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Male Sprague-Dawley rats were instrumented with telemetry probes and arterial and venous catheters for determination of blood pressure (BP), heart rate (HR), blood sampling, and intravenous (iv) infusions. An intracerebroventricular (ICV) cannula was placed into the brain lateral ventricle for infusion of leptin or vehicle. After control measurements, streptozotocin (STZ) was injected iv (50 mg\/kg) to induce diabetes, and 5 days later leptin ( n = 6) or saline vehicle ( n = 5) was infused ICV for 12 days via osmotic pumps. Beginning on day 6 of leptin treatment, the ganglionic blocker hexamethonium (15 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>iv) was infused, while leptin infusion was continued, to assess the role of the autonomic nervous system. Induction of diabetes was associated with increases in blood glucose (98 \u00b1 7 to 350 \u00b1 19 mg\/dl), food intake (23 \u00b1 3 to 43 \u00b1 3 g\/day), decreases in HR (\u221270 \u00b1 11 beats\/min), polyuria, and increased water consumption, which were all completely normalized by ICV leptin infusion. Although hexamethonium attenuated leptin\u2019s effect on HR, it failed to impair leptin\u2019s ability to restore euglycemia or to prevent the polyuria or increased water intake in STZ-diabetic rats. We also found that after pretreatment with hexamethonium ( n = 8), ICV leptin infusion, during continued ganglionic blockade, completely normalized blood glucose in diabetic rats. In addition, selective hepatic vagotomy did not attenuate leptin\u2019s ability to restore euglycemia in diabetic rats. These results suggest that leptin\u2019s powerful chronic CNS antidiabetic actions are mediated primarily via nonautonomic mechanisms.<\/jats:p>","DOI":"10.1152\/ajpendo.00301.2016","type":"journal-article","created":{"date-parts":[[2016,12,7]],"date-time":"2016-12-07T02:21:34Z","timestamp":1481077294000},"page":"E420-E428","source":"Crossref","is-referenced-by-count":12,"title":["Role of autonomic nervous system in chronic CNS-mediated antidiabetic action of leptin"],"prefix":"10.1152","volume":"312","author":[{"given":"Alexandre A.","family":"da Silva","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi; and"},{"name":"Bar\u00e3o de Mau\u00e1 University Center, Ribeir\u00e3o Preto, S\u00e3o Paulo, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John E.","family":"Hall","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi; 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