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

Captopril is an inhibitor of angiotensin I converting enzyme and is used for treating intractable chronic hypertension. However, the use of captopril during pregnancy is limited because of reported fetal and neonatal side effects. This study explored the efficacy of sublingual captopril in postpartum management of severe preeclampsia. Captopril controlled the systolic and diastolic pressures within normal range in two patients. The other three patients responded moderately and were switched to hydralazine, clonidine, or nifedipine after 12 hours. The systolic and diastolic pressures of these three patients remained moderately elevated over the 24-hour duration of the study while their pulse rates increased. Captopril did not significantly increase the pulse rate in any of the patients studied, and no other side effects were noted. All patients had normal pressures at their 2- and 6-week postpartum check-up. We conclude that sublingual captopril may be used safely and effectively in managing postpartum hypertension in patients with severe preeclampsia.
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PMID:Captopril in severe preeclampsia. 195 84

The effect of chronic angiotensin I converting enzyme inhibition on the pressure-natriuresis relation was studied in Wistar-Kyoto and spontaneously hypertensive rats. Enalapril maleate (25 mg.kg-1.day-1 in drinking water) was started at 4-5 weeks of age. At 7-9 weeks of age, the pressure-natriuresis relation was studied while the rats were under Inactin anesthesia 1 week after the right kidney and adrenal gland were removed. Neural and hormonal influences on the remaining kidney were fixed by surgical renal denervation, adrenalectomy, and infusion of a hormone cocktail (330 microliters.kg-1.min-1) containing high levels of aldosterone, arginine vasopressin, hydrocortisone, and norepinephrine dissolved in 0.9% NaCl containing 1% albumin. Changes in renal function resulting from alterations in renal artery pressure were compared between enalapril-treated and control rats. Mean arterial pressure (+/- SEM) under anesthesia was 118 +/- 5, 94 +/- 4, 175 +/- 3, and 124 +/- 2 mm Hg for control Wistar-Kyoto (n = 10), enalapril-treated Wistar-Kyoto (n = 10), control spontaneously hypertensive (n = 9), and enalapril-treated spontaneously hypertensive (n = 9) rats, respectively. When renal artery pressure was set at values above approximately 125 mm Hg, control spontaneously hypertensive rats excreted less sodium and water than control Wistar-Kyoto rats. Enalapril treatment resulted in a significant and similar shift to the left of the pressure-natriuresis relation in both strains of rats so that a lower renal artery pressure was required to excrete a similar amount of sodium when compared with their respective untreated controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jan
PMID:Effect of enalapril treatment on the pressure-natriuresis curve in spontaneously hypertensive rats. 198 83

Changes in our concepts of angiotensin I converting enzyme are reviewed briefly. The actions of this enzyme go beyond liberating angiotensin II from angiotensin I or inactivating bradykinin. Its very wide distribution in the body and its activity in vitro indicate involvement in the metabolism of other biologically active peptides. The recent molecular cloning of the human enzyme confirmed the existence of a hydrophobic C-terminal peptide that forms the short transmembrane domain of this plasma membrane-bound enzyme. The much longer external portion contains two homologous active site domains but probably only one functional active center. Finally, in spite of the great progress made in studying angiotensin converting enzyme, there are many challenging problems waiting to be solved.
Hypertension 1990 Oct
PMID:Angiotensin I converting enzyme and the changes in our concepts through the years. Lewis K. Dahl memorial lecture. 217 Feb 73

