Altered contractile responses of arteries from spontaneously hypertensive rat: The role of endogenous mediators and membrane depolarization
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
27721001
DOI
10.1016/j.lfs.2016.10.005
PII: S0024-3205(16)30587-2
Knihovny.cz E-zdroje
- Klíčová slova
- Adrenergic contraction, Femoral artery, Neuropeptide Y, Propranolol, SHR, Tyramine, Vascular contractility,
- MeSH
- arterie fyziologie MeSH
- draslík metabolismus MeSH
- hypertenze MeSH
- membránové potenciály MeSH
- noradrenalin metabolismus MeSH
- potkani inbrední SHR fyziologie MeSH
- potkani inbrední WKY MeSH
- svalová kontrakce MeSH
- svaly hladké cévní fyziologie MeSH
- tyramin metabolismus MeSH
- vazokonstrikce * MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- draslík MeSH
- noradrenalin MeSH
- tyramin MeSH
AIMS: The goal of our study was to reveal the important mechanism(s) responsible for the enhanced contractility of isolated arteries from animals suffering genetic hypertension. MAIN METHODS: Contractile force of endothelium-denuded arteries, modulated by various interventions, was measured by wire myography. KEY FINDINGS: 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 α-adrenoceptor blockade lowered tyramine-induced contraction more in SHR arteries; similar effect was achieved by guanethidine-induced sympathectomy. Partial depolarization of WKY arteries by 20mM K+ enhanced its contraction to SHR level. The blockade of β-adrenoceptors by propranolol or selective β2-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. SIGNIFICANCE: The differences of SHR and WKY arteries were not related to vascular expression of α- and β-adrenoceptors or G-proteins. Enhanced contractility of SHR arteries is related to both increased presence of endogenous norepinephrine in vascular wall and also to altered vascular smooth muscle membrane potential.
Citace poskytuje Crossref.org
Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension
