Reactivity and sensitivity of mesenteric vascular beds and aortic rings of spontaneously hypertensive rats to endothelin: effects of calcium entry blockers

Criscione, Leoluca; Nellis, P.; Riniker, B.; Thomann, H; Burdet, Richard

doi:10.1111/j.1476-5381.1990.tb12047.x

Cited by 47 publications

(22 citation statements)

References 21 publications

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“…This indiwerful relaxation cates that the functional alterations of the intraluminal surface ovascular hyperof the endothelium become more pronounced with increasing rats (Dohi et endothelium to noradrenaline did not differ in 2K1C rats and WKY. In the spontaneously hypertensive rat, the responsive-8 to 12 weeks) ness of vascular smooth muscle to endothelin-1 relative to its by intraluminal normotensive controls is still controversial; increased ition of endothe- Miyauchi et al, 1989;Criscione et al, nation induced by 1990), decreased (Dohi & Luscher, 1990b;Auch-Schwelk & Itered. Although Vanhoutte, unpublished observations) and normal responses vith acetylcholine (Diederich et al, 1989;Criscione et al, 1990) to endothelin-1 tivation in norhave been reported.…”

Section: Discussionmentioning

confidence: 99%

“…In the spontaneously hypertensive rat, the responsive-8 to 12 weeks) ness of vascular smooth muscle to endothelin-1 relative to its by intraluminal normotensive controls is still controversial; increased ition of endothe- Miyauchi et al, 1989;Criscione et al, nation induced by 1990), decreased (Dohi & Luscher, 1990b;Auch-Schwelk & Itered. Although Vanhoutte, unpublished observations) and normal responses vith acetylcholine (Diederich et al, 1989;Criscione et al, 1990) to endothelin-1 tivation in norhave been reported. Although some of the differences may be ence was signifiexplained by the differences in the experimental conditions or to renovascular the anatomical origin of the arteries used, the present study ge-matched norfurther supports the notion, at least in mesenteric resistance arteries, that hypertension is associated with a decreased sensitivity to the peptide.…”

Section: Discussionmentioning

confidence: 99%

“…However, the role of endothelin in hypertension is not clear since the responsiveness of arteries obtained from hypertensive animals to the peptide is still controversial. Increased Miyauchi et al, 1989;Criscione et al, 1990), decreased (Dohi & Luscher, 1990b;Auch-Schwelk & Vanhoutte, 1989) and normal responses (Diederich et al, 1989;Criscione et al, 1990) to endothelin-1 have been reported in vessels from spontaneously hypertensive rats. The responsiveness of resistance arteries to endothelin-1 in renovascular hypertension would be of pathophysiological interest, since this type of hypertension is characterized by an increased activity of the renin-angiotensin system (Brunner et al, 1962;Fourcade et al, 1971;Ploth et al, 1977;Huang et al, 1981;Miyazaki et al, 1986;Wilson et al, 1989) and because angiotensin II stimulates the production of endothelin in cultured endothelial cells (Emori et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Renovascular hypertension impairs formation of endothelium‐derived relaxing factors and sensitivity to endothelin‐1 in resistance arteries

Dohi¹,

Criscione

Lüscher³

1991

British J Pharmacology

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1 Endothelium-dependent vascular regulation was investigated in mesenteric resistance arteries of Goldblatt two kidney-one clip (2K1C) renovascular hypertensive rats. 2 Third order branches of mesenteric arteries were dissected free and mounted on glass cannulae in an organ chamber. Changes in vascular diameter were measured in pressurized and perfused arteries with a video dimension analyzer. 3 Acetylcholine evoked endothelium-dependent relaxations that were much more pronounced with intraluminal than with extraluminal application. In 2K1C rats the relaxation induced by intraluminal, but not extraluminal acetylcholine was decreased compared to normotensive Wistar Kyoto rats (WKY). Increased duration of hypertension further decreased the response to intraluminal but not extraluminal acetylcholine. 4 Endothelin-1 and noradrenaline caused contractions which were augmented by removal of the endothelium. This augmentation was reduced in 2K1C rats compared to WKY; the difference was small with noradrenaline but more pronounced with endothelin-1. 5 In arteries without endothelium the sensitivity, but not the maximal contraction to endothelin-1 was lower in 2K1C rats, while the response to noradrenaline was not different in 2K1C rats and WKY. The sensitivity to the peptide was not further affected by increasing the duration of hypertension. 6 Thus, renovascular hypertension leads to an impaired intraluminal, but not extraluminal activation of the release of endothelium-derived relaxing factor and a decreased inhibitory effect of the endothelium against endothelin-1-and noradrenaline-induced contractions in mesenteric resistance arteries. Furthermore, the sensitivity, but not the maximal response of vascular smooth muscle to endothelin-1 was reduced.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Renovascular hypertension impairs formation of endothelium‐derived relaxing factors and sensitivity to endothelin‐1 in resistance arteries

Dohi¹,

Criscione

Lüscher³

1991

British J Pharmacology

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Section: Biological Actionsmentioning

confidence: 99%

“…The next issue to be taken into account is the responsiveness to ET, since the biological action of ET could also be determined by sensitivity on the receptor side. However, changes in the pressor response in vivo [56,57] and in the vasoconstrictive response of isolated arteries in vitro [58][59][60][61] of SHR are inconclusive.Increased sensitivity to ET-1 despite the normal plasma levels reported in some studies in SHR [56,59] 35%. Both the glomerular filtration rate and renal plasma flow increased by approximately 50% over the control.…”

mentioning

confidence: 99%

Recent Advances in Endothelin Research on Cardiovascular and Endocrine Systems.

