Renal Vasodilatation Caused by Captopril in Conscious Normotensive and Goldblatt Hypertensive Dogs

Zimmerman, Ben G.; Mommsen, Craig; Kraft, E

doi:10.3181/00379727-164-40896

Cited by 26 publications

(20 citation statements)

References 5 publications

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“…Hence, it is not surprising that ACEinhibitors such as trandolaprilat and perindoprilat significantly augment the endothelium-dependent relaxations evoked by the kinin (Vidal & Vanhoutte, 1988, and unpublished observations). These observations help to explain the conversion of the vasoconstrictor effect of bradykinin into a vasodilator response, as has been reported in vitro as well as the potentiation in vivo of the vasodilator effect of bradykinin (Adamski & Grega, 1988;Kikta & Fregly, 1982;Zimmerman et al, 1980 In the presence of 10-9 M bradykinin PG F20,L 2x 10-6M (c) Other endothelium-dependent vasodilators: Preliminary evidence suggests that certain ACEinhibitors can potentiate endothelium-dependent relaxations to some (e.g. acetylcholine, adenosine diphosphate), but not all (e.g.…”

Section: Endothelium-derived Relaxing Factormentioning

confidence: 86%

Why are converting enzyme inhibitors vasodilators?

Vanhoutte

Auch-Schwelk

Biondi

et al. 1989

Brit J Clinical Pharma

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1. The primary action of the converting enzyme inhibitors to prevent the formation of angiotensin II can explain a decrease in peripheral vascular resistance in patients with elevated, but not in those with normal or reduced plasma renin levels. 2. The inhibition of the breakdown of bradykinin will potentiate the vasodilator properties of the endogenously produced peptide. These include direct relaxation of certain vascular smooth muscle, production of vasodilator prostanoids and release of endothelium‐derived relaxing factor(s). The greater release of the latter in the kidney could exert a negative feedback on the release of renin. 3. In addition, converting enzyme inhibitors may directly (by a prejunctional effect) and indirectly (by curtailing the production of angiotensin II) reduce the release of noradrenaline in the blood vessel wall. 4. Converting enzyme inhibitors may also directly reduce the responsiveness of vascular smooth muscle to vasoconstrictor stimuli (e.g. alpha‐adrenoceptor activation). 5. The different effects of these therapeutic agents may concur to induce peripheral vasodilatation.

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Section: Endothelium-derived Relaxing Factormentioning

confidence: 86%

Why are converting enzyme inhibitors vasodilators?

Vanhoutte

Auch-Schwelk

Biondi

et al. 1989

Brit J Clinical Pharma

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“…However, as reported by REGOLI et al (1962) andGROSS et al (1964), since the contralateral kidney is depleted of renin, it is possible that circulating, rather than intrarenal, angiotensin is responsible for this tonic influence, and since captopril also potentiates bradykinin, it is possible that kinins also have a greater influence on renal vascular tone in this type of hypertensive rats than in NCR. ZIMMERMAN et al (1980) have observed that captopril causes a greater hypotensive effect and an increase in plasma renin activity (PRA) in two-kidney, one-clipped hypertensive dogs, but that the vasodilative effect of captopril on the renal vascular area is not significantly different between hypertensive and control dogs. In explaining their results, they have described that other factors besides the degree of activation of renin-angiotensin system determine the renal vascular response to captopril.…”

Section: Discussionmentioning

confidence: 99%

“…Captopril also induces reduction of the total peripheral resistance with the lowering of arterial pressure in essential hypertension (FUJITANI et al, 1979;TARAZI et a!.,1980). However, hardly any study has been done on the dilative effects of captopril on various regional vascular areas except the study in two-kidney, oneclip renovascular hypertensive dogs by ZIMMERMAN et al (1980). They have reported that a similar dilative effect of captopril was observed in the renal vascular area of these hypertensive and normotensive control animals.…”

mentioning

confidence: 89%

Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

1988

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Mean arterial pressure and three regional blood flows-renal, superior mesenteric, and hindquarter flows-were monitored in conscious normotensive control rats (NCR), in two-kidney, one-clip (two-kidney), and in one-kidney, one-clip (one-kidney) hypertensive rats. After administering captopril, an angiotensin-converting enzyme inhibitor, mean arterial pressure decreased in all three groups. However, lowering of arterial pressure was not statistically significant in any of the groups. Renal flow increased significantly in the intact artery of two-kidney hypertensive rats, whereas it did not significantly increase in the clipped artery of one-kidney hypertensive rats and in the intact artery of NCR. Superior mesenteric flow increased significantly only in one-kidney hypertensive rats. Hindquarter flow did not significantly change in the three groups. Regional resistance reduced significantly in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it did not reduce significantly in these two vascular areas in one-kidney hypertensive rats and in NCR. The present findings show that the reninangiotensin-mediated vasoconstriction plays a role in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it hardly plays a role in these three vascular beds in one-kidney hypertensive rats.