Global cerebral ischemia (four vessel model) was induced in renovascular hypertensive rats (two kidney, one clip model) chronically treated with intraperitoneal administration of angiotensin I converting enzyme inhibitors, either captopril (100 mg/kg per day) or Wy-44,655 (10 mg/kg per day). Mortality following cerebral ischemia was higher in renovascular hypertensive rats than in normotensive controls. Reduction of blood pressure with captopril or Wy-44,655, lowered mortality. In surviving renovascular hypertensive and normotensive rats cerebral ischemia induced hyperactivity and lesions of the CA1 area of the hippocampus. Prolonged treatment with captopril--but not with Wy-44,655--reduced hyperactivity and the extent of the CA1 lesions. In conclusion, hypertension increases mortality following cerebral ischemia but does not affect the extent of brain injury in survivors. Prior treatment with converting enzyme inhibitors lowers mortality. Treatment with captopril attenuates brain injury in survivors.
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PMID:The angiotensin I converting enzyme inhibitors, captopril and Wy-44,655 attenuate the consequences of cerebral ischemia in renovascular hypertensive rats. 220 71

The influence of aprotinin as a kallidinogenase inactivator on the antihypertensive effect of angiotensin I converting enzyme inhibitor (CEI) was studied in two-kidneyed and one-clipped hypertensive rats. Sixteen two-kidneyed and one-clipped hypertensive rats and sham-operated normotensive rats were prepared for this experiment. They were divided into two groups: those with the aprotinin infusion and those without. The effects of the oral administration of CEI were compared as regards mean arterial pressure (MAP) and urinary kallikrein activity (UKA). In 8 hypertensive rats under glucose infusion, MAP fell from 184.4 +/- 4.5 to 106.3 +/- 5.2 mm Hg, and UKA changed from 1.37 +/- 0.18 nkat/12 h to 0.61 +/- 0.11 nkat/12 h after the administration of CEI. In the remaining hypertensive rats under aprotinin infusion, MAP decreased from 175.0 +/- 3.0 to 140.6 +/- 5.1 mm Hg, and UKA slightly changed from 0.72 +/- 0.25 nkat/12 h to 0.59 +/- 0.12 nkat/12 h. Thus, the decrease of MAP after the administration of CEI was suppressed by the aprotinin infusion, and this significant difference was supported by the decrease of UKA. As for 16 normotensive rats, CEI did not alter MAP, nor did aprotinin have any effect on it. However, UKA tended to decrease after the administration of CEI. These results suggest that both the kallikrein-kinin system and the renin-angiotensin system play an important role in the maintenance of high blood pressure in two-kidneyed and one-clipped chronically hypertensive rats.
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PMID:Role of the kallikrein-kinin system in two-kidneyed and one-clipped hypertensive rats. 243 36

Intrarenal administration of angiotensin I converting enzyme (ACE) inhibitors carried out in norepinephrine- (NE; 2-4 micrograms/kg per min) or in angiotensin II- (ANG II; 60-90 ng/kg per min) induced acute hypertension in conscious unrestrained rabbits. Intrarenal administration of captopril (5 mg/kg) and MK-422 (1 mg/kg) caused no significant effect when injected intravenously. However, it showed a prompt and marked depressor effect in NE- but not in ANG II-induced hypertension. This effect was not observed after intrarenal infusion of saralasin (2 and 10 micrograms/kg per min) in NE-induced hypertension. While pretreatment with aprotinin or indomethacin failed to inhibit the depressor action, 2-bromoethylamine hydrobromide (BEA), which is known to induce necrosis of the renal papilla, produced complete abolition of the depressor effect of an intrarenal injection of MK-422 in NE-induced hypertension. These results indicate that the kidney plays an important role in the depressor action of ACE inhibitors in NE- but not in ANG II-induced acute hypertension, and that this effect may be related to the potentiation of antihypertensive renomedullary lipids rather than the inhibition of the renin-angiotensin system or the potentiation of bradykinin or prostaglandins.
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PMID:The renal antihypertensive effect of angiotensin I converting enzyme inhibitors. 244 69