Naruse¹,

Naruse²,

Demura³

1994

Endocr J

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IntroductionSince the quite exciting discovery in 1988 of endothelin (ET) in the culture medium of aortic endothelial cells by Yanagisawa and coworkers [1], evidence has accumulated to support its important roles in the regulation of blood pressure and body fluid homeostasis and its pathophysiological significance in various cardiovascular diseases. The discovery of ET and the opponent substances including nitric oxide [2] and natriuretic peptides [3] during the last decade was epoch-making in the field of "Cardiovascular Endocrinology". Because of its impressive potency and the long duration of its pressor action [1], the roles of ET in the regulation of cardiovascular homeostasis have been extensively studied.However, the co-expression or close localization of ET and its receptors in various tissues other than the vascular vessels suggest non-vascular roles of ET [4][5][6]. In the present review, we firstly integrate the information relevant to its physiological role in blood pressure regulation and possible pathogenic role in hypertension.We secondarily focus on the possible roles of ET in the endocrine system, especially in the pituitary and adrenal.Substantial review articles on ET in the kidney [7,8], ET and the heart [9], the growth regulating properties of ET [10], and ET in bronchial diseases [11, 12] have been published. Structure of ET and ET ReceptorThe molecular and biochemical aspects of ET family peptides and ET receptors have been reviewed by Masaki and Yanagisawa [13] and others [14][15][16]. We here describe the fundamentals. ET PeptidesThe ET molecule consists of 21 amino acid residues with two intramolecular disulfide bonds between cystein residues at 1 and 15 and 3 and 11, respectively. The ring structure and the hydrophobic amino acid residues at the C-terminus are indispensable to its full biological activities. There are three distinct isof orms of ET: ET-1, . The difference in the amino acid sequence is seen in the ring structure, while they share the same sequence in the linear C-terminal portion. Interspecies differences are minimal [13][14][15][16]. Interestingly, the amino acid sequence of a family of rare snake venoms, the sarafotoxins, is very similar to the sequence of ET [16], composing the ET-sarafotoxin family and suggesting the importance of the peptide in evolution.PreproET-1, the precursor of the peptide, is synthesized through the gene transcription and translation. Expression of the preproET-1 mRNA in the endothelial cells is stimulated by various humoral and physical factors: thrombin, TGF-f3, interleukin-1, TNF-a, angiotensin II (Ang II), vasopressin, and shear stress (for review see [13][14][15] produced.In addition, the existence of ET was also shown by immunoassay in a variety of tissues other than the vascular endothelium [22]. The ET-1 content is the highest in the posterior pituitary and the lung followed by the anterior pituitary, brain, and adrenal gland. The ET-3 content is highest in the posterior and anterior pituitaries.The ET-1 content is significantly hi...

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Endothelin‐1 modulates vascular smooth muscle structure and vasomotion: Implications in cardiovascular pathology

Ohlstein

Douglas

1993

Drug Development Research

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Endothelin-I modulates vascular smooth muscle tone by exerting potent vasoconstrictor actions through the ETA receptor subtype located on the membranes of vascular smooth muscle cells. This receptor subtype also mediates the growth-promoting actions of this peptide in vascular smooth muscle cells. The ETA receptor is distinct, however, from the endothelin receptor subtype located on the endothelium; the anatomically and functionally distinct ET, receptor mediates the release of the endothelium-derived factor nitric oxide, a labile substance which not only produces potent vasodilation but also possesses anti-mitogenic activity. This report describes the interaction between these two vasoactive factors i n the control of cardiovascular function. Under normal conditions the endothelium serves to modulate the contractile and proliferative actions of endothelin-I . However, many cardiovascular disorders (e.g., hypertension, atherosclerosis, vascular restenosis, subarachnoid hemorrhage, etc.) are associated with both abnormal endothelial cell function, resulting in an inability to synthesize and/or release nitric oxide, and elevated circulating levels of endothelin-I. Since the resultant loss/inhibition of nitric oxide will augment both the contractile and proliferative actions of endothelin-I, this has the potential to promote vasoconstriction and smooth muscle hyperplasidhypertrophy at the site of any such lesion. Since evidence i s accumulating that both endothelin-I and nitric oxide play pivotal roles in the control of both vascular smooth muscle tone and growth, any imbalance between these two counter-regulatory systems is likely to have profound pathological consequences within the cardiovascular system. 0 1993 Wiley-Liss, Inc.

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Reactivity and sensitivity of mesenteric vascular beds and aortic rings of spontaneously hypertensive rats to endothelin: effects of calcium entry blockers

Cited by 47 publications

References 21 publications

Renovascular hypertension impairs formation of endothelium‐derived relaxing factors and sensitivity to endothelin‐1 in resistance arteries

Renovascular hypertension impairs formation of endothelium‐derived relaxing factors and sensitivity to endothelin‐1 in resistance arteries

Recent Advances in Endothelin Research on Cardiovascular and Endocrine Systems.

Endothelin‐1 modulates vascular smooth muscle structure and vasomotion: Implications in cardiovascular pathology

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