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

Quality of life issues have become increasingly important in tailoring antihypertensive therapy to individual patients. The application of quality of life data to the practice setting is frequently difficult, however. The effective use of this information requires an understanding of its definition and measurement, as well as of study methods. Quality of life findings may be specific to particular disease states, patient populations, and pharmacologic agents. The addition of hydrochlorothiazide to concurrent methyldopa, propranolol, or captopril therapy has been reported to reduce patients' overall sense of well-being. beta-Adrenergic blockers may exert either positive or negative effects on quality of life. Angiotensin-converting enzyme (ACE) inhibitors may have positive effects on quality of life; however, the cost of therapy is an important consideration. Information on calcium antagonists is limited. The findings of the Treatment of Mild Hypertension Study (TOMHS) may eventually provide comparative quality of life data on the four first-line antihypertensive therapies.
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PMID:Applying quality of life data in practice. Considerations for antihypertensive therapy. 275 13

An undetermined percentage of the 60 million hypertensive Americans have potentially correctable renovascular hypertension (RVHT). Conventional plasma renin activity (PRA) determinations and radionuclide renography have limited sensitivity and specificity as screening tests for RVHT. Angiotensin-converting enzyme inhibition with captopril stimulates renin secretion and causes transient decreases in glomerular filtration rate and effective renal plasma flow within the stenotic kidney. Review of recent studies in hypertensive patients suggests that captopril stimulation of both PRA determinations and conventional renography may enhance the sensitivity and specificity of these studies in detecting RVHT.
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PMID:The captopril tests: a new concept in detecting renovascular hypertension? 266 28

The failure of recent antihypertensive trials to document clearly a reduction in the risk of coronary heart disease (nonfatal or fatal myocardial infarction and sudden death) has important clinical implications. Although the causes of this phenomenon are unknown, it is possible that lipid and metabolic side effects of the antihypertensive drugs used in these studies negated the beneficial effects of blood pressure reduction. Angiotensin-converting enzyme (ACE) inhibitors are lipid neutral and associated with few metabolic side effects, and may be considered over agents that cause adverse effects on such parameters as serum cholesterol, glucose, potassium, and uric acid levels. ACE inhibitors are now emerging in the United States as important first-line therapy for the treatment of hypertension.
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PMID:ACE inhibitors in hypertension: a US perspective. 267 Feb 18

Angiotensin-converting enzyme (ACE) inhibitors are being increasingly prescribed for the treatment of hypertension and heart failure. Not only are they efficacious but the incidence of serious adverse events with ACE inhibitors is similar to that with placebo. 'First-dose hypotension' mainly affects the renin-dependent patient. Neutropenia and agranulocytosis have been reported rarely for the nonsulfhydryl compounds. Comparative safety data are provided for captopril, enalapril, and quinapril, a new nonsulfhydryl ACE inhibitor that has been investigated extensively in over 2,000 patients. Results show that the proportion of patients reporting associated adverse events was lower with quinapril (11%) than with captopril (17%) or enalapril (15%). Similarly, there was a lower proportion of patients withdrawn due to adverse events with quinapril.
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PMID:The safety of ACE inhibitors for the treatment of hypertension and congestive heart failure. 267 Feb 22

