Effects of Enalapril Alone, and in Combination With Hydrochlorothiazide, on Renin-Angiotensin-Aldosterone, Renal Function, Salt and Water Excretion, and Body Fluid Composition

Bauer, John H.; Gaddy, Patricia

doi:10.1016/s0272-6386(85)80177-3

Cited by 37 publications

(7 citation statements)

References 42 publications

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“…However, ERPF/RBF is increased (+3% to -18%) [30,[174][175][176][177][178][179][180][181][182], and RVR is reduced (-23% to -29%) [30,[176][177][178]180]. Bauer and Gad@ [30] have observed marked improvement in GFR (+21%) and ERPF (+32%) in essential hypertensive patients with impaired renal function (inulin clearance -< 80 ml/min/ 1.73 m") treated for 8 weeks with enalapril monotherapy. Reams and Bauer subsequently reported [181] that the long-term (96 week) oral administration of enalapril monotherapy (10-40 rag/day) to patients with normal renal function had no significant effect on GFR (0%) or ERPF (+6%), whereas both GFR and ERPF were markedly improved (+54% and +57%, respectively) in essential hypertensive patients with impaired renal function (inulin clearance -< 80 ml/min/ 1.73 me).…”

Section: Enalaprilmentioning

confidence: 97%

“…The short-term (-<3 month) oral administration of enalapril monotherapy (5-40 rag/day) to patients with essential hypertension has no consistent effect on GFR (-8% to +8%) [30,[174][175][176][177][178][179][180][181][182] (Table 3). However, ERPF/RBF is increased (+3% to -18%) [30,[174][175][176][177][178][179][180][181][182], and RVR is reduced (-23% to -29%) [30,[176][177][178]180].…”

Section: Enalaprilmentioning

confidence: 99%

“…Bauer and Gad@ [30] have reported that essential hypertensive patients receiving combined therapy with enalapril and a diuretic may demonstrate marked improvement in renal function (see Table 3). However, an improvement in GFR (+ 55%) and ERPF ( + 32%) was observed only in essential hypertensive patients with moderately impaired renal function (inulin clearance -< 80 ml/min/1.73 m z but -> Table 3).…”

Section: Enalaprilmentioning

confidence: 99%

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Acute and chronic effects of angiotensin converting enzyme inhibitors on the essential hypertensive kidney

Reams

Bauer

1990

Cardiovasc Drug Ther

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The natural course of essential hypertensive renal disease is characterized by a slowly progressive impairment of renal function. Initially, the changes are functional and reversible; however, structural changes gradually occur, leading to hypertensive nephrosclerosis. Similarities exist between the early functional hemodynamic changes observed in the essential hypertensive kidney and the physiologic renal effects of angiotensin II. To the degree that the initial functional changes are the result of excessive endogenous production of angiotensin II, interruption of the integrity of this humoral system could be expected to reverse the pathophysiologic sequence of events leading to hypertensive nephrosclerosis. This review focuses on the pathophysiology of the essential hypertensive kidney, the intrarenal effects of angiotensin II, and the acute and chronic effects of angiotensin converting enzyme (ACE) inhibition therapy on the essential hypertensive kidney. The data reviewed suggest that ACE inhibition therapy does reverse the initial functional hemodynamic changes observed in the essential hypertensive kidney and may protect the glomerulus from hemodynamically mediated injury.

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Section: Enalaprilmentioning

confidence: 97%

Section: Enalaprilmentioning

confidence: 99%

Section: Enalaprilmentioning

confidence: 99%

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Acute and chronic effects of angiotensin converting enzyme inhibitors on the essential hypertensive kidney

Reams

Bauer

1990

Cardiovasc Drug Ther

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“…Thus, the study of Eliahou et al [24] also demon strated, as our study does, that the control of hypertension per sc may not be adequate to prevent the deterioration in renal function. Furthermore, others have reported that converting enzyme inhibitors are more potent in prevent ing the progression of renal insufficiency than other anti hypertensive agents [25,26], and the long-term therapy of patients with renal failure and hypertension with enalapril may increase the glomerular filtration rate [27], Anderson and Brenner [28] suggested that the different effects of antihypertensive drugs on renal function, de spite comparable control of hypertension, are due to dif ferent actions on systemic and glomerular hypertension. Agents that ameliorate glomerular hypertension arc more effective in preventing the progression of renal insuffi ciency and may even increase the glomerular filtration rate.…”

Section: Discussionmentioning

confidence: 99%

Comparison between the Effects of Indapamide and Hydrochlorothiazide on Creatinine Clearance in Patients with Impaired Renal Function and Hypertension

Madkour

Gadallah²,

Riveline³

et al. 1995

Am J Nephrol

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The long-term effects of indapamide or hydrochlorothiazide on blood pressure and renal function were examined in patients with impaired renal function and moderate hypertension. Both drugs controlled hypertension and blood pressure remained normal during the 2 years of the study. Despite this comparable control of hypertension, indapamide therapy was associated with a 28.5 ± 4.4% increase in creatinine clearance while treatment with hydrochlorothiazide was associated with a 17.4 ± 3.0% decrease in creatinine clearance. The results of the study indicate that indapamide is superior to hydrochlorothiazide in the treatment of patients with impaired renal function and moderate hypertension.

