The effect of converting enzyme inhibition with SQ20,881 on plasma and urinary kinins, prostaglandin E, and angiotensin II in hypertensive man.

Vinci, Joseph M.; Horwitz, David L.; Zusman, Randall M.; Pisano, John J.; Catt, Kevin J.; Keiser, Harry R.

doi:10.1161/01.hyp.1.4.416

Cited by 119 publications

(33 citation statements)

References 42 publications

(24 reference statements)

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“…19 " 23 Our finding of a slight hypotensive effect of high-dose captopril monotherapy in LPH patients is compatible with the antihypertensive effects of captopril other than through antagonism of angiotensin H-medicated vasoconstriction. However, since this therapeutic response was only slight, we conclude that the major therapeutic effect is upon blockade of angiotensin II production.…”

supporting

confidence: 73%

Synergistic effect of captopril with hydrochlorothiazide for the treatment of low-renin hypertensive black patients.

et al. 1983

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A common etiologic role for the renin-angiotensin system in essential hypertension was postulated 1 after a vasodepressor response was noted in 85% of patients with essential hypertension during converting enzyme inhibition. Curiously, however, captopril, a converting enzyme inhibitor that can be administered by mouth, occasionally causes a blood pressure fall in patients with low-renin hypertension (LRH), 2 3 suggesting that it has antihypertensive activity other than through blockade of angiotensin IIinduced vasoconstriction.Many patients with LRH exhibit enhanced aldosterone secretion in response to administered angiotensin II, 4 -5 as do patients with primary aldosteronism with bilateral zona glomerulosa hyperplasia, 6 ' 7 and have thus been postulated to have a mild form of primary

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supporting

confidence: 73%

Synergistic effect of captopril with hydrochlorothiazide for the treatment of low-renin hypertensive black patients.

et al. 1983

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“…In vivo the same agent increased prostaglandin in patients with essential hypertension who were ingesting a moderate sodium intake, but not when ingesting a low sodium intake (27). Unfortunately, even on the higher sodium intake teprotide reduced plasma AII concentration, making it impossible to ascertain the relative influence of changes in AII and prostaglandins in the depressor response.…”

Section: Methodsmentioning

confidence: 99%

Captopril-induced Changes in Prostaglandin Production

Swartz¹,

Williams²,

Hollenberg³

et al. 1980

J. Clin. Invest.

328

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A B S T R A C T Captopril is a potent hypotensive agent whose efficacy has hitherto been attributed to its ability to alter either angiotensin II formation or kinin degradation. Our purpose was to examine captopril's acute effect on prostaglandin production, because changes in neither the renin-angiotensin nor the kallikrein-kinin systems appear adequate to account for the fall in arterial pressure. The plasma levels of' angiotensin II, kinins, and prostaglandins were determined in response to increasing doses (5, 12.5, and 25 mg) of captopril and these responses were compared with the change in arterial pressure observed in nine supine normal male subjects studied on both a high (200 meq) and low (10 meq) sodium intake.Captopril significantly (P < 0.01) increased the levels of the 13,14-dihydro-15-keto metabolite of prostaglandin E2 (PGE2-M), a potent vasodilator, with similar responses being observed on both a high aind a low sodium intake. No significant changes in the plasma levels of 6-keto-prostaglandin F,a, or thromboxane B2, the stable products of prostacyclin and thromboxane A2, respectively, occurred.The depressor response to captopril correlated with the change in PGE2-M (r = 0.52, t = 5.44, P < 0.0001). On the other hand, although significant (P < 0.02) decrements in angiotensin II and increments in plasma kinins accompanied the hypotensive response in sodium-restricted subjects, in sodium-loaded subjects where the renin-angiotensin system was suppressed, nio change in angiotensin II, and only a modest change in kinins was noted, even though significant (P < 0.01) decrements in diastolic blood pressure occurred (-10+2 mm Hg).Thus, changes in depressor prostaglandin production can better account for the hypotensive response to

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“…aprotinin (10,18), and indomethacin (19,20) ( 10. 18, 19 (25)(26)(27)(28). The consensus view is that the action o f captopril in reducing blood pressure cannot be entirely explained by its inhibition o f ACE.…”

Section: Resultsmentioning

confidence: 99%

The Effect of Captopril on Urinary Protein Excretion in Puromycin Aminonucleoside Nephrosis in Rats

et al. 1985

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ABSTIL4ff. We investigated the effect of captopril, an orally active angiotensin converting enzyme inhibitor, on urinary protein excretion in puromycin aminonucleoside nephrotic rats. The administration of captopril(10 mg/100 g body weight) decreased proteinuria on days 10-14 following the administration of puromycin aminonucleoside (73.0 versus 125.0 rng, p c 0.01), without affecting glomerular filtration rate. The beneficial effect of captopril was not abolished by the continuous intravenous infusion of angiotensin I1 (10 pg/kg/h for 9 days) or subcutaneous injections of aprotinin (50,000 KIU/day for 3 days). Indomethacin, in moderate (5 mg/kg/day for 3 days) or high (10 mg/ kg/day) doses, abolished the captopril attenuation in urinary protein excretion. The salutory effect of captopril was characteized by a reduction in the fractional excretion of protein without compromising the glomerular filtration rate. No difference in renal ultrastructure was noted in captopril-treated versus control animals. Captopril was ineffective in reducing urinary protein excretion in rats with adriamycin-induced glomerulopathy. W e conclude that captopril acts to reduce proteinuria in renal disease states arising from depletion of the glomerular basement membrane polyanion. The mechanism of action is postulated to be an alteration in renal hemodynamics, namely increased blood flow and a decrease in the ultrafiltration coefficient, that are the consequence of increased intrarenal prostaglandin production. (Pediatr Res 19: 828-834, 1985) Abbreviations AI, angiotensin I AII, angiotensin I1 ACE, angiotensin converting enzyme BW, body weight FEpr, fractional excretion of protein G B M , glomeruiar basement membrane GFR, glomerular filtration rate ka ultrafiltration coefficient PAN, puromycin aminonucleoside Q A , renal blood flow Many vasoactive substances are capable of altering quantitative urinary protein excretion in normal and disease states.The

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The effect of converting enzyme inhibition with SQ20,881 on plasma and urinary kinins, prostaglandin E, and angiotensin II in hypertensive man.

Cited by 119 publications

References 42 publications

Synergistic effect of captopril with hydrochlorothiazide for the treatment of low-renin hypertensive black patients.

Synergistic effect of captopril with hydrochlorothiazide for the treatment of low-renin hypertensive black patients.

Captopril-induced Changes in Prostaglandin Production

The Effect of Captopril on Urinary Protein Excretion in Puromycin Aminonucleoside Nephrosis in Rats

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