The effect of subarachnoid hemorrhage on mechanisms of vasodilation mediated by cyclic adenosine monophosphate

Journal of Neurosurgery
H Onoue, Z S Katusic

Abstract

This study was designed to determine whether subarachnoid hemorrhage (SAH) affects the function of the K+ channels responsible for relaxation of canine cerebral arteries in response to adenylate cyclase activation. The effect of K+ channel inhibitors on the arterial relaxation response to forskolin, a direct adenylate cyclase activator, was studied in rings of basilar arteries obtained from normal dogs and dogs in which SAH was induced (double-hemorrhage model). The levels of adenosine 3',5'-cyclic monophosphate (cAMP) were measured using the radioimmunoassay technique. In rings with the endothelium removed, relaxation induced by forskolin was not affected by SAH. The relaxation response to forskolin was reduced by charybdotoxin (10(-7) mol/L), a selective Ca++-activated K+ channel inhibitor, in normal arteries and arteries subjected to autologous blood injection. This inhibitory effect of charybdotoxin was significantly greater in arteries involved in SAH than in normal vessels. The relaxation response to forskolin was reduced by 4-aminopyridine (10(-3) mol/L), a delayed rectifier K+ channel inhibitor, only in arteries involved in SAH. In contrast, the relaxation response to forskolin was not affected by glyburide (10(-5) mol/...Continue Reading

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Citations

Nov 22, 2011·World Neurosurgery·Robert G WhitmoreSherman C Stein
Feb 27, 2007·Stroke; a Journal of Cerebral Circulation·Gavin W BritzAl C Ngai
Aug 17, 2002·Neurosurgery·Samuel D MacomsonEllen G Shaver
Mar 17, 2000·Neurosurgery·H H Dietrich, R G Dacey
Oct 4, 2006·Current Opinion in Anaesthesiology·J F Zander
Oct 25, 2002·Cardiovascular Drug Reviews·Katsufumi MizushigeHitoshi Suzuki
Nov 24, 1999·The American Journal of Physiology·C G Sobey, L Quan

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