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

Orthotopic heart transplant recipients treated with immunosuppressive regimens based on cyclosporine have a high incidence of hypertension. Cyclosporine-induced nephrotoxicity characterized by afferent glomerular arteriolar vasoconstriction also develops in these patients. Calcium channel antagonists produce afferent glomerular arteriolar vasodilation. Angiotensin-converting enzyme inhibitors (ACEI) dilate the efferent arteriole and have been suggested to decrease glomerular filtration rate in subjects taking cyclosporine. To test the hypothesis that calcium channel antagonists would improve glomerular filtration rate in heart transplant patients receiving ACEI treatment, we reviewed the charts of our patients whose treatment for hypertension had been changed from an ACEI to a calcium channel antagonist. A change in renal function was assessed by the average of serum creatinine level, blood urea nitrogen, and creatinine clearance within 3 months before and after the change from ACEI to calcium channel antagonist. Blood pressure was assessed on two different occasions before and after conversion to calcium channel antagonist. The data were analyzed by a paired Student t test. Serum blood urea nitrogen and creatinine levels decreased significantly when patients were treated with calcium channel antagonists (p < 0.05). Creatinine clearance increased in all patients when the treatment was converted to a calcium channel antagonist (CCA) (ACEI = 56.4 +/- 19.3 ml/min versus CCA = 71.06 +/- 23.77, N = 9; p < 0.005). A 5-mm Hg decrease occurred in mean arterial pressure when treatment was changed from ACEI to calcium channel antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of calcium channel antagonists on renal function in hypertensive heart transplant recipients. 145 46

Angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists are important classes of antihypertensive agents. Within their respective classes, ACE inhibitors and calcium antagonists share common pharmacokinetic properties, but in contrast to ACE inhibitors, some calcium antagonists may cause a significant increase in plasma digoxin concentrations. Clinically, both classes of agents have been shown to be safe and effective in large-scale, long-term clinical trials. ACE inhibitors appear to be very well tolerated and may be associated with fewer adverse effects than some calcium antagonists. ACE inhibitors appear to blunt diuretic-induced hypokalemia, hypercholesterolemia, hyperuricemia, and hyperglycemia. Both classes of agents can be used safely in patients with renal disease, diabetes mellitus, peripheral vascular disease, and chronic obstructive pulmonary disease. They may also be used in the elderly. While ACE inhibitors are particularly useful in hypertension accompanied by congestive heart failure, calcium antagonists can be very useful when angina pectoris is present in the hypertensive patient.
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PMID:Comparative pharmacokinetic and clinical profiles of angiotensin-converting enzyme inhibitors and calcium antagonists in systemic hypertension. 154 35

Angiotensin-converting enzyme (ACE) inhibitors are useful first-line drugs in the therapy of mild and moderate hypertension. Adverse reactions to this drug class are rarely serious. Hypotension, cough, rash, and taste disturbance are uncommon; reduced glomerular filtration and hyperkalemia occur infrequently; angioedema is rare and neutropenia is extremely rare. Quinapril is a new ACE inhibitor that is converted to biologically active quinaprilat in the liver. This ACE inhibitor has a rapid onset of action and inhibits local tissue converting enzyme systems in kidney, heart, and brain, as well as in the circulating renin-angiotensin system. Clinically significant adverse effects of quinapril occur at low rates. In 1,771 patients receiving quinapril, the reported incidence of the first occurrence of orthostatic hypotension was comparable to that seen in patients receiving placebo. In other studies, headache was reported by up to 4.7% of patients receiving quinapril, which is comparable to reported incidences of headache in patients receiving other ACE inhibitors. Other adverse events reported at rates greater than 1% include cough with associated rhinitis and bronchitis, dizziness, and somnolence. Such adverse events have only rarely led to the withdrawal of patients from clinical studies of quinapril.
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PMID:Adverse effects of angiotensin-converting enzyme inhibitors in antihypertensive therapy with focus on quinapril. 154 39

