Clinical Pharmacokinetics of Ramipril

Meisel, Simcha; Shamiss, Ari; Rosenthal, Talma

doi:10.2165/00003088-199426010-00002

Cited by 52 publications

(34 citation statements)

References 20 publications

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“…The superiority of telmisartan over ramipril in this time period is consistent with the established pharmacokinetic profiles of these agents. [21][22][23] It is also consistent with the results of other trials using 24-h ABPM that have shown superior efficacy of telmisartan compared with antihypertensives from a range of classes, including losartan, 24,25 valsartan, 15,16 amlodipine 26 and perindopril. 27 Evidence that reduction of morning BP provides clinical benefit comes from a study of patients with type II diabetes, hypertension and nephropathy, in whom a reduction of morning SBP in response to antihypertensive treatment was shown to correlate significantly with a slowing of the progression of renal damage.…”

Section: Discussionsupporting

confidence: 79%

Antihypertensive efficacy of telmisartan vs ramipril over the 24-h dosing period, including the critical early morning hours: a pooled analysis of the PRISMA I and II randomized trials

et al. 2009

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Section: Discussionsupporting

confidence: 79%

Antihypertensive efficacy of telmisartan vs ramipril over the 24-h dosing period, including the critical early morning hours: a pooled analysis of the PRISMA I and II randomized trials

et al. 2009

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“…Ramipril has the advantage of being a long-acting substance compared with other ACE inhibitors, with an effective half-life of 13-17 h in adults [13]. It may therefore be given once daily and has few side effects [14,15].…”

Section: Introductionmentioning

confidence: 99%

Effect of ramipril on ambulatory blood pressure and albuminuria in renal hypertension

Soergel

Verho²,

Wühl

et al. 2000

Pediatric Nephrology

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Inhibition of the angiotensin-converting enzyme (ACE) exerts a renoprotective effect in adult patients with chronic kidney disease. We evaluated prospectively changes in blood pressure (BP), protein excretion and renal function after administration of the long-acting ACE inhibitor ramipril as monotherapy during 6 months in 14 moderately hypertensive children aged 5-18 years with various nephropathies. Four patients initially had a decreased glomerular filtration rate (GFR below 60 ml/min/1.73 m2). BP was evaluated by ambulatory 24-h monitoring. After 2 weeks of treatment by oral ramipril (1.5 mg/m2 once daily), mean values of systolic and diastolic 24-h ambulatory BP fell by more than 5 mmHg in nine patients. In eight patients the dose was doubled. At the end of the study systolic BP was below the 95th percentile in 9 and diastolic BP in 13 patients. The initially reduced nocturnal dip increased significantly. Of 11 patients with an increased albumin excretion (median 1.3 g/g creatinine), 6 responded to ramipril by a median reduction of 78% (range 24-83%), whilst in 5 albuminuria increased (median +19%). GFR was well preserved and no other adverse effects from the drug were noted. The study demonstrates that ramipril is an efficacious antihypertensive agent in children with renal hypertension. It is well tolerated, even in mild renal insufficiency. In addition, the drug has a persistent antiproteinuric action in about half of the patients contributing to conserve renal function.

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“…Since ANGII is known as a negative feedback regulator of renin secretion and of renin gene expression (6,7), it is thought that the renin stimulatory effects of ACE inhibitors are related to the inhibition of AnglI formation and consequently to the lowering of circulating and tissue AnglI levels (8).…”

mentioning

confidence: 99%

Tonic stimulation of renin gene expression by nitric oxide is counteracted by tonic inhibition through angiotensin II.

Schricker

Hegyi

Hamann

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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This study was designed to examine the possible involvement of prostaglandins and nitric oxide (NO) in the renin stimulatory effect ofangiotensin 11 (AngII) antagonists. To this end, plasma renin activities (PRAs) and renal renin mRNA levels were assayed in rats that were treated with the Angconverting enzyme inhibitor ramipril or with the AnglI AT1-receptor antagonist losartan. Ramipril and losartan increased PRA values from 7.5 + 1.6 to 86 ± 6 and 78 ± 22 ng of AngI per h per ml and renin mRNA levels from 112 ± 9% to 391 + 20%o and 317 ± 10%o, respectively. Inhibition of prostaglandin formation with indomethacin did not influence basal or ramiprilaffected PRA. Basal renin mRNA levels also were unchanged by indomethacin, while increases in renin mRNA levels after ramipril treatment were slightly reduced by indomethacin. Inhibition of NO synthase by nitro-L-arginine methyl ester (L-NAME) reduced PRA values to 3.2 ± 0.9, 34 ± 13, and 12.1 ± 2.7 ng of AngI per h per ml in control, ramipril-treated, and losartan-treated animals, respectively. Renin mRNA levels were reduced to 77 + 14% under basal conditions and ramipril-and losartan-induced increases in renin mRNA levels were completely blunted after addition of L-NAME. The AngIH antagonists, furthermore, induced an upstream recruitment of reninexpressing cells in the renal afferent arterioles, which was also blunted by L-NAME. These findings suggest that renin mRNA levels are tonically increased by NO and that the action of NO is counteracted by AngII.One of the most prominent in vivo effects of angiotensin (Ang)-converting enzyme (ACE) inhibitors is a marked stimulation of renin secretion and renin gene expression in the kidneys (1-5). Since ANGII is known as a negative feedback regulator of renin secretion and of renin gene expression (6, 7), it is thought that the renin stimulatory effects of ACE inhibitors are related to the inhibition of AnglI formation and consequently to the lowering of circulating and tissue AnglI levels (8).There is evidence that several in vivo effects of ACE inhibitors are not, as originally thought, due to the inhibition of AnglI formation but to the inhibition of kinin degradation (9-12). Inhibition of kinin degradation results in elevated tissue levels of autacoids such as prostaglandins and nitric oxide (NO), the formation of which is stimulated by kinins (11)(12)(13)(14). Although NO is reported to inhibit the renin system (15-17), contradictory findings suggest that NO stimulates the renin system (18-25) and also that prostaglandins stimulate the renin system (for review, see ref. 26). With such a stimulatory effect of NO and prostaglandins on the renin system, it is possible that the renin stimulatory effect of ACE inhibitors could be related to an enhanced formation of prostaglandins and NO.To investigate the mode of action of ACE inhibitors on the renin system, we studied renin release and renin mRNA levels in the kidneys of conscious rats that were treated with the ACE inhibitor ramipril (27) or with the Angll AT1-rec...

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Clinical Pharmacokinetics of Ramipril

Cited by 52 publications

References 20 publications

Antihypertensive efficacy of telmisartan vs ramipril over the 24-h dosing period, including the critical early morning hours: a pooled analysis of the PRISMA I and II randomized trials

Antihypertensive efficacy of telmisartan vs ramipril over the 24-h dosing period, including the critical early morning hours: a pooled analysis of the PRISMA I and II randomized trials

Effect of ramipril on ambulatory blood pressure and albuminuria in renal hypertension

Tonic stimulation of renin gene expression by nitric oxide is counteracted by tonic inhibition through angiotensin II.

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