Renal failure is progressive irrespective of the underlying primary renal disease or continued disease activity. Intrarenal haemodynamic changes may contribute to progressive loss of renal function, and may be modified by pharmacological therapies. Angiotensin-converting enzyme (ACE) inhibitors may have a specific therapeutic advantage in the treatment of hypertension associated with progressive renal disease. We have studied the effects of an ACE inhibitor and a calcium channel blocker on systemic BP, glomerular filtration, proteinuria and histological injury in animal models of progressive renal disease (the remnant kidney and diabetes). Systemic BP was lowered similarly by each treatment in both models. Beneficial effects on renal structure, proteinuria, and glomerular filtration only occurred in the ACE inhibitor-treated animals. Intrarenal haemodynamic effects of ACE inhibitors may therefore offer an advantage over other antihypertensive agents in progressive renal disease. Where there is reduced renal perfusion, intrarenal haemodynamic effects of ACE inhibitors may lead to compromised renal function. Acute renal failure is a common consequence of ACE inhibitor therapy in patients with bilateral renal artery stenosis, or renal artery stenosis to a single functioning kidney. Acute studies have suggested that these effects are reversible; function returns following withdrawal of ACE inhibitor therapy. We examined the long-term effects of ACE inhibitor therapy in rats with the two-kidney, one-clip (Goldblatt) model of hypertension. Rats were treated for 12 months with an ACE inhibitor or a vasodilator. After 1 year of treatment the clipped kidney from the ACE inhibitor-treated rats was small, fibrotic, and had no glomerular filtration. No functional improvement of the clipped kidney occurred following ACE inhibitor withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin-converting enzyme inhibition in renal disease; contrasting effects on renal function in renal artery stenosis and progressive renal injury. 267 36

1. The circulating and tissue renin-angiotensin systems (RAS) contribute importantly to cardiovascular homeostasis. Systemic and/or local activation of the RAS is seen in many pathological conditions of the cardiovascular system (e.g. hypertension and congestive heart failure). Increased angiotensin production participates in the pathophysiology of these and other disease states. Accordingly, inhibitors of the renin angiotensin system have a broad spectrum of therapeutic efficacy. 2. Angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents that do not adversely affect serum lipid levels. In addition, they reduce left ventricular hypertrophy. 3. ACE inhibitors cause coronary vasodilation and reduce ventricular work and wall stress. They have been shown to reduce experimental infarct size and to increase anginal threshold in humans. 4. After experimental or human myocardial infarction that results in significant left ventricular dysfunction, ACE inhibitors prevent ventricular dilatation and development of congestive heart failure, and may improve survival. 5. ACE inhibitors can prevent ventricular fibrillation and contractile impairment (stunned myocardium) associated with reperfusion injury after experimental myocardial ischaemia. 6. ACE inhibitors reduce preload and afterload, improve exercise capacity, reduce ventricular arrhythmias, and improve patient survival in clinical cardiac failure. 7. Taken together, inhibition of the RAS may potentially result in primary as well as secondary protective effects on the cardiovascular system.
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PMID:Clinical implications for therapy: possible cardioprotective effects of ACE inhibition. 269 Sep 9

In tissues rich in kallikrein, vasodilator kinins, acting as paracrine hormones, may play a role in the local regulation of blood flow. We studied the role of kinins in the regulation of blood flow in the rat submandibular gland using a kinin analogue with antagonistic properties, [DArg0]Hyp3-Thi5-8[DPhe7]bradykinin. When infused into the carotid artery (20 micrograms/min/rat), this antagonist blocked the effect of bradykinin (25-250 ng/kg, intracarotid injection) on glandular blood flow. In nephrectomized rats, the antagonist also blocked the increase in glandular blood flow caused by enalaprilat, a kininase II converting enzyme inhibitor. At a dose of 20 micrograms/min/rat, the antagonist produced no detectable change in basal glandular blood flow; however, at a higher dose (100 micrograms/min/rat), it caused a significant decrease (p less than 0.001). In eight of 10 rats, blood flow decreased by 75% or more; this effect was not blocked by the alpha-adrenergic receptor antagonist phentolamine. After antagonist infusion was stopped, blood flow returned toward normal. Sympathetic nerve stimulation of the gland induced vasoconstriction followed by poststimulatory vasodilatation. In rats displaying severe vasoconstriction after the antagonist, postsympathetic vasodilatation was abolished even when stimulation was performed after the antagonist infusion had been stopped and blood flow returned toward normal. Although a direct vasoconstrictor effect of the kinin antagonist cannot be completely ruled out, these data suggest that, in the rat submandibular gland, kinins may play a role in regulation of basal blood flow and vasodilatation after converting enzyme inhibitor or sympathetic stimulation.
Hypertension 1989 Jul
PMID:Role of kinin in regulation of rat submandibular gland blood flow. 273 39

