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

This review compares the metabolism and pharmacokinetic profiles of captopril, the first orally active angiotensin-converting enzyme (ACE) inhibitor, and 2 newer ACE inhibitors, enalapril and quinapril. Captopril differs from both enalapril and quinapril in that its chemical structure contains a sulfhydryl group, the presence of which may be important in the development of adverse reactions. Captopril also differs from enalapril and quinapril in its ability to be metabolized in plasma. Enalapril and quinapril are both de-esterified, most likely in the liver, to their active metabolites, enalaprilat and quinaprilat. All 3 ACE inhibitors are eliminated primarily via renal excretion, and renal dysfunction markedly increases the area under the time versus plasma concentration curves. Hepatic dysfunction also slows the conversion of enalapril and quinapril to their active metabolites. There is evidence that both captopril and enalapril, but not quinapril, may accumulate with repeated dosing. The pharmacokinetics of these agents are not significantly modified by co-administration of other drugs. However, captopril does cause marked increases in trough plasma levels of digoxin. Overall, the pharmacokinetic profiles of captopril, enalapril, and quinapril make them suitable for a wide range of patients with hypertension or congestive heart failure.
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PMID:Comparative pharmacokinetics of captopril, enalapril, and quinapril. 154 41

To assess the effects of genetic predisposition of essential hypertension on early renal function in recent insulin-dependent diabetics, we studied inulin, para-aminohippuric, sodium, and lithium clearances in 69 unselected diabetics with (n = 20) and without (n = 49) a family history of essential hypertension. Despite similar metabolic control, glomerular filtration rate and mean arterial pressure were significantly higher in diabetics with than in those without a family history of hypertension. However, no difference was found between the two groups regarding renal vascular resistance, sodium excretion, or fractional proximal and distal sodium reabsorption. Renal responses to acute captopril (75 mg) administration were evaluated in 27 patients (six with family history of hypertension). Captopril decreased filtration fraction and mean arterial pressure similarly in both groups, whereas glomerular filtration rate and renal vascular resistance decreased more dramatically in diabetics with family history of hypertension. These findings indirectly suggest an abnormal response to angiotensin of vascular tone in recent diabetics with familial predisposition to hypertension. Renal response to acute nicardipine (2.5 mg i.v.) administration was analyzed in 24 patients (five with family history of hypertension). In both groups, nicardipine similarly decreased mean arterial pressure and renal vascular resistance and induced a marked natriuretic effect due to a predominant reduction in proximal reabsorption of sodium. However, the increase in sodium excretion was twofold to threefold more pronounced in diabetics with a family history of hypertension. Whether these early renal abnormalities may contribute to the risk of diabetic nephropathy, as suggested by retrospective studies, remains to be determined.
Hypertension 1992 Apr
PMID:Renal abnormalities in normotensive insulin-dependent diabetic offspring of hypertensive parents. 155 69

Captopril renal scintigraphy is a well-known noninvasive tool in the diagnosis of renovascular hypertension. The authors present a case of a patient with malignant hypertension whose captopril renal scintigraphy suggested bilateral and equal renovascular hypertension. His renal angiogram, however, demonstrated no renal artery stenosis or abdominal aortic atherosclerotic disease. False-positive captopril renal scintigraphy has been reported but can usually be attributed to the patient's hypotensive episode after captopril administration, volume or salt depletion, or chronic glomerulonephropathy. This patient demonstrated mild blood pressure changes after captopril administration and was not volume or salt depleted. His creatinine was 1.6 mg/dl on admission but demonstrated appropriate renal function on subsequent noncaptopril renal scintigraphy.
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PMID:Abnormal captopril renogram in a patient without renovascular hypertension. 157 20

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

Micropuncture experiments were performed on intact and remnant kidneys of male Sprague-Dawley rats before and after angiotensin converting enzyme inhibition with captopril (0.5 mg kg-1 iv). Partially nephrectomized rats were studied at 2 and 8 weeks post-surgery before the development of systemic hypertension. At 2 weeks, nephrectomized rats had a numerically higher tubular stop-flow pressure than controls (43 +/- 2 mmHg vs. 38 +/- 2 mmHg; P = 0.08) and a higher post- to pre-glomerular resistance ratio (Re/Ra) (0.40 +/- 0.03 vs. 0.31 +/- 0.03; P = 0.08). At 8 weeks, stop-flow pressure and post- to pre-glomerular resistance ratios were similar in remnant and intact kidneys. Captopril had no effect on stop-flow pressure in 2 week post-surgery nephrectomized rats or either control group, but it increased stop-flow pressure in 8 week post-surgery nephrectomized rats (40 +/- 2 to 44 +/- 2 mmHg, P = 0.04). This increase in stop-flow pressure was associated with an increase in the post- to pre-glomerular resistance ratio (0.33 +/- 0.02-0.42 +/- 0.02, P = 0.009). Stop-flow pressure was positively correlated with the post- to pre-glomerular resistance ratio in 2-week post-surgery nephrectomized rats and their respective controls when combined (r = 0.89, P = 0.0001) and 8-week post-surgery nephrectomized rats and their respective controls combined (r = 0.78, P = 0.0001). Stop-flow pressure was not significantly correlated with mean arterial pressures or welling-point pressures in these groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril and time dependent changes in post- to pre-glomerular resistance ratios in remnant kidneys of pre-hypertensive rats. 158 10