The author reviews contemporary views on the pathogenetic participation of selected humoral factors (of the renin-angiotensin-aldosterone system, natriuretic hormone and atrial natriuretic factor) in the development of arterial hypertension in humans. Hypertension may be due to absolute or relative excess of factors with a pressor and antinatriuretic action or to deficiency of depressor and natriuretic substances. In essential hypertension and the majority of other types of hypertension the position is more complicated. Humoral substances are there involved in a complex way in dynamic interaction with other genetic, nervous, cardiovascular and other mechanisms. Investigation of humoral substances has helped to elucidate the causes of endocrine-hypertension, to expand our knowledge on the multifactorial genesis of essential hypertension, to differentiate its subtypes, and it led also practical therapeutic outcome such as the use of inhibitors of the angiotensin I converting enzyme or spirolactone.
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PMID:[Humoral mechanisms in the pathogenesis of arterial hypertension with emphasis on the renin-angiotensin-aldosterone system and natriuretic substances]. 252 99

Renal artery stenosis is one of the most important forms of secondary hypertension. For years, the only causative treatment was nephrectomy. With rapid advances in cardiovascular and transplantation surgery, operative procedures in renovascular hypertension become more and more sophisticated. Revascularization is superior to medical management of renovascular hypertension in terms of preserved renal function. In recent years, surgical result have been excellent, and even patients with rather complex forms of renovascular hypertension have been successfully operated upon. New classes of antihypertensive drugs, particularly beta-blockers and angiotensin I converting enzyme inhibitors, have enabled the control of blood pressure in most patients with renovascular hypertension but do not assure preservation of renal function. Finally, a fascinating technique, the percutaneous transluminal renal angioplasty, has rapidly advanced to become one of the most popular methods in the treatment of hypertension secondary to renal artery stenosis. However, percutaneous transluminal renal angioplasty is the treatment of choice for most nonostial, nonocclusive lesions.
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PMID:[Renovascular hypertension]. 252 91

The influence of chronic treatment with the angiotensin I converting enzyme (ACE) inhibitor enalapril on blood pressure, kidney function, and survival was examined in stroke-prone spontaneously hypertensive rats (SHRSP). Male SHRSP that were fed a Japanese rat chow plus a 1% NaCl drinking solution beginning at 7-8 weeks of age developed severe hypertension and stroke; 14 of 18 untreated control SHRSP died by 14 weeks of age and exhibited evidence of cerebrovascular lesions. When enalapril (15 mg/kg/day) was included in the drinking solution of 15 SHRSP, blood pressure was initially reduced by only a slight degree, whereas survival improved markedly; only one of 10 SHRSP died before the rest were killed at 18 to 21 weeks. The remaining five enalapril-treated SHRSP lived beyond 36 weeks and on histological examination exhibited no evidence of cerebrovascular lesions. Chronic enalapril treatment also prevented the greater urinary excretion of protein and severe renal lesions observed in untreated SHRSP but did not affect urinary salt and water excretion. In anesthetized rats, glomerular filtration rate and tubular reabsorption of water were lower in untreated control SHRSP when compared with enalapril-treated SHRSP. Mean arterial pressure was comparable in both groups. These data support a possible role for ACE inhibition in the prevention of stroke and maintenance of kidney function independent of any marked change in blood pressure of SHRSP. Whether the protective effects of ACE inhibition relate to reduced angiotensin II formation, increased tissue kinins, or another mechanism remains to be determined.
Hypertension 1989 Feb
PMID:Enalapril prevents stroke and kidney dysfunction in salt-loaded stroke-prone spontaneously hypertensive rats. 253 41

When patients with functional unilateral renal artery stenosis are treated with an angiotensin I converting enzyme inhibitor (ACE-inhibitor) a risk is present for loss of the function of the affected kidney without clinical symptoms. Renal function should therefore be controlled in these patients before and after initiation of the treatment. Even a slight increase in serum creatinine must be followed by reassessment of the treatment and investigation for renocascular hypertension must be considered.
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PMID:[Unnoticed loss of renal function during treatment with angiotensin I converting enzyme inhibitor. A new risk in patients with unrecognized unilateral stenosis of the renal artery]. 258 87


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