Prostacyclin generation by cultured human vascular endothelial cells with reference to angiotensin I-converting enzyme.

Sawada, Shohei; Toyoda, Takeo; Takamatsu, Hajime; Niwa, Isamu; Maebo, Norihiko; Tsuji, Hajime; Nakagawa, Masao; Ijichi, Hamao

doi:10.1253/jcj.50.242

Cited by 19 publications

(2 citation statements)

References 11 publications

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“…It has been repeatedly demonstrated in the intact organism that ACE-inhibitors augment the Nakagawa et al, 1987;Sawada et al, 1986). Thus, if prostanoids contribute to the antihypertensive effects of ACE-inhibitors, it most likely is through an indirect effect (e.g.…”

Section: Prostacyclinmentioning

confidence: 99%

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: Prostacyclinmentioning

confidence: 99%

Why are converting enzyme inhibitors vasodilators?

Vanhoutte

Auch-Schwelk

Biondi

et al. 1989

Brit J Clinical Pharma

View full text Add to dashboard Cite

show abstract

“…In vitro, ACE-inhibitors do not augment, or even reduce the production of prostanoids (e.g. Kirschenbaum & Chaudhari, 1988;Nakagawa et al, 1987;Sawada et al, 1986). Thus, if prostanoids contribute to the antihypertensive effects of ACE-inhibitors, it most likely is through an indirect effect (e.g.…”

Section: Prostacyclinmentioning

confidence: 99%

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1989

Brit J Clinical Pharma

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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 endotheliumderived 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. oa-adrenoceptor activation). 5 The different effects of these therapeutic agents may concur to induce peripheral vasodilatation. Keywords adrenergic neurotransmission bradykinin endothelium-derived contracting factor endothelium-derived relaxing factor prostacyclin shear stress

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