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“…Recently, Nussberger et al 2129 thoroughly dissected these complexities in man; results indicate that failure of some prior studies 27 to demonstrate decline of plasma Ang II during enalapril administration likely derives from 1) substances that cross-react with anti-Ang II antibody (Ang I plus metabolites of Ang I and Ang II), and 2) in vitro generation of Ang II in plasma samples despite presence of inhibitors and cooling of samples. 21 These observations further suggest that, during chronic enalapril administration with high circulating levels of Ang I, elimination of in vitro Ang II generation may require high levels of CEI or immediate extraction of samples.…”

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confidence: 99%

Chronic MK421 fails to modify evolution of hypertension in neonatally coarcted pups.

Bagby

Fuchs

1989

Hypertension

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In inbred dogs with neonataiiy induced coarctation hypertension, prior serial studies during the first year after aortic banding showed extracellular volume excess with normal plasma renin activity (PRA). The present studies test the hypothesis that slowly evolving aortic constriction in this model will yield intrarenal angiotensin II excess, peripherally undetectable, with continuous slightly positive sodium balance, and thus that chronic blockade of angiotensin II formation will prevent generation of hypertension. Accordingly, we used MK421 (enalapril, 3 mg/kg twice daily), a long-acting angiotensin converting enzyme inhibitor, or placebo, administered orally, from the time of banding through 4 months after banding in sex-matched littermates randomly assigned to one of four groups: coarcted/MK421; control/MK421; coarcted/placebo; control/placebo. Results indicate that MK421 caused identical lowering of absolute forelimb systolic blood pressure in coarcted and control pups but failed to modify evolution of a significant (/?<0.005) systolic blood pressure difference hi coarcted versus control dogs. Thus, neither temporal course nor final magnitude of relative hypertension was altered by MK421. Efficacy of MK421 was documented by 83% inhibition of the pressor response to angiotensin I at nadir of drug effect and by sustained increases in angiotensin I and renin concentration throughout the period of study. Coarcted and control pups responded similarly to MK421 for all measured variables. Glomerular nitration rate and extracellular volume (measured by [ M C]inulin disappearance) did not differ among groups. Thus, chronic administration of MK421 failed to prevent hypertension and did not impair maintenance of normal renal function in the evolving phase of neonataiiy induced coarctation hypertension. We conclude that, although angiotensin II may participate in the untreated model, it does not appear essential to generation of hypertension. We propose that the renal pressure-natriuresis mechanism regulates distal pressure, that stenosis-related resistance independently determines the proximal-distal difference, and that chronic converting enzyme inhibition lowers the set point of the former without influencing stenosis evolution, thus secondarily lowering proximal pressure by an equal degree. {Hypertension 1989; 13:91-101) A ortic coarctation has been studied as an exper-L \ imental model of renovascular hyperten-A. \~ sion 1 and classified with other models wherein all functional renal mass lies distal to a vascular stenosis (e.g., renal artery stenosis present bilaterally or affecting a single kidney).2 Acute aortic constriction is followed by transient activation of the renin-angiotensin system as blood pressure rises, 3 -5 whereas the phase of established hypertension exhibits normal plasma renin activity (PRA) (see References 1, 6, and 7) coupled with expanded extracellular fluid volume. Received May 11, 1988; accepted September 26, 1988. In neonataiiy induced coarctation hypertension (NICH) in the inbred Lab...

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Effects of Enalapril Alone, and in Combination With Hydrochlorothiazide, on Renin-Angiotensin-Aldosterone, Renal Function, Salt and Water Excretion, and Body Fluid Composition

Cited by 37 publications

References 42 publications

Acute and chronic effects of angiotensin converting enzyme inhibitors on the essential hypertensive kidney

Acute and chronic effects of angiotensin converting enzyme inhibitors on the essential hypertensive kidney

Comparison between the Effects of Indapamide and Hydrochlorothiazide on Creatinine Clearance in Patients with Impaired Renal Function and Hypertension

Chronic MK421 fails to modify evolution of hypertension in neonatally coarcted pups.

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