Increased tail artery vascular responsiveness to angiotensin II in cold-treated rats

Chronic exposure of rats to cold for 1-3 weeks results in a mild form of hy pertension. The renin-angiotensin system (RAS) has been implicated in this model of cold-induced hypertension. Previously we have characterized the va scular responsiveness in cold-acclimated animals, using aortic tissue, and recent studies have focused on the thermoregulatory responses of angiotensi n II (AngII), utilizing the tail artery of the rat. Therefore in the curren t study we evaluated the vascular responsiveness of cold-treated rats to An gII in both aorta and tail artery at 2 and 4 weeks of cold exposure (5 +/- 2C). Systolic blood pressures were significantly elevated in cold-treated a nimals compared with control animals at both 2 and 4 weeks of cold exposure . At both of these time pointsbody weights were reduced and ventricular wei ghts were increased in cold-treated animals. After 2 weeks of cold exposure the vascular responsiveness of the aorta to AngII was significantly lower than that of controls. This vascular responsiveness to AngII was elevated a nd returned to control levels after 5 weeks of cold exposure. However, this pattern was not observed in the tail artery.The vascular responsiveness of tail artery rings from cold-treated rats to AngII was significantly greate r than that of control animals during both 2 and 5 weeks of exposure to col d. The vascular contractile responses of both the aorta and tail artery to KCl in the cold-treated animals was not different from that of the control animals maintained at ambient room temperature, suggesting that the vascula r smooth muscle contractile components were not altered by the cold exposur e. Thus, the in vitro vascular reactivity to the receptor-mediatedvasoconst rictor AngII was decreased in the sparsely innervated aorta and increased i n the more densely innervated tail artery of the cold-treated animals when compared with controls. These results suggest that the increased responsive ness of AngII on the smooth muscle of the tail artery may play a role in ad aptation to the cold and the maintenance of cold-induced hypertension.