Altered contractile responses of arteries from spontaneously hypertensive rat: The role of endogenous mediators and membrane depolarization
Language English Country Netherlands Media print-electronic
Document type Journal Article
PubMed
27721001
DOI
10.1016/j.lfs.2016.10.005
PII: S0024-3205(16)30587-2
Knihovny.cz E-resources
- Keywords
- Adrenergic contraction, Femoral artery, Neuropeptide Y, Propranolol, SHR, Tyramine, Vascular contractility,
- MeSH
- Arteries physiology MeSH
- Potassium metabolism MeSH
- Hypertension MeSH
- Membrane Potentials MeSH
- Norepinephrine metabolism MeSH
- Rats, Inbred SHR physiology MeSH
- Rats, Inbred WKY MeSH
- Muscle Contraction MeSH
- Muscle, Smooth, Vascular physiology MeSH
- Tyramine metabolism MeSH
- Vasoconstriction * MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Potassium MeSH
- Norepinephrine MeSH
- Tyramine 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.
References provided by Crossref.org
Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension
