ENDOTHELIN IS BLOOD VESSEL SELECTIVE: STUDIES ON A VARIETY OF HUMAN AND DOG VESSELS <i>IN VITRO</i> AND ON REGIONAL BLOOD FLOW IN THE CONSCIOUS RABBIT

Cocks, T. M.; Broughton, Archer; Dib, Mobin; Sudhir, Krishnankutty; Angus, James A.

doi:10.1111/j.1440-1681.1989.tb01551.x

Cited by 41 publications

(17 citation statements)

References 9 publications

(4 reference statements)

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“…The intense, long-lasting renal vasoconstriction at the higher doses is particularly noteworthy. The same phenomenon has been observed in several species (Cocks et al, 1989;Minkes & Kadowitz, 1989) and in vitro (Firth et al, 1988;Cairns et al, 1988) and is associated with a marked decline in renal function (Lopez-Farr6 et al, 1989). On this basis endothelin has been implicated as a mediator in the pathogenesis of acute renal failure (Firth et al, 1988).…”

Section: Discussionmentioning

confidence: 62%

“…Thus, no direct relaxation of arterial segments from a variety of species has ever been demonstrated (Cocks et al, 1989;Eglen et al, 1989;Saito et al, 1989). On the other hand, endothelin has been shown to dilate the rat perfused mesenteric vascular bed when tone was induced by methoxamine (Warner et al, 1989a,b;Randall et al, 1989) and to release the vasodilator eicosanoid, prostacyclin, from rat perfused lungs in vitro (de Nucci et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

“…Porcine endothelin-1 (endothelin) elicits complex cardiovascular effects in a number of species (Lippton et al, 1988;Wright & Fozard, 1988;Yanagisawa et al, 1988;Cocks et al, 1989;Gardiner et al, 1989a;Given et al, 1989;Han et al, 1989;Kitayoshi et al, 1989;Lopez-Farre et al, 1989;Minkes & Kadowitz, 1989;Tsuchiya et al, 1989;Winquist et al, 1989a). In anaesthetized, ganglion-blocked, spontaneously hypertensive (SH) rats, for example, both vasoconstriction and vasodilatation are seen in vascular beds such as the hindquarter or carotid, whereas other regions, including renal and mesenteric, respond to endothelin solely with vasoconstriction (Wright & Fozard, 1988).…”

Section: Introductionmentioning

confidence: 99%

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Differences in regional vascular sensitivity to endothelin‐1 between spontaneously hypertensive and normotensive Wistar‐Kyoto rats

Wright

Fozard

1990

British J Pharmacology

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1 The systemic and regional haemodynamic effects of porcine endothelin-1 (endothelin) have been measured in anaesthetized spontaneously hypertensive (SH) rats rendered areflexic by ganglion blockade; comparisons were made with age-matched Wistar-Kyoto (WKY) control animals. 2 In both SH and WKY rats endothelin (0.1-1 nmol kg-1 i.v.) elicited an initial, short-lived (<2 min), fall in blood pressure which was associated with substantial increases in hindquarter and carotid vascular conductances. Both the blood pressure falls and the peripheral vasodilator responses were greater in SH than in WKY rats. 3 The initial depressor effects of endothelin were followed by marked and sustained increases in blood pressure associated with constriction in carotid, hindquarter, renal and mesenteric vascular beds. Vasoconstrictor responses were quantitatively similar in the two rat strains. 4 Pretreatment with indomethacin (5mgkg-t i.p. or i.v.) did not alter the responses to endothelin, 1 nmol kg-1, in SH rats. 5 The regional haemodynamic effects of intravenously administered acetylcholine (0.01-1 pg kg-), nitroprusside (0.3-lOpgkg-') and angiotensin II (0.01-0.1 ugkg-1) were similar in SH and WKY rats. 6 Endothelin (10-10-3 x 10 -8M) contracted aortic rings from both SH rats and WKY control animals. Removal of the endothelium enhanced significantly the sensitivity of tissues from both WKY and SH rats to endothelin; the increase in sensitivity was greater in tissues from SH than WKY rats. 7 The results demonstrate qualitative similarities in the complex haemodynamic effects of endothelin in SH rats and WKY control animals. However, the SH rats display substantially greater vasodilator responses to endothelin than WKY. Eicosanoid generation is not the mechanism of the vasodilator action of endothelin in SH rats under the conditions of our experiments.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Differences in regional vascular sensitivity to endothelin‐1 between spontaneously hypertensive and normotensive Wistar‐Kyoto rats

Wright

Fozard

1990

British J Pharmacology

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“…Vasodilator responses to endothelin-1 have equally been demonstrated in a variety of isolated blood vessel prep-arations (see, e.g., Cocks et al, 1989;Folta et al, 1989;Randall et al, 1989;Warner et al, 1989;Baydoun et al, 1990;Hasunuma et al, 1990;Kitazumi et al, 1990;Perreault & De Marte, 1991).…”

Section: Introductionmentioning

confidence: 99%

The role of nitric oxide in the regional vasodilator effects of endothelin‐1 in the rat

Fozard

Part

1992

British J Pharmacology

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1 The role of nitic oxide (NO) derived from L-arginine in the regional vasodilator effects of endothelin-1 has been investigated in anaesthetized, spontaneously hypertensive (SH) rats in which autonomic reflexes were abolished by ganglion blockade. The experimental design incorporated animals infused with phenylephrine to mimic the peripheral vasoconstrictor effects of the NO biosynthesis inhibitors and a single dose per animal paradigm to obviate problems of tachyphylaxis to the vasodilator effects of endothelin-1. 2 Infusion of the inhibitor of NO synthase, N-monomethyl-L-arginine (L-NMMA) at a dose (5mgkg-min-1) which maximally raised blood pressure did not influence either the fall in blood pressure or the vasodilator responses induced in the hindquarters and carotid vascular beds by endothelin-1 (1 nmol kg ', i.v.). The duration (but not the initial magnitude) of the vasodepressor response to endothelin-1 was however significantly attenuated (by 49%) during infusion of the more potent inhibitor of NO synthase, NG-nitro-L-arginine methyl ester (L-NAME), 2mg kg-min-'.3 Increasing the dose of L-NAME to 10 and 25mgkg-'min-1 significantly attenuated, but did not abolish, the falls in blood pressure and hindquarters vasodilator responses to acetylcholine, 1 pg kg-1, and endothelin-1, 1nnmolkg-min-u. The effects were selective in that vasodepressor responses to the endothelium-independent vasodilator, sodium nitroprusside, 1-l0mg kg min , were unaltered.4 The data indicate that NO generated de novo from L-arginine mediates a significant component of the vasodilator effect of endothelin-1 in the anaesthetized, ganglion-blocked SH rat. However, a major component of the vasodepressor effects of both endothelin-1 and acetylcholine may occur independently of this mechanism.

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“…3 Endothelins-1, 2 and 3 induce transient vasodilatation due to NO and prostacyclin release, before the development of sustained vasoconstriction. 39,40 Vasoconstriction to ET-1 is mediated by vascular smooth muscle cell ET A -and ET B -receptors. Endothelial cell ET B -receptors mediate vasodilatation through production of endothelium-derived vasodilators (Figure 2).…”

Section: Vascularmentioning

confidence: 99%

Role of endothelin in cardiovascular disease

Agapitov

Haynes

2002

J Renin Angiotensin Aldosterone Syst

154

119

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Endothelins are a family of peptides, which comprises endothelin-1 (ET-1), endothelin-2 (ET-2) and endothelin-3 (ET-3), each containing 21 amino-acids. ET-1 is a peptide secreted mostly by vascular endothelial cells, the predominant isoform expressed in vasculature and the most potent vasoconstrictor currently known. ET-1 also has inotropic, chemotactic and mitogenic properties. In addition, it influences salt and water homeostasis through its effects on the renin-angiotensin-aldosterone system (RAAS), vasopressin and atrial natriuretic peptide and stimulates the sympathetic nervous system.

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ENDOTHELIN IS BLOOD VESSEL SELECTIVE: STUDIES ON A VARIETY OF HUMAN AND DOG VESSELS IN VITRO AND ON REGIONAL BLOOD FLOW IN THE CONSCIOUS RABBIT

Cited by 41 publications

References 9 publications

Differences in regional vascular sensitivity to endothelin‐1 between spontaneously hypertensive and normotensive Wistar‐Kyoto rats

Differences in regional vascular sensitivity to endothelin‐1 between spontaneously hypertensive and normotensive Wistar‐Kyoto rats

The role of nitric oxide in the regional vasodilator effects of endothelin‐1 in the rat

Role of endothelin in cardiovascular disease

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