The angiotensin-converting enzyme (ACE) inhibitors available today include captopril (Capoten), enalapril (Vasotec), enaloprilat (Vasotec IV), lisinopril (Prinivil, Zestril), benazepril (Lotensin), fosinopril (Monopril), and ramipril (Atace). These drugs are used in the treatment of hypertension and congestive heart failure. They also are used in treating renovascular hypertension not amenable to surgery and are being studied to decrease left ventricular size after infarction and to determine whether they slow the rate of internal hyperplasia. Angiotensin-converting enzyme inhibitors have negative inotropic and chronotropic effects. This chapter discusses the ACE inhibitors and their actions, uses, adverse effects, contraindications, and nursing implications.
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PMID:Angiotensin-converting enzyme inhibitors. 157 40

A universal underlying abnormality in the pathogenesis of hypertension, atherosclerosis, myocardial dysfunction, and diabetic glomerulosclerosis involves alteration in smooth muscle cell structure, function, and growth. Angiotensin II, through its effects on contractility, growth, and the sympathetic nervous system, may potentially play a key role in this pathologic process and, thus, contribute to the development of these cardiovascular and renal complications of diabetes mellitus. Angiotensin-converting enzyme inhibitors and some direct renin inhibitors prevent or slow the progression of some of these complications, which further suggests a pathologic role for the reninangiotensin system in diabetes mellitus.
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PMID:Effect of the renin-angiotensin system in the vascular disease of type II diabetes mellitus. 158 Feb 75

Angiotensin-converting enzyme (ACE) inhibitors are effective hypotensive agents in hypertension of different types and degree. Probably, they lower pressure by reducing angiotensin II (AII); the varied timing of their hypotensive effect suggests that AII increases blood pressure in more than one way. Infusion studies show two effects of AII: at moderate dose, a rapid vasoconstrictor action; at lower dose, a slow-developing but ultimately large hypertensive effect. Vascular hypertrophy develops during the slow pressor response; at least part of the hypertrophy results from a nonpressor mechanism. In vitro studies show that AII has mitogenic and trophic actions on vascular smooth muscle cells in culture and that it stimulates synthesis of extracellular matrix proteins. One of these actions may produce the nonpressor component of vascular hypertrophy. ACE inhibitors lower pressure in the spontaneously hypertensive rat (SHR) and when given in young animals produce a hypotensive effect that endures long after the period of treatment. An action of endogenous AII, possibly a paracrine effect within the vessel wall, may cause vascular hypertrophy in young SHR with long-lasting effects on arterial pressure.
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PMID:Angiotensin II, angiotensin-converting enzyme inhibitors, and blood vessel structure. 158 Feb 78

Inhibitors of two zinc metallopeptidases, angiotensin I converting enzyme (ACE) and neutral metalloendopeptidase-24.11 (EP-24.11), are antihypertensive agents. In this issue of Hypertension, Genden and Molineaux report that yet another peptidase inhibitor, metalloendopeptidase-24.15, EC 3.4.24.15 (EP-24.15), lowers blood pressure in normotensive rats. In this editorial we discuss the possible role of kinins as common mediators of part of the vasodepressor action of these peptidase inhibitors. Genden and Molineaux report that the marked fall in blood pressure caused by the EP-24.15 inhibitor is almost abolished by a kinin receptor antagonist, supporting the hypothesis that kinins play a role in the regulation of normal blood pressure. We have confirmed that the EP-24.15 inhibitor used by these investigators lowers blood pressure. Up to now, EP-24.15 has not been implicated in in vivo metabolism of kinins. Although a number of kininases have been identified, our own previous work indicated that the metabolic pathway responsible for clearing kinins from the circulation involves the action of kininase II (angiotensin I converting enzyme) and renal peptidases. Nevertheless, the main metabolic pathway involved some other unidentified enzyme, since in these experiments disappearance of kinins from the circulation was only marginally reduced by a "cocktail" of inhibitors of ACE, EP-24.11, and carboxypeptidase N. It could be that EP-24.15 is involved in kinin metabolism. However, a number of questions need to be answered with regard to the mechanism by which the EP-24.15 inhibitor lowers blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Sep
PMID:Zinc metallopeptidase inhibitors. A novel antihypertensive treatment. 188 49

