Impairment of the Modulatory Role of Nitric Oxide on the Endothelin-1-elicited Contraction of Cerebral Arteries: A Pathogenetic Factor in Cerebral Vasospasm after Subarachnoid Hemorrhage?

Alabadí, José A.; Torregrosa, Germán; Miranda, Francisco Javier Noya; Salom, Juan B.; Centeno, José M.; Alborch, Enrique

doi:10.1097/00006123-199707000-00039

Cited by 38 publications

(20 citation statements)

References 28 publications

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“…An increased vascular response to ET-1 has been reported in different pathophysiological conditions such as cerebral ischemia (Salom et al, 2000), subarachnoid hemorrhage (Alabadi et al, 1997), and hypertension (Cardillo et al, 1999). The vascular hyperreactivity to ET-1 described in this study, together with the increased plasma levels of this peptide in ethanol-treated rats (Nanji et al, 1994), could play a role in the pathogenesis of cerebral ischemia associated with ethanol consumption.…”

Section: Discussionsupporting

confidence: 62%

Ethanol Consumption Enhances Endothelin-1-Induced Contraction in the Isolated Rat Carotid

Tirapelli

Casolari²,

Montezano³

et al. 2006

J Pharmacol Exp Ther

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We investigated the mechanisms involved in the enhancement of endothelin (ET)-1 vascular reactivity induced by ethanol consumption. Ethanol intake for 2, 6, and 10 weeks enhanced the ET-1-induced contractile response of endothelium-intact but not endothelium-denuded rat carotid rings independently of the treatment duration. Conversely, phenylephrine-induced contraction was not affected by ethanol intake. The contraction induced by IRL1620 ,Ala 11,15 )-ET-1-(8 -21)], a selective ET B agonist, was increased after treatment with ethanol in endothelium-intact but not in endothelium-denuded carotid rings. Moreover, ET-1-and IRL1620-induced relaxation was reduced in endothelium-intact phenylephrine-precontracted rings from ethanol-treated rats. Acetylcholine-induced relaxation was not affected by ethanol treatment. N G -Nitro-Larginine methyl ester, 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one, indomethacin, and tetraethylammonium reduced the relaxation induced by IRL1620 in carotid glands from control but not ethanol-treated rats. The mRNA levels for ET A and ET B receptors were not altered by ethanol consumption. However, ethanol treatment reduced the protein expression of ET B receptors. Furthermore, immunohistochemical assays showed reduced immunostaining for endothelial ET B receptors after treatment with ethanol. We conclude that ethanol consumption enhances ET-1-induced contraction in the rat carotid and that this response is not different among the three periods of treatment used in this study. Finally, the potentiation of ET-1-induced vascular reactivity is probably caused by reduced expression of relaxing endothelial ET B receptors.

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Section: Discussionsupporting

confidence: 62%

Ethanol Consumption Enhances Endothelin-1-Induced Contraction in the Isolated Rat Carotid

Tirapelli

Casolari²,

Montezano³

et al. 2006

J Pharmacol Exp Ther

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“…This would suggest that NO is released from a non-endothelial (neuronal) NO source as well as from endothelium in response to 5-HT, in a similar way as described in the responses of the goat middle cerebral artery to 5-HT (Miranda et al, 1996) and endothelin-1 (Alabadí et al, 1997). In carotid and cerebral arteries, vasodilator perivascular nerves that synthesise and release NO by means of nNOS have been identified (Tomimoto et al, 1994;Ignacio et al, 1997).…”

Section: Discussionmentioning

confidence: 73%

Experimental diabetes induces hyperreactivity of rabbit renal artery to 5-hydroxytryptamine

Miranda¹,

Alabadí²,

Lloréns³

et al. 2002

European Journal of Pharmacology

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The influence of diabetes on the response of isolated rabbit renal arteries to 5-hydroxytryptamine (5-HT) was examined. 5-HT induced a concentration-related contraction that was higher in arteries from diabetic rabbits than in arteries from control rabbits. Endothelium removal did not significantly modify 5-HT contractions in arteries from control rabbits but enhanced the response to 5-HT in arteries from diabetic rabbits. Incubation with N G -nitro-L-arginine (L-NA) enhanced contractions to 5-HT in arteries from control and diabetic rabbits. In arteries with endothelium, this L-NA enhancement was lower in diabetic rabbits than in control rabbits. In arteries without endothelium, incubation with L-NA enhanced the maximal contractions to 5-HT in control rabbits but did not in diabetic rabbits. Indomethacin inhibited 5-HT-induced contraction of arteries from control rabbits and enhanced the maximal contraction to 5-HT of arteries from diabetic rabbits. In summary, diabetes enhances contractile response of rabbit renal artery to 5-HT. In control animals, this response is regulated by both endothelial and non-endothelial (neuronal) nitric oxide (NO) and by a vasoconstrictor prostanoid. Diabetes impairs the release of non-endothelial NO and the vasoconstrictor prostanoid. D