Advances in renal angiography and revascularization techniques have renewed interest in developing a better noninvasive screening test for identifying patients with potentially correctable renovascular hypertension. Captopril renography is a promising diagnostic tool in the evaluation of the hypertensive patient. This review highlights the important pathophysiological changes in renal hemodynamics and humoral response attributable to significant renal artery stenosis, and underscores the dramatic effects of angiotensin-converting enzyme inhibition on the renovascular bed. The review also summarizes the available clinical information in captopril renography, and presents consensus recommendations on appropriate patient selection, radionuclide(s) of choice, and suggested diagnostic criteria.
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PMID:State-of-the-art review: captopril renography--pathophysiological considerations and clinical observations. 158 12

Rats harboring the mouse Ren-2 transgene develop hypertension despite low levels of plasma renin activity. We tested the hypothesis that these rats exhibit an increase in vascular angiotensin formation caused by the presence of the transgene. We measured the release of angiotensins I and II from isolated perfused hindquarters by high-performance liquid chromatography and radioimmunoassay. Female rats heterozygous for the transgene had significantly elevated mean arterial pressure compared with control rats (189.3 +/- 9.5 versus 110.0 +/- 5.4 mm Hg, p less than 0.05). Plasma angiotensin II was significantly decreased in transgenic rats. Transgenic rat hindquarters released more angiotensin I (121 +/- 37 versus 39 +/- 12 fmol/30 min, n = 7 each) and more angiotensin II (210 +/- 21 versus 62 +/- 12 fmol/30 min, p less than 0.05, n = 7 each) than control rat hindquarters. Captopril increased angiotensin I release and decreased angiotensin II values in both transgenic and control rat hindquarters. Bilateral nephrectomy 24 hours before hindquarter perfusion greatly reduced angiotensin release from control rat hindquarters but not from transgenic rat hind limbs. We also tested for the presence of Ren-2 messenger RNA in mesenteric and aortic tissue by RNase protection assay and Northern blot analysis. We found that Ren-2 messenger RNA was present in mesenteric and aortic tissue of transgenic but not of control rats. We conclude that the Ren-2 transgene is expressed in vascular tissue of transgenic rats and may be responsible for substantial increases in vascular angiotensin formation.
Hypertension 1992 Jun
PMID:Increased vascular angiotensin formation in female rats harboring the mouse Ren-2 gene. 159 69

We have previously demonstrated that loss of renal functional reserve (renal response to protein loading) in two-kidney, one clip Goldblatt hypertension is characterized by no change in glomerular filtration rate or single nephron glomerular filtration rate and decreased absolute proximal tubular reabsorption during glycine administration. Captopril restores proximal reabsorption and renal functional reserve in this condition. Because captopril suppresses angiotensin II generation and increases bradykinin, prostaglandins, and potentially nitric oxide, we have investigated the role of angiotensin II blockade in restoring proximal reabsorption and renal functional reserve by comparing captopril with DuP 753, an angiotensin II receptor antagonist, in Goldblatt rats. One month after clipping, two period micropuncture studies (control and glycine) were performed on the unclipped kidney. Normal rats and three groups of clipped rats were studied: an untreated group (HYP), a group treated with captopril (CEI), and a group treated with DuP 753 (DuP) 5 days before micropuncture. Glycine increased glomerular filtration rate, nephron plasma flow, and single nephron glomerular filtration rate in normal rats. Systemic and glomerular hypertension in HYP rats was associated with loss of renal functional reserve and a decrease in absolute proximal reabsorption during glycine. Captopril and DuP 753 normalized systemic and glomerular capillary pressure and prevented the decrease in proximal reabsorption during glycine; however, only CEI rats increased single nephron glomerular filtration rate and glomerular filtration rate after glycine. In conclusion, abnormal responses of both glomerular and tubular function are responsible for the loss of renal functional reserve in Goldblatt rats. Inhibitory angiotensin II activity is responsible for decreasing proximal reabsorption during glycine; however, factors other than angiotensin II limit the glomerular response to glycine.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Angiotensin II and renal functional reserve in rats with Goldblatt hypertension. 159 82

Modern noninvasive techniques, such as doppler sonography or color-encoded doppler sonography, have only rarely been used for diagnosis of renovascular hypertension in children. In the following case report, we describe the successful diagnosis of renovascular hypertension in a 13-year-old girl by using color-encoded doppler sonography and Captopril renal scintigraphy. The patient was admitted with hypertension of 180/130 mmHg. Laboratory findings showed elevated plasma renin and aldosterone concentrations. No abnormalities were found by abdominal sonography, isotope renography, intravenous pyelography, or in venous digital subtraction angiography. However, subsequent color-encoded doppler sonography clearly showed evidence of an artery stenosis of the right kidney. Furthermore, isotope renography one hour after oral administration of captopril revealed an almost complete loss of glomerular filtration rate of the right kidney. Based on these findings, arterial digital subtraction angiography, including transluminal angioplasty, was performed. During this treatment procedure, the right renal artery stenosis could be confirmed and was subsequently dilated without complication. In the following twelve months the patient remained normotensive and required no further antihypertensive drug treatment.
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PMID:[Unilateral renal artery stenosis. Color-coded Doppler sonography and captopril scintigraphy in a 13-year-old patient]. 160

Hypertension in the neonate is commonly related to renal disease. More specifically, renovascular hypertension in neonates is often associated with the placement of a umbilical artery catheter. Many medications, including angiotensin-converting enzyme (ACE) inhibitors, have been used in the treatment of neonatal hypertension. Captopril, an ACE inhibitor, is an oral agent that is effective in renovascular hypertension. We describe the use of intravenous enalapril, another ACE inhibitor, in successfully treating severe renovascular hypertension refractory to standard medical therapy in two term neonates.
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PMID:Treatment of neonatal renovascular hypertension with intravenous enalapril. 162 14


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