title: Intracellular Ca2+ and force generation determined in resistance arteries of normotensive and hypertensive rats.
abstract: OBJECTIVE
  Dysfunctional cellular Ca2+ handling has been proposed to underlie the heightened vascular reactivity observed in the spontaneously hypertensive rat (SHR) model of genetic hypertension. We tested the hypothesis that basal or agonist-induced mobilization of intracellular Ca2+ is elevated in mesenteric resistance arteries of SHR compared with the normotensive Wistar-Kyoto (WKY) rat.
  
  
  METHODS
  A method using fura-2 for the simultaneous measurement of intracellular Ca2+ and isometric force generation in isolated mesenteric resistance arteries was employed to measure agonist-induced changes in Ca2+ and force during activation with 100 mmol/l K+ or 10 mumol/l norepinephrine. Arteries with normalized diameter 220-240 microns from male rats aged 14-15 weeks were examined.
  
  
  RESULTS
  No differences were detected between the rat strains in basal Ca2+ concentration or the steady-state concentration of Ca2+ achieved in response to either 100 mmol/l K+ or 10 mumol/l norepinephrine. The relationship between Ca2+ and force during the contractile responses to K+ and norepinephrine was analyzed. No differences between the strains in the level of active stress, normalized to unit intracellular Ca2+, were detected in the steady-state responses to K+ or norepinephrine.
  
  
  CONCLUSIONS
  The present results do not support the hypothesis that alterations in either the basal concentration of intracellular Ca2+ or the amount of intracellular Ca2+ mobilized in response to high levels of norepinephrine or K+ are present in resistance arteries of SHR compared with those of WKY rats. Moreover, these findings suggest that elevations in Ca2+ do not contribute to heightened peripheral resistance in SHR.
authors.affiliation: Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.
authors.forename: R D
authors.initials: RD
authors.lastname: Bukoski
authors.forename: B A
authors.initials: BA
authors.lastname: Lastelic
authors.forename: H
authors.initials: H
authors.lastname: Xue
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.forename: K
authors.initials: K
authors.lastname: Bian
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D007425:Intracellular Membranes / Q000378:metabolism*; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012016:Reference Values; D014655:Vascular Resistance; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D011188:Potassium; D002118:Calcium; D009638:Norepinephrine