Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the angiotensin-converting enzyme inhibitor captopril on blood pressure, heart rate, plasma prolactin, and renin activity were examined in a single-blind, placebo-controlled trial on 30 patients with essential hypertension (15 given drug, 15 placebo). Captopril, 25 mg administered orally, reduced the blood pressure and increased the plasma renin activity. Captopril decreased mean plasma prolactin from 17.5 +/- 1.4 ng/mL to 9.1 +/- 1.0 ng/mL (p less than 0.001). Significant correlation was found between captopril-induced change from control values of plasma prolactin (delta plasma prolactin) vs delta plasma renin activity (r = -0.688, p less than 0.001). These results suggest that acute administration of captopril was accompanied by a reduction in plasma prolactin and that this reduction may be of clinical significance during therapy of hypertension.
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PMID:Effect of captopril on plasma prolactin in patients with essential hypertension. 219 85

The effect of single dose (50 mg) Captopril (C) used either alone or associated to diuretics (50 mg hydrochlorothiazide -HCTI) in the treatment of mild-moderate essential arterial hypertension was studied in a multicentric study. Eighty eight patients were chosen. After a minimum of 4 month follow-up period 53.4% responded (BDP less than 95 mm Hg) to single dose C (group 1:47 patients), 89.77% to 50 mg C in single dose together with 50 mg HTIT (group 2: 32 patients), 95.45% of two 50 mg doses of C and 50 mg HCIT (group 3: 5 patients), and 97.72% responded to 3 doses of C and 50 mg of HCTI (group 4: 2 patients). The decrease in blood pressure values was statistically significant (p, 000, Wilcoxon test) in groups 1 and 2, having a mean decrease in blood pressure (BP) of 14%. In group 1 (n = 42) the SBP which initially was 165.72 +/- 11.32, decreased to 148.28 +/- 11.5 and the DBP decreased from 101.55 +/- 5.68 to 87.28 +/- 6.59. In group 2 (n = 32) the SBP decreased from 173.50 +/- 14.08 to 152.44 +/- 20.8 and the DBP from 103.34 +/- 5.29 to 87.47 +/- 6.39. The response to monotherapy could not be statistically correlated either to early essential hypertension or to the patients age. Treatment was discontinued in three cases due to the secondary effects, cough, ageusia and nervousness, showing the remaining patients a good tolerance. No changes were observed in the analytical parameters. This study shows the usefulness and tolerance of single dose C as the initial treatment of mild to moderate essential hypertension.
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PMID:[Captopril in single doses in the treatment mild-moderated arterial hypertension]. 219 35

Captopril given for 5 days to normotensive subjects caused a significant fall in blood pressure. The fall in blood pressure was greater on a low sodium diet (19.6%) and less on a high sodium diet (11%) whereas on a normal sodium intake it was 16.5%. This fall in blood pressure was related to the initial level of angiotensin II and the fall in angiotensin II and was also associated with large falls in plasma aldosterone and, on the normal sodium intake, a loss of sodium that amounted to approximately 140 mmol/normal subject studied over the 5 days. Patients with essential hypertension who were studied on their normal diets had a similar fall in blood pressure for a given plasma renin activity. Angiotensin converting enzyme inhibitors are therefore used in hypertension not because they are specific for patients with high blood pressure but because they are effective in lowering blood pressure in both normotensive and hypertensive subjects and cause few side effects. They are also particularly effective when used in conjunction with sodium restriction, diuretics, or calcium entry antagonists but less effective when combined with a beta-blocker.
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PMID:Why use angiotensin converting enzyme inhibitors to lower blood pressure? 241 21

Blood pressure, diameter, volume distensibility, and compliance of brachial artery were measured noninvasively in patients with sustained essential hypertension before and after Captopril in 11 patients and before and after isosorbide dinitrate (ISDN) in 11 other patients. Both drugs caused a similar significant decrease in mean arterial pressure (MAP) (p less than 0.001) and increase in arterial compliance (p less than 0.001), defined as the product of arterial volume by distensibility. ISDN increased arterial compliance through a dominant increase in arterial diameter (0.524 +/- 0.029 vs. 0.455 +/- 0.022 cm; p less than 0.001) and hence volume, whereas Captopril increased compliance through an increase in volume distensibility (0.20 +/- 0.02 vs. 0.12 +/- 0.02% change volume/mm Hg; p less than 0.001) with minimal changes in arterial diameter. The study provided evidence that of the two vasodilating drugs, ISDN and Captopril, only Captopril caused a predominant pharmacological relaxing effect on the wall of hypertensive human brachial arteries studied in situ.
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PMID:Comparative effects of captopril and isosorbide dinitrate on the arterial wall of hypertensive human brachial arteries. 243 55

