To clarify the mechanisms of cold-induced vasoconstriction (CIVC), 'in vivo' and 'in vitro' experiments were conducted. In urethane anesthetized rabbits, the central ear artery was isolated and perfused with Ringer Lock's solution at a constant flow rate. Cold water application to the ear increased the ear vessdl resistance. The increase was reduced by xylocaine application on the perivascular sympathetic nerves. The perivascular sympathetic nerve discharges were reflexly increased upon exposure to cold. These results indicate that a neurogenic factor plays a significant role in CIVC. Since the non-neurogenic fraction of cold-induced increase in ear vessel resistance was not altered by NaCN addition in the perfusate, participation of myogenic factor in CIVC appears to be minimal, if at all. The 'in vitro' experiment, however, revealed that bold temperature does affect vascular smooth muscle functions. It was found that a helical strip of the central ear artery contracted transiently when a warm bath solution (37℃) was replaced by a cold one (10℃). The contraction was still observed in a Ca-free solution. However, a helical strip which had been metabolically inctivated with NaCN became unresponsive to cold exposure. Caffeine elicited a similar transient contraction which did not require Ca either in the bath solution; it was facilitated in a cold bath. Contraction either by high K, norepinephrine (NE) or tyramine was reduced in a cold bath as compared with that in a warm bath. NE as well as K contraction disappeared in a Ca-free solution. Ouabain, an inhibitor of Na/K pump, did not elicit a contraction either in a warm or cold bath within a period of 5min. It was concluded that a considerable fraction of CIVC is produced by a somatosympathetic vasoconstrictor reflex; however, the possibility exists that, under certain circumstances where blood vessels are extremely cooled, a myogenic mechanism, probably a cold-induced Ca release from intracellular Ca stores, may contribute to CIVC. On such occasions, certain other mechanisms, such as NE release from the nerve terminal as well as vascular responsiveness to the released NE, and potential-dependent Ca-influx, are affectdd in such a way as to negate CIVC. Neither reduced Na/K pump activity or purely physical shortening of collagen or elastic fibers, appear to contribute to CIVC.

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