title: Electromechanical alterations in the cerebrovasculature of stroke-prone rats.
abstract: OBJECTIVE
  Cerebrovascular pressure-dependent constriction (PDC) is associated with smooth muscle (SM) depolarization and Ca(2+) influx through voltage-gated channels. We studied the alterations in electromechanical contraction in the middle cerebral arteries (MCAs) of stroke-prone Wistar-Kyoto spontaneously hypertensive rats (SHRsp) in relation to the stroke-related loss of PDC.
  
  
  METHODS
  Constriction to pressure, elevated [K(+)](o) and/or [Ca(2+)](o), and SM membrane potentials (E(m)) were measured in isolated pressurized MCAs of SHRsp and stroke-resistant SHR.
  
  
  RESULTS
  MCAs of SHRsp exhibited an age-related decrease in PDC before hemorrhagic stroke and a loss of PDC after stroke. At 100 mm Hg, the MCAs of poststroke SHRsp maintained partial constriction that was not altered with pressure but was inhibited by nifedipine (1 micromol/L). The MCAs of poststroke SHRsp constricted to vasopressin (0.17 micromol/L) but not to elevated [K(+)](o). When pressure was reduced from 100 to 0 mm Hg, the MCAs from young prestroke SHRsp exhibited SM hyperpolarization (-38 to -46 mV), whereas those of poststroke SHRsp maintained a constant, depolarized E(m) (-34 mV). Alterations in E(m) with varying [K(+)](o) suggested that there was a decrease in SM K(+) conductance in the MCAs of poststroke SHRsp.
  
  
  CONCLUSIONS
  The observation that the MCAs of poststroke SHRsp depolarize but do not constrict to elevated [K(+)](o) suggests the presence of dysfunctional voltage-gated Ca(2+) channels. The inability to alter E(m) with pressure or to constrict to depolarization could partially contribute to the loss of PDC in the MCAs of poststroke SHRsp.
authors.affiliation: Division of Basic Medical Sciences, Memorial University, St John's, Newfoundland, Canada. jsmeda@morgan.ucs.mun.ca
authors.forename: J S
authors.initials: JS
authors.lastname: Smeda
authors.forename: S
authors.initials: S
authors.lastname: King
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002536:Cerebral Arteries / Q000503:physiopathology*; D004594:Electrophysiology; D020022:Genetic Predisposition to Disease; D006973:Hypertension / Q000235:genetics*; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D009543:Nifedipine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D011312:Pressure; D051381:Rats; D011918:Rats, Inbred SHR / Q000235:genetics; D011921:Rats, Inbred WKY / Q000235:genetics; D012016:Reference Values; D020521:Stroke / Q000235:genetics* / Q000503:physiopathology*; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014666:Vasomotor System / Q000503:physiopathology; D014667:Vasopressins / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D009543:Nifedipine; D011188:Potassium; D002118:Calcium