Altered contractile responses of arteries from spontaneously hypertensive rat: The role of endogenous mediators and membrane depolarization

0467207 - FGÚ 2017 RIV GB eng J - Journal Article
Bencze, Michal - Behuliak, Michal - Vavřínová, Anna - Zicha, Josef
Altered contractile responses of arteries from spontaneously hypertensive rat: The role of endogenous mediators and membrane depolarization.
Life Sciences. Roč. 166, Dec 1 (2016), s. 46-53. ISSN 0024-3205. E-ISSN 1879-0631
R&D Projects: GA ČR(CZ) GAP304/12/0259; GA MZd(CZ) NV15-25396A
Institutional support: RVO:67985823
Keywords : femoral artery * SHR * vascular contractility * adrenergic contraction * tyramine * propranolol * neuropeptide Y
Subject RIV: FA - Cardiovascular Diseases incl. Cardiotharic Surgery
Impact factor: 2.936, year: 2016

Spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) arteries were stimulated by norepinephrine, increased extracellular K+ or tyramine. Strain difference was not observed in the contraction elicited by exogenous norepinephrine but SHR arteries responded more to tyramine (causing endogenous norepinephrine release from neuronal varicosities). K+-induced contraction was enhanced in SHR arteries, with no involvement of endogenous catecholamines. The alpha-adrenoceptor blockade lowered tyramine-induced contraction more in SHR arteries; similar effect was achieved by guanethidine-induced sympathectomy. Partial depolarization of WKY arteries by 20 mM K+ enhanced its contraction to SHR level. The blockade of beta-adrenoceptors by propranolol or selective beta2-antagonist ICI-118,551 induced contraction of SHR endothelium-denuded arteries but was without significant effects on WKY arteries unless they were stimulated with K+. Both tyramine-induced and propranolol-induced contractions were attenuated by flupirtine and abolished by nifedipine.
Permanent Link: http://hdl.handle.net/11104/0265318