Angiotensin I-converting enzyme (ACE) is a peptidyldipeptide hydrolase that is located mainly on the luminal surface of vascular endothelial cells but also in cells derived from the monocyte-macrophage system. Physiologically, ACE is a key enzyme in the renin-angiotensin system, converting angiotensin I into the potent vasopressor angiotensin II and also inactivating the vasodilator bradykinin. Increased serum ACE activity (SACE) has been reported in pathologies involving a stimulation of the monocytic cell line, primarily granulomatous diseases. Sarcoidosis is the most frequent and the better studied of these diseases; high SACE is not only a well-established marker for the diagnosis but is also a useful tool for following its course and evaluating the effect of therapy. SACE can also be increased in nonsarcoidotic pulmonary granulomatous diseases such as silicosis and asbestosis, in extrathoracic granulomatous pathologies such as Gauchers disease and leprosis, and, to a lesser extent, in nongranulomatous disorders such as hyperthyroidism or cholestasis. On the other hand, monitoring sarcoidosis obviates the measurement of ACE activity in other biological fluids, e.g., broncho-alveolar and cerebrospinal fluids, in the search of a locoregional dissemination or dis-simulation of the disease. Decreased SACE has been reported in vascular pathologies involving an endothelial abnormality, e.g., deep vein thrombosis, and in endothelium dysfunctions related to the toxicity of chemo- and radiotherapy used in cancers, leukemias, and hematopoietic or organ transplantations. SACE is also of interest for monitoring arterial hypertension treated with specific synthetic ACE inhibitors. These various reasons for determining ACE activity have led to the development of numerous methods. The most widely used is the spectrophotometric assay using hippuryl-histidyl-leucine as substrate. Fluorimetric and radiochemical assays using both classic and novel substrates have been proposed, but they are time consuming, require special apparatus, and are not suited to automation. Kinetic spectrophotometry of furylacryloyl-phenylalanyl-glycyl-glycine hydrolysis is now used extensively because it is easy to automatize. Efforts are now required to standardize one or more of these assays. Indeed, "normal" plasma values differ not only according to the substrate, but also to the method of determination and to sex and age.
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PMID:Angiotensin-converting enzyme: clinical applications and laboratory investigations on serum and other biological fluids. 166 62

Several antihypertensive agents have been found to influence serum lipid profiles. Thiazide diuretics increase total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels and slightly reduce high-density lipoprotein (HDL) cholesterol. Most beta-blockers substantially increase triglycerides and lower HDL cholesterol. Angiotensin-converting enzyme inhibitors, calcium channel antagonists, alpha- and beta-blockers, and beta-blockers with intrinsic sympathomimetic activity are lipid neutral. alpha 1-Antagonists (e.g., terazosin and prazosin) lower total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels and improve total cholesterol/HDL ratios. Observational epidemiologic studies indicate that the lipid effects of antihypertensive agents are large enough to account for substantial differences in the predicted incidence of coronary heart disease. Combination therapy with the alpha 1-antagonist terazosin plus either thiazides or beta-blockers also ameliorates the adverse lipid effects of these agents used alone. A reasonable approach to managing the lipid problems often associated with hypertension is to advise a cholesterol-lowering, low-sodium diet and weight reduction and to select drugs that alone or in combination do not adversely affect lipid profiles.
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PMID:Antihypertensive therapy: taking lipids into consideration. 167 22

The effect of beta-blocking agents and enalapril as antihypertensive drugs has been compared in 47 patients with IgA nephropathy. The deterioration rate was calculated from the regression line of 51Cr-EDTA clearance and expressed in ml/min/year. The annual loss in glomerular filtration rate (GFR) was greater in patients treated with different beta-blocking agents (-4.9 +/- 6.8 ml/min/year) compared to patients treated with Enalapril (1.7 +/- 7.4 ml/min/year), in spite of the fact that these patients had a lower initial GFR. Nine patients were initially treated with beta-blocking agents (-9.5 +/- 9.3 ml/min/year) and then with an angiotensin-converting enzyme inhibitor (5.5 +/- 11.2 ml/min/year). Angiotensin-converting enzyme inhibitors should therefore be preferred in the treatment of hypertension in IgA nephropathy.
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PMID:Deterioration rate in hypertensive IgA nephropathy: comparison of a converting enzyme inhibitor and beta-blocking agents. 168 30


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