Improved Renal Function During Chronic Lisinopril Treatment in Moderate to Severe Primary Hypertension

Ag, Dupont; Volckaert, A; Ingels, Michel; Am, Bossuyt; Mh, Jonckheer; Ro, Six

doi:10.1097/00005344-198706107-00032

Cited by 10 publications

(4 citation statements)

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“…As in another study [6], we observe no change in cardiac output after lisinopril. On the contrary, Gara- vaglia et al [7] report a significant decrease in cardiac output during lisinopril monotherapy, which they attribute to a decrease in venous tone, as suggested by a redistribution of the intravascular volume from the cardiopulmonary area to the periphery.…”

Section: Discussionsupporting

confidence: 82%

“…Other studies have reported a more striking significant increase in renal plasma flow during long-term lisinopril administration [6,7]. In these conditions, BP is significantly decreased and the only other significant change observed is a reduction in RVRI.…”

Section: Discussionmentioning

confidence: 82%

“…Several investigators have already studied the hemodynamic consequences of lisinopril administration [5][6][7][8]. Conflicting results have been reported concerning the effects of lisinopril on cardiac output [6,7] and renal hemodynamics [5][6][7][8], and, to our knowledge, the comparison of the effects of the first dose of lisinopril to those of the same dose in chronically treated hypertensive patients has never been reported.…”

mentioning

confidence: 99%

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Acute and chronic effects of lisinopril on renal and systemic hemodynamics in hypertension

Degaute

Leeman

Reuse

et al. 1992

Cardiovasc Drug Ther

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Acute and chronic effects of the converting enzyme inhibitor lisinopril on renal and systemic hemodynamics were studied in 12 patients with mild to moderate essential hypertension. After a washout period, cardiac output (measured by Doppler echography), renal plasma flow, and glomerular filtration rate (measured by isotopic techniques) were determined before and after oral administration of 20 mg lisinopril (visit 1). The same protocol was repeated after 3 months of lisinopril therapy 20 mg once daily (visit 2). Acute administration of lisinopril, both in untreated hypertensive patients (visit 1) and during long-term treatment (visit 2), decreased blood pressure (p < 0.05) and increased renal plasma flow (p < 0.05), while cardiac output and glomerular filtration rate were unchanged. Comparison of baseline parameters between visits 1 and 2 showed that chronic treatment with lisinopril decreased blood pressure and renal vascular resistance and that these effects were still significant 24-hours postdosage. We conclude that lisinopril is an effective antihypertensive agent with favorable renal hemodynamic effects.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 82%

mentioning

confidence: 99%

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Acute and chronic effects of lisinopril on renal and systemic hemodynamics in hypertension

Degaute

Leeman

Reuse

et al. 1992

Cardiovasc Drug Ther

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“…Though clearly sufficient to permit reasonably firm conclusions about common renal mechanisms of action of antihypertensive drugs, studies in humans of the renal hemodynamic effects over extended periods would benefit from being more rigorous and numerous. Many have been motivated by an attempt to display “favorable” renal effects, by which is usually meant no reduction in GFR or RBF (Textor et al, 1982 ; Bauer, 1984 ; Sugino et al, 1984 ; Dupont et al, 1987 ; Smith et al, 1987 ; Reams et al, 1988 ; Degaute et al, 1992 ; De Rosa et al, 2002 ), when it is clear that neither of these is a prerequisite for clinical efficacy. Furthermore, some studies misleadingly identify a fall in RVR as contributing to an antihypertensive effect only in proportion to the contribution this fall makes to the decrease in overall SVR (Koshy et al, 1977 ; Preston et al, 1979 ; Warren et al, 1981 ; Thananopavarn et al, 1982 ; Bauer, 1984 ; Dupont et al, 1987 ; Smith et al, 1987 ; van den Meiracker et al, 1989 ; Fridman et al, 2000 ).…”

Section: Discussionmentioning

confidence: 99%

How Do Antihypertensive Drugs Work? Insights from Studies of the Renal Regulation of Arterial Blood Pressure

2016

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Though antihypertensive drugs have been in use for many decades, the mechanisms by which they act chronically to reduce blood pressure remain unclear. Over long periods, mean arterial blood pressure must match the perfusion pressure necessary for the kidney to achieve its role in eliminating the daily intake of salt and water. It follows that the kidney is the most likely target for the action of most effective antihypertensive agents used chronically in clinical practice today. Here we review the long-term renal actions of antihypertensive agents in human studies and find three different mechanisms of action for the drugs investigated. (i) Selective vasodilatation of the renal afferent arteriole (prazosin, indoramin, clonidine, moxonidine, α-methyldopa, some Ca++-channel blockers, angiotensin-receptor blockers, atenolol, metoprolol, bisoprolol, labetolol, hydrochlorothiazide, and furosemide). (ii) Inhibition of tubular solute reabsorption (propranolol, nadolol, oxprenolol, and indapamide). (iii) A combination of these first two mechanisms (amlodipine, nifedipine and ACE-inhibitors). These findings provide insights into the actions of antihypertensive drugs, and challenge misconceptions about the mechanisms underlying the therapeutic efficacy of many of the agents.

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Anti-Adrenergic Therapy in Hypertensive Patients with Concomitant Disease

Abraham¹

2001

Prevention of Disease Progression Throughout the Cardiovascular Continuum

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Improved Renal Function During Chronic Lisinopril Treatment in Moderate to Severe Primary Hypertension

Cited by 10 publications

References 0 publications

Acute and chronic effects of lisinopril on renal and systemic hemodynamics in hypertension

Acute and chronic effects of lisinopril on renal and systemic hemodynamics in hypertension

How Do Antihypertensive Drugs Work? Insights from Studies of the Renal Regulation of Arterial Blood Pressure

Anti-Adrenergic Therapy in Hypertensive Patients with Concomitant Disease

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