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“…ACE inhibitors are well known to reduce arterial pressure and have been used extensively for patients with hypertension. ACE inhibitors have been used to reduce blood pressure in animal models [12][13][14] and human hypertension. [15][16][17][18][19] In conclusion, these results suggest that hypotensive effects of SDG isolated from flaxseed is mediated through inhibition of angiotensin-converting enzyme.…”

Section: Discussionmentioning

confidence: 99%

Secoisolariciresinol Diglucoside (SDG) Isolated from Flaxseed, an Alternative to ACE Inhibitors in the Treatment of Hypertension

Prasad

2013

Int J Angiol

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Flaxseed comprises 32 to 45% of its mass as oil of which 51% is α-linolenic acid and 15 to 18% is linoleic acid. 1,2 Flaxmeal which is devoid of oil is approximately 55 to 68% of the total flaxseed and contains approximately 16.4 mg/g of secoisolariciresional diglucoside (SDG). 3 SDG content of flaxseed varies between 0.6 and 1.8 g per 100 g. 4 SDG has been isolated from flaxseed. 5 SDG is a phytoestrogen, 6 and phytoestrogens from dietary soy have been shown to have mild hypotensive effect. 7 Prasad 8 has reported that SDG administered intravenously (IV) has a dose-dependent hypotensive effects in Sprague Dawley male rats. He also reported that hypotensive effect starts immediately reaching to a maximum within 15 minutes, after which the pressure tended to recover, but the recovery was not complete even after 4 hours of SDG administration. He also reported that the hypotensive effects of SDG is mediated through the stimulation of guanylate cyclase enzyme. Plant flavonoids have inhibitory effects on angiotensin-converting enzyme (ACE). 9 Substances derived from soy are ACE inhibitors. 10 The renin-angiotensin-aldosterone system (RAAS) plays a major role in the regulation of blood pressure. Within RAAS, ACE converts angiotensin I to angiotensin II which increases the blood pressure by vasoconstriction and by stimulating the production of aldosterone, which promotes sodium and water retention. The ACE Keywords ► arterial pressures ► angiotensin I ► angiotensinconverting enzyme inhibitor ► secoisolariciresinol diglucoside ► flaxseed AbstractSecoisolariciresionol diglucoside (SDG) is a plant lignan isolated from flaxseed and is phytoestrogen. SDG is a potent and long-acting hypotensive agent. Plant phytoestrogens have inhibitory effects on angiotensin-converting enzyme (ACE). The hypotensive effects of SDG, a phytoestrogen, may be mediated through inhibition of ACE. The objective of this study was to investigate if SDG-induced hypotension is mediated through inhibition of ACE. The Sprague Dawley male rats were anesthetized and trachea was cannulated. The right jugular vein was cannulated to administer the drug and the carotid artery was cannulated to record arterial pressures using PIOEZ-1 miniature model transducer (Becton, Dickinson and Company, Franklin Lakes, NJ) and Beckman dynograph (Beckman Instruments, Inc., Schiller Park, IL). The effects of angiotensin I (0.2 µg/kg, intravenously [IV]) in the absence and presence of SDG (10 mg/kg, IV), and SDG alone on systolic, diastolic, and mean arterial pressures were measured before and after 15, 30, and 60 minutes of drug administration. SDG decreased the systolic, diastolic, and mean arterial pressure by 37, 47, and 43%, respectively, at 15 minutes and 18.8, 21.2, and 20.3%, respectively, at 60 minutes. Angiotensin I increased the arterial pressure. SDG decreased angiotensin I-induced rise in the systolic, diastolic, and mean arterial pressures by 60, 58, and 51%, respectively, at 15 minutes and 48, 46, and 30%, respectively, at 60 minutes. The data suggest that SDG...

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Renal Vasodilatation Caused by Captopril in Conscious Normotensive and Goldblatt Hypertensive Dogs

Cited by 26 publications

References 5 publications

Why are converting enzyme inhibitors vasodilators?

Why are converting enzyme inhibitors vasodilators?

Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

Secoisolariciresinol Diglucoside (SDG) Isolated from Flaxseed, an Alternative to ACE Inhibitors in the Treatment of Hypertension

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