Endothelium dependence of dilation of pial arterioles in mouse brain by calcium ionophore.
Previous studies have shown that local selective in situ injury of pial arteriolar endothelium eliminates the dilations produced by acetylcholine or bradykinin. One means of producing such injury employs a helium-neon laser in the presence of intravascular Evans blue. Since the endothelium-dependent dilations produced by acetylcholine or bradykinin may be initiated by interaction with endothelial surface receptors, it is possible that the light simply inactivates or destroys these receptors. We used calcium ionophore A-23187, another dilating agent known from in vitro studies of large arteries to be endothelium-dependent, which moves calcium into endothelial cells rather than interacting with surface receptors. Our data in 10 mice show that before injury, 10(-5)M A-23187 dilated arterioles to 109 +/- 2% of control diameter. After selective endothelial injury by helium-neon laser, dilation was essentially abolished (101 +/- 1% of baseline diameter; p less than 0.01, Wilcoxon test). Undamaged sites along the arteriole still dilated to A-23187. Our data indicate that the laser must do more than inactivate surface receptors and are the first in vivo microvascular (vessels of less than 100 micron diameter) data showing endothelium dependence of the response to A-23187.
D000818:Animals; D001160:Arterioles / Q000187:drug effects; D000001:Calcimycin / Q000494:pharmacology*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000502:physiology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010841:Pia Mater / Q000098:blood supply*; D014664:Vasodilation
D000001:Calcimycin