Reoxygenation and Calcium-Induced Cerebroarterial Contractions as Affected by Vasodilator Agents

Abstract

Summary: In helical strips of dog cerebra� arterie . s . ex posed to Ca2+ -free medium under hYPoxlc condltions (95% N 2 and 5% CO 2 ), prostaglandin (PO) F 2 1l produced a slight tonic contraction. The addition . of Ca2+ evok � d a phasic contraction followed by relax�t � on and a sus . t � med contraction, and reoxygenation ehclt � d an addltIOnal The mechanical responses of isolated cerebral ar teries to vasodilator substances differ from those of extracerebral arteries. For instance, Ca 2 + entry blockers, including verapamil, diltiazem, nifed ipine, nicardipine, and flunarizine, relax cerebral arteries more than extracerebral arteries (Shimizu et aI., 1980; Van Nueten and Vanhoutte, 1981; Ya mamoto et aI., 1983), whereas relaxations caused by acetylcholine and isoproterenol are not so evi dent in cerebral arteries as in others (Toda, 1974a(Toda, , 1979. Prostaglandin (PG) 1 2 , nitroglycerin, and Ca 2 + entry blockers produce marked relaxations of cerebral arteries; however, their mechanisms of ac tion are quite different. PGI 2 and nitroglycerin relax the arteries, possibly by accumulation of cellular cyclic AMP and cyclic GMP, respectively (Kuko-

Vasodilatory effects of cinnamaldehyde and its mechanism of action in the rat aorta

“…When aorta rings were exposed to Ca 2+ -free media, addition of phenylephrine 10 −6 M elicited a small tonic contraction induced mainly by intracellular Ca 2+ release from endoplasmic reticulum stores 15. Pretreatment of endothelium-denuded rings with cinnamaldehyde 5.0 × 10 −5 g/mL significantly reduced phenylephrine-induced contraction under extracellular Ca 2+ -free conditions (Figure 6C).…”

“…Vascular endothelium plays a key role in maintaining normal function of the vasculature 15. Endothelial cells release endothelium-dependent vasodilators, such as nitric oxide and prostacyclin (prostaglandin I 2 ), upon stimulation of various factors in the blood stream and as a result of physiological stress 15,16.…”

“…Endothelial cells release endothelium-dependent vasodilators, such as nitric oxide and prostacyclin (prostaglandin I 2 ), upon stimulation of various factors in the blood stream and as a result of physiological stress 15,16. Nitric oxide is mainly formed by nitric oxide synthase using L-arginine as a substrate.…”

“…This complex further activates myosin light chain kinase to phosphorylate myosin light chains and cause muscle contraction 24. The intracellular Ca 2+ concentration can be regulated by extracellular Ca 2+ influx through both the voltage-dependent Ca 2+ channel and the receptor-operated Ca 2+ channel, or by intracellular Ca 2+ release from endoplasmic reticulum Ca 2+ stores 15. KCl mainly activates potential-dependent Ca 2+ channels to promote calcium influx and vasoconstriction.…”

The effects of beraprost Na, a stable prostacyclin analog, on animal models of stroke

“…However, it is reported that beraprost increases pre-and postischemic pial arterial diameter of cats (Tanaka et al, 1988), and dilates the isolated cerebral artery from the dog (Akiba et al, 1986) and human (Kobayashi et al, 1989) at concentrations more than 10 -8M. Furthermore, diltiazem, a vasodilator with very weak antiplatelet activity (Lippton et al, 1984;Bian and Toda, 1988), improved survival and convulsion rates in AA-induced sudden death in rabbits. From these facts, although the antithrombotic effect may play a major role, the involvement of vasodilation cannot be denied completely.…”