ENHANCED VASCULAR NEUROPEPTIDE Y-IMMUNOREACTIVE INNERVATION IN 2 HYPERTENSIVE RAT STRAINS

Considerable evidence indicates an enhanced sympathetic innervation of resistance arterial smooth muscle in the spontaneously hypertensive r at (SHR) compared with its normotensive Wistar-Kyoto (WKY) control. In addition to sympathetic hyperinnervation, an increased vascular inner vation by neuropeptide Y-containing fibers, which are known to exert a vasoconstrictive and trophic action in vascular smooth muscle, has al so been described. In addition to genetic hypertension, the SHR expres ses hyperactive behavior and hyperreactivity to stress. To determine w hether the enhanced neuropeptide Y-immunoreactive vascular innervation is specifically associated with hypertension and/or these behavioral abnormalities, four genetically related, inbred rat strains were used: SHR, which are hypertensive and hyperactive; WKY rats, which are neit her hypertensive nor hyperactive; WKHA, which are hyperactive but norm otensive; and WKHT, which are hypertensive but not hyperactive. The pr esent study demonstrated that whereas the hypertensive strains (SHR an d WKHT) exhibited smooth muscle hypertrophy in both superior mesenteri c and caudal arteries in adulthood (10 months) but not at a prehyperte nsive age (1 month), both arteries exhibited significantly increased n europeptide Y-immunoreactive innervation at both ages. It was further observed that the mesenteric artery in WKHA, a normotensive strain, ha d significant smooth muscle hypertrophy at 10 months; however, neurope ptide Y innervation in this artery was no different from that of WKY c ontrols. The findings indicate that there is a cosegregation of neurop eptide Y hyperinnervation of the vasculature with the hypertensive phe notype, evident as early as 1 month of life in the hypertensive strain s, and this should be considered further as a contributory factor in g enetic hypertension. Vascular smooth muscle hypertrophy, while evident in adult hypertensive rats, was also observed in the mesenteric arter y (but not the caudal artery) of adult WKHA rats, suggesting that othe r factors besides genetic hypertension, possibly hyperreactivity to st ress, are responsible for this specific hypertrophic change in WKHA ra ts.