Leptin is a protein produced by adipocytes. Leptin is known to markedly and
rapidly increase sympathetic nerve activity to the kidney and hindlimb of
experimental animals. Recent studies suggest that leptin may stimulate endo
thelial production of nitric oxide, which could oppose sympathetically indu
ced vasoconstriction. We tested the hypothesis that such actions of leptin
may produce peripheral functional sympatholysis. In Sprague-Dawley rats, we
intermittently stimulated the abdominal sympathetic trunk and measured ren
al and hindlimb blood flows before and after 3 h of infusion of leptin (100
0 mug/kg, n = 7) or vehicle (n = 7). Leptin did not change arterial pressur
e, heart rate, or renal or hindlimb conductance over the course of 3 h. In
addition, leptin did not significantly alter sympathetically mediated vasom
otor responses to electrical stimulation, as compared with vehicle. Thus, w
e conclude that leptin does not change regional blood flows, and that lepti
n also does not appear to have vascular or neural actions to cause peripher
al functional sympatholysis. (C) 2001 American Journal of Hypertension, Ltd
.