title: Altered contractile responses of arteries from spontaneously hypertensive rat: The role of endogenous mediators and membrane depolarization.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  Contractile force of endothelium-denuded arteries, modulated by various interventions, was measured by wire myography.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic. Electronic address: michalbencze@gmail.com.
authors.forename: Michal
authors.initials: M
authors.lastname: Bencze
authors.affiliation: Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
authors.forename: Michal
authors.initials: M
authors.lastname: Behuliak
authors.affiliation: Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic; Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic.
authors.forename: Anna
authors.initials: A
authors.lastname: Vavřínová
authors.affiliation: Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
authors.forename: Josef
authors.initials: J
authors.lastname: Zicha
mesh_terms: D000818:Animals; D001158:Arteries / Q000502:physiology*; D006973:Hypertension; D008297:Male; D008564:Membrane Potentials; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009638:Norepinephrine / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D011918:Rats, Inbred SHR / Q000502:physiology*; D011921:Rats, Inbred WKY; D014439:Tyramine / Q000378:metabolism; D014661:Vasoconstriction
chemical_list: D011188:Potassium; D009638:Norepinephrine; D014439:Tyramine
keywords: Adrenergic contraction; Femoral artery; Neuropeptide Y; Propranolol; SHR; Tyramine; Vascular contractility