Responsiveness of Monkey Skeletal Muscle Arteries to Vasoconstrictor Substances before and after Cold Storage

The stainless steel cannula inserting method was used to observe effects of α-adrenoceptor agonists, 5-HT and KCl before and after cold storage (3–5 days, at 4°C) in skeletal muscle branches of the simian deep femoral artery. Epinephrine (EPI), norepinephrine (NE), phenylephrine (PE), methoxamine (MT) and 5-hydroxytryptamine (5-HT) induced marked monophasic vasoconstrictions in a dose-dependent manner. 5-HT induced a greater vasoconstriction in larger diameter vessels (old animals) than that in smaller ones (young animals), suggesting age-related responses. A selective α2-stimulant, Clonidine (CLO) or xylazine (XYL), produced only a slight vasoconstriction. Tyramine (TYR) also produced only a slight vasoconstrictor response. The order of potencies for inducing vasoconstrictions was EPI≥5-HT≥NE>MT=PE≫KCI>CLO=XYL=TYR. The vasoconstrictor responses to all used adrenergic agonists and 5-HT were not significantly influenced by the prolonged cold storage. However, KCI-induced constrictions were significantly suppressed by the cold storage. These results suggest that the postjunctional α-adrenoceptor in simian skeletal muscle arteries is mainly of the α1 -type. Since cold storage caused a significant suppression of the KCI-induced response but not those of adrenoceptor agonists and 5-HT, it was considered that the mechanism of calcium entry to the vascular smooth muscle of skeletal muscle arteries might be significantly damaged by the cold storage.