The major complication of extracorporeal membrane oxygenation (ECMO) for the treatment of neonatal respiratory failure is bleeding related to heparinization. Systolic hypertension has emerged as another serious side effect in our experience. Thirty-eight of the first 41 newborns we treated with ECMO developed a systolic blood pressure greater than 90 mm Hg. The mean hypertension index (HI blood = hours greater than 90/hr on ECMO) was 0.17 +/- 0.16. Possible biochemical mediators were assayed in 17 patients. Plasma renin activity (PRA), aldosterone, epinephrine, norepinephrine, prostaglandin E2, thromboxane, and antidiuretic hormone were elevated. Angiotensin-converting enzyme (ACE) and prostacyclin were not elevated. Eighteen patients (44%) had intracranial hemorrhage (ICH), and 11 patients (27%) had clinically significant ICH. The HI was significantly (p less than 0.005) lower in those patients without ICH (0.11 +/- 0.01) than in those patients with ICH (0.25 +/- 0.04). PRA at hour 12, day 2, and day 3 was significantly higher (p less than 0.05) in patients experiencing ICH (62 +/- 42; 93 +/- 15; 73 +/- 30 ng/ml/hr) than in those without ICH (27 +/- 25; 14 +/- 8; 12 +/- 4 ng/ml/hr). An aggressive approach to medical management evolved that included hydralazine, nitroglycerine, and captopril, which protected against ICH. Two of 23 patients (9%) treated with the protocol sufferred clinically significant ICH, whereas nine of 18 patients (50%) treated before implementation of the protocol experienced ICH. The ACE inhibitor captopril was most effective in the control of hypertension. We conclude that systolic hypertension is common during neonatal ECMO, is associated with ICH, and is related to a high PRA. Aggressive management of hypertension during ECMO can reduce the incidence of ICH, and captopril is an important component of this aggressive medical management.
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PMID:Hypertension during extracorporeal membrane oxygenation: cause, effect, and management. 282 41

Angiotensin-converting enzyme occupies a central position in the dynamics of the renin-angiotensin system. We prospectively studied serum angiotensin-converting enzyme activity in 112 women at various stages of pregnancy and in the postpartum period because converting enzyme levels have not been well documented in pregnant women with medical disorders which might be expected to influence intravascular volume or blood pressure. Enzyme activity is lower during pregnancy than it is in the same population at 6 weeks postpartum. Levels of serum angiotensin converting enzyme activity remain relatively stable during gestation but drop during the immediate postpartum period. Diabetes, chronic hypertension, and pregnancy induced hypertension fo not markedly change serum angiotensin converting enzyme activity.
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PMID:Constancy of serum angiotensin-converting enzyme activity in normal and complicated pregnancy. 282 98

Angiotensin-converting enzyme (ACE) has been identified as a prominent brush border membrane-bound enzyme of human jejunum. In this study, we purified brush border membrane vesicles enriched in ACE, and characterized the ACE with regard to (a) its stability in the membrane, (b) substrate hydrolysis kinetics compared with pulmonary endothelial ACE, and (c) pharmacologic interaction with Ramipril. These investigations resulted in the following findings. The uninhibited enzyme is stable in native membranes in vitro, with a half-life of 195 +/- 7 h. Kinetic analysis of ACE hydrolysis activity revealed the presence of a single enzyme species, which yielded a high Vmax and displayed a Km similar to purified ACE from lung endothelium. Brush border ACE was inhibited by Ramipril, one of the most specific and potent orally administered ACE inhibitors indicated for hypertension. We determined the brush border ACE value of IC50 = 3 X 10(-9) M Ramipril-diacid, which is the same value for serum and lung ACE. Brush border ACE remains 100% inhibited by 10 microM Ramipril during at least 8 days in vitro. The data indicate that ACE is a prominent jejunal brush border enzyme that behaves pharmacologically and kinetically like its peripheral circulation counterpart. This study suggests that high doses of orally administered ACE inhibitors may affect intestinal epithelial function.
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PMID:Human intestinal brush border angiotensin-converting enzyme activity and its inhibition by antihypertensive Ramipril. 283 Nov 5


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