140-+/- 2 to 138 +/- 3 mEq/L. There was neither finding of orthostatic hypotension nor escape from the antihypertensive effect. These results indicate that chronic inhibition of angiotensin I-converting enzyme with an orally active compound offers an effective and well-tolerated approach to treatment of hypertension.
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PMID:Antihypertensive effect of the oral angiotensin I-converting enzyme inhibitor in long-term treatment of hypertensive patients. 704 Jul 24

The effect of treatment with two different antihypertensive agents on the function of small arteries from 17 patients with essential hypertension randomly assigned to receive either the angiotensin I-converting enzyme inhibitor cilazapril or the beta-blocker atenolol was investigated. Subcutaneous small arteries obtained from gluteal fat biopsies were studied on a wire myograph before treatment and at 1 and 2 years of treatment. Blood pressure was mildly elevated in both groups of patients (mean, 150/100 mm Hg) and was well controlled throughout the 2 years of treatment (mean, 130/85 mm Hg). We previously reported, in arteries from patients treated with cilazapril, an improvement at 1 year of treatment of the vasoconstrictor effect of endothelin-1, which had been significantly attenuated in the untreated hypertensive patients compared with normotensive subjects. After 2 years of treatment, this normalization of endothelin-1 response was still present in small arteries of patients treated with the angiotensin I-converting enzyme inhibitor, whereas in patients treated with atenolol, responses were still unchanged after 2 years of treatment. Endothelial function was tested by examining the response of norepinephrine-precontracted arteries to acetylcholine. Untreated hypertensive patients exhibited a slightly but significantly blunted vasorelaxation in response to 10 mumol/L acetylcholine compared with normotensive subjects. After 1 and 2 years of effective antihypertensive treatment, cilazapril-treated patients exhibited responses to acetylcholine that were not different from those of normotensive subjects, whereas atenolol-treated patients still had impaired responses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of effects of angiotensin I-converting enzyme inhibition and beta-blockade for 2 years on function of small arteries from hypertensive patients. 772 19


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