Patients with essential hypertension were studied to clarify the role of the kallikrein-kinin system in the hypotensive actions of angiotensin I converting enzyme inhibitors. Captopril, alacepril, ramipril, and altiopril administered in single doses rapidly decreased blood pressure and plasma angiotensin II levels, and increased plasma and urinary kinins as well as plasma renin activity. Following administration of captopril for 14 days, similar effects were observed. Urine volume and urinary sodium excretion were augmented after acute and chronic administration of captopril. The patients who received ramipril and altiopril were divided into renin subgroups. In the normal-renin group, the change in blood pressure was accompanied by an increase in plasma kinin level and a decrease in plasma angiotensin II level. However, in the low-renin group, although these drugs reduced blood pressure and increased plasma kinin, no significant change was observed in plasma angiotensin II levels. These findings suggest that (a) in patients with normal renin activity, the hypotensive effect of converting enzyme inhibitors might be caused by an increase in plasma kinin and a decrease in plasma angiotensin II, but in the low-renin group, the increase in plasma kinin levels may be more important; and (b) the augmentation of urine volume and urinary sodium excretion may also be related to the hypotensive effects of the converting enzyme inhibitors during long-term administration.
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PMID:Role of kallikrein-kinin system in the hypotensive mechanisms of converting enzyme inhibitors in essential hypertension. 247 7

We investigated the possibility that angiotensin II (ANGII) augments the sensitivity of the pituitary to corticotropin releasing factor (CRF) by comparing, in patients with essential hypertension, the responses of plasma adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin activity to a bolus injection of either 0.5 or 1.0 microgram/kg of synthetic ovine CRF in control conditions and after chronic treatment with the converting enzyme inhibitor captopril to block the formation of ANGII; the effects of CRF were examined up to 4 h after its administration. In control studies, we found that the two doses of CRF induced similar increments in ACTH and cortisol, the levels of which remained elevated throughout the studies; these changes were associated with increments in plasma aldosterone that were dose dependent, less pronounced, and of shorter duration and with a slight decrease in plasma renin activity. Captopril treatment increased basal plasma renin activity and lowered plasma aldosterone while leaving basal ACTH and cortisol unchanged. During converting enzyme inhibition, the responses of ACTH and cortisol to CRF were similar to those observed in control studies, whereas the changes in plasma aldosterone and plasma renin activity were, respectively, smaller and greater. From these results, it appears that during ANGII blockade the sensitivity of ACTH to CRF stimulation is unaffected, whereas that of the adrenals to ACTH is selectively reduced at the level of the zona glomerulosa.
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PMID:Effects of angiotensin II blockade on the responses of the pituitary-adrenal axis to corticotropin-releasing factor in humans. 248 58

This study was undertaken to further clarify the role of kallikrein-kinin and renin-angiotensin systems in the hypotensive mechanisms of the angiotensin-I converting enzyme inhibitor by using highly sensitive and specific radioimmunoassays in patients with essential hypertension. Captopril was administered for 14 days (chronic effect), and the acute effects of captopril, alacepril and ramipril were also studied in the in-patients with essential hypertension. All of these converting enzyme inhibitors rapidly decreased the blood pressure and plasma angiotensin II levels, and increased plasma and urinary kinin and plasma renin activity in the acute effect. Following the administration of captopril for 14 days, these decreases and increases were maintained. The change of blood pressure was significantly correlated negatively with that of plasma kinin levels and positively with that of plasma angiotensin II levels in both the acute and chronic effect of converting enzyme inhibitors. Urine volume and urinary sodium excretion were markedly augmented, while both the change of urine volume and that of urinary sodium excretion were negatively correlated with the change of blood pressure in the chronic effect. These findings suggest that the hypotensive effect of converting enzyme inhibitors might be caused by an increase of plasma kinin and a decrease of plasma angiotensin II, and in part by an augmentation of urine volume and urinary sodium excretion. In this drug treatment, the renal kallikrein-kinin system may also play some role in the increase of urine volume and urinary sodium excretion through the increased kinin in the kidney.
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PMID:Significance of kallikrein-kinin and renin-angiotensin systems in the hypotensive mechanism of angiotensin-I converting enzyme inhibitors in essential hypertensives. 253 50

