Responses of the Canine Saphenous Vascular Bed to Various Biogenic and Foreign Substances

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Responses of the dog saphenous vascular bed to a variety of vasoactive substances were studied under constant flow perfusion. Adrenergic compounds, except isoproterenol, induced a constriction. Releasers of norepinephrine from the sympathetic nerve endings, such as DMPP, tolazoline, TEA and guanethidine also constricted the saphenous vascular bed, and catecholamine-uptake blocking agents such as cocaine and desipramine behaved in the same way. Phentolamine, one of the adrenergic blocking agents, and bretylium, a typical antireleaser of norepinephrine, caused a dilatation. Cholinergic compounds produced a dilatation. Serotonin, angiotensin and vasopressin produced a constriction, while histamine, bradykinin, kallikrein and eledoisin produced a dilatation. Relaxants of the vascular smooth muscle, nitroglycerin, papaverine, dipyridamole and xanthine derivatives dilated the saphenous vascular bed. Ergot alkaloids caused a constriction. Morphine markedly dilated the saphenous vascular bed and nicotinic acid had no activity at all.