VASCULAR CONTRACTIONS TO SEROTONIN ARE AUGMENTED BY COOLING

Human saphenous veins (HSV; n = 17) were obtained at surgery and assayed immediately. The veins were cut into rings, suspended in organ chambers and connected to force transducers for the recording of isometric tension. Tail arteries (RTA) from male Sprague-Dawley rats were similarly prepared. In quiescent rings, cooling from 37 to 24-degrees-C had no significant effect. In the presence of alpha-adrenoceptor blockade, potassium chloride (KCl, 10-80 mM) caused concentration-dependent contractions that were inhibited slightly by cooling. Serotonin (5-HT, 10(-8) - 10(-5) M) elicited concentration-dependent contractions in both the HSV and RTA with EC50'S (-log concentration required to induce contractions 50% of maximal) of 6.31 +/- 0.03 and 6.55 +/- 0.06, respectively. These contractions were subject to blockade with the S2-selective 5-HT antagonist, ketanserin. When either HSVs or RTAs were contracted with 5-HT and cooled, a potent augmentation of the contractions ensued. The data indicate that, while acute moderate cooling does not significantly augment either resting tone or KCl-induced contractions of HSV or RTA, S2-receptor-mediated events are enhanced, yielding potent augmentations of the vascular response to the platelet-derived compound, serotonin. The relationship between temperature and serotonergic receptor responsiveness may be of clinical importance as a mechanism contributing to cold-induced vasospasm.