Title of article :
Does leptin cause functional peripheral sympatholysis?
Author/Authors :
Ali Jalali، نويسنده , , Donald A. Morgan، نويسنده , , William I. Sivitz، نويسنده , , Marcelo L. G. Correia، نويسنده , , Allyn L. Mark، نويسنده , , William G. Haynes، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2001
Abstract :
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 endothelial production of nitric oxide, which could oppose sympathetically induced 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 renal and hindlimb blood flows before and after 3 h of infusion of leptin (1000 μg/kg, n = 7) or vehicle (n = 7). Leptin did not change arterial pressure, heart rate, or renal or hindlimb conductance over the course of 3 h. In addition, leptin did not significantly alter sympathetically mediated vasomotor responses to electrical stimulation, as compared with vehicle. Thus, we conclude that leptin does not change regional blood flows, and that leptin also does not appear to have vascular or neural actions to cause peripheral functional sympatholysis.
Keywords :
Leptin , blood flow , Sympathetic nerve , nerve stimulation. , Nitric oxide
Journal title :
American Journal of Hypertension
Journal title :
American Journal of Hypertension