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“…1,2 This mechanism is essentially supported by demonstrations that NOS inhibitor enhanced the constrictor effects of exogenous ET-1 in several in vivo and ex vivo preparations. [3][4][5][6][7][8][9][10][11][12][13][14] Thus, an assumption underlying these observations is that the constrictor actions of exogenous and endogenous ET-1 are similarly affected by NO; (2) NO inhibition of ET-1 release. 1,2 Although the detailed mechanism underlying the NO inhibition of acute ET-1 release has not been clearly established, possibilities include decreased conversion of the immediate precursor to ET-1, big ET-1, to ET-1 15 and inhibition of pathways involved in the exocytosis of Weibel-Palade bodies, 16 endothelial granules that store ET-1.…”

Section: • Online Data Supplementmentioning

confidence: 99%

Nitric Oxide Inhibition of Endothelin-1 Release in the Vasculature

Rapoport

2014

Hypertension

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A key function of endothelial derived nitric oxide (NO) is to limit the constrictor capacity of endothelin (ET)-1.1,2 Thus, an imbalance between NO and ET-1 can result in ET-1-dependent increased vascular tone.1 Indeed, the importance of sustained, NO inhibition of the ET-1 drive to increase tone is exemplified in vivo by the rapid, ET-1-mediated arterial pressure elevation after acute NO synthase (NOS) inhibition. Moreover, the ET-1 pressor effect after NOS inhibition is independent of other pressor systems and, thus, reflects the relative importance of NO suppression of this ET-1 drive.2 Two, nonmutually exclusive mechanisms thought to underlie the ET-1 dependency of the increased vascular tone responsible for the NOS inhibitor-induced pressure elevation are (1) NO inhibition of constriction to endogenously released ET-1.1,2 This mechanism is essentially supported by demonstrations that NOS inhibitor enhanced the constrictor effects of exogenous ET-1 in several in vivo and ex vivo preparations. 3-14Thus, an assumption underlying these observations is that the constrictor actions of exogenous and endogenous ET-1 are similarly affected by NO; (2) NO inhibition of ET-1 release. 1,2Although the detailed mechanism underlying the NO inhibition of acute ET-1 release has not been clearly established, possibilities include decreased conversion of the immediate precursor to ET-1, big ET-1, to ET-1 15 and inhibition of pathways involved in the exocytosis of Weibel-Palade bodies, 16 endothelial granules that store ET-1. 17 However, it should be noted that in vivo findings that actually demonstrate the fundamental phenomenon of NO inhibition of ET-1 release are generally lacking.2 Thus, studies purported to demonstrate NO inhibition of ET-1 release have relied largely on isolated vessels and cultured endothelium, as described herein.This review assessed these in vitro findings, with a specific focus toward elucidating the mechanism underlying the NO-mediated negative regulation of ET-1-dependent increased arterial pressure, as demonstrated after acute NOS inhibitor in vivo.2 Findings referred to are mainly those of ET-1 release rather than contractility (eg, those in which ET receptor antagonist prevented the NOS inhibitor-induced decreased flow/increased pressure/tension). 12,18-25 The rationale for this emphasis is that findings based on contractility could reflect NOS inhibitor enhancement of ET-1 constriction rather than increased ET-1 release. Furthermore, we also focus on whether laminar shear stress influences the manifestation of NO inhibition of ET-1 release. That is, the endothelium of arteries that are anatomically linear is subjected to high levels of shear stress while, for example, at bifurcated arterial locations is subjected to low levels of shear stress, regions associated with atherosclerosis. 26 Acute NOS Inhibition/No Donors and ET-1 Release ArteriesIn rat heart perfused at constant flow, increased amounts of ET-1 were detected in the coronary effluent of samples collected for the final 5 to 15 minutes ...

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Impairment of the Modulatory Role of Nitric Oxide on the Endothelin-1-elicited Contraction of Cerebral Arteries: A Pathogenetic Factor in Cerebral Vasospasm after Subarachnoid Hemorrhage?

Cited by 38 publications

References 28 publications

Ethanol Consumption Enhances Endothelin-1-Induced Contraction in the Isolated Rat Carotid

Ethanol Consumption Enhances Endothelin-1-Induced Contraction in the Isolated Rat Carotid

Experimental diabetes induces hyperreactivity of rabbit renal artery to 5-hydroxytryptamine

Nitric Oxide Inhibition of Endothelin-1 Release in the Vasculature

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