Angiotensin converting enzyme (ACE) generates angiotensin II and is also capable of degrading bradykinin into inactive peptides. It has been suggested that the effects of ACE inhibitors are partially mediated by increased prostaglandin synthesis induced by a simultaneous rise in bradykinin. Captopril increases PG excretion and indomethacin (INDO) attenuates its effects. Enalapril is a long acting ACE inhibitor, and its molecule does not have the sulphydryl group present in captopril. In order to evaluate the participations of PG in a the ENA effects of enalapril (ENA) on arterial pressure (AP), plasma renin activity (PRA), plasma aldosterone (ALDO) and renal hemodynamics (RH) in essential hypertension (EHT), we compared the effects of ENA alone and associated with INDO. Nine EHT patients received on different occasions: ENA 10 mg, INDO 25 mg and ENA-INDO. Arterial pressure, PGE2, ALDO, PRA, RH and plasma and urinary ENA as enalaprylate were measured after each treatment. Maximal ENA absorption occurred after 4 hours, however it was still detectable after 72 hr. ENA decreased AP after 6 hr in spite of unchanged PGE2 excretion; PRA did not change and ALDO decreased transiently. INDO delayed ENA absorption, slightly attenuated the fall in AP and suppressed PGE2 excretion when given with ENA. INDO alone suppressed PGE2 and did not alter AP. No significant changes occurred in RH with the treatments. Our results suggest that the antihypertensive effect of ENA is independent of PG, and that the slight attenuation induced by INDO may be attributed to a delay in intestinal absorption. In EHT patients under normovolemic conditions, renal function is not altered by ACE inhibition.
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PMID:[Role of prostaglandins in the antihypertensive effect of the converting enzyme inhibitor, enalapril]. 256 Oct 22

A study was made of the effect of a single intake of captopril on the neurohumoral mechanisms of the regulation of renal circulation in 25 patients with essential hypertension (EH). Captopril induced an increase of the effective renal blood flow (ERB) and of the effective renal plasma flow along with a considerable lowering of the renal vascular resistance. No relationship was found between these changes and the time course of changes in the activity of plasma renin, aldosterone and vasopressin concentration in blood plasma. The relationship was established between the changes in the ERB and the time course of changes in baroreceptor sensitivity that significantly increased in the majority of EH patients under the effect of captopril.
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PMID:[Neurohumoral mechanisms regulating renal blood circulation in patients with hypertension undergoing captopril block of angiotensin-converting enzyme]. 257 61

The usual regimens of captopril--twice or thrice daily administration--are based on the duration of the decrease in plasma angiotensin II induced by captopril. In a study performed to evaluate the hypotensive effect of once daily captopril, 13 white patients with mild-to-severe uncomplicated hypertension were treated with one tablet of captopril 100 mg daily, taken 1-1.5 h before lunch, for 8 weeks. Arterial blood pressure was measured weekly, 22-23.5 h after medication. The patients' diet contained no more than 120 mmol/day of sodium. In the first week supine blood pressure fell from 210 +/- 3/128 +/- 4 (mean +/- SEM) to 179 +/- 5/116 +/- 5 mm Hg (p less than 0.001/p less than 0.01 compared with pretreatment). After the large decrease in the first week changes in systolic and diastolic pressures tailed off; they tended to fall towards stable values that would be maintained on prolonged treatment. At the end of the eighth week the supine values were 155 +/- 3/104 +/- 3 (p less than 0.001/p less than 0.001). Changes in erect blood pressure paralleled those in the supine posture. No side effects were detected. These results confirm that captopril is efficacious when given alone to patients with essential hypertension who are taking a low sodium diet. Blood pressures were not, however, reduced to normotensive levels. Captopril's hypotensive effect in once daily administration appears to be independent of its effects on circulating angiotensin II. Captopril alone 100 mg/day is thus indicated in essential hypertension and should be prescribed once daily to obtain the best possible compliance.
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PMID:Once-daily administration of captopril and hypotensive effect. 258 Jan 69


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