Journal
AMERICAN JOURNAL OF HYPERTENSION
Volume 14, Issue 7, Pages 615-618Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0895-7061(01)01287-0
Keywords
leptin; blood flow; sympathetic nerve; nitric oxide; nerve stimulation
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Funding
- NHLBI NIH HHS [HL14388, HL55006] Funding Source: Medline
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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 mug/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. (C) 2001 American Journal of Hypertension, Ltd.
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