Captopril does not affect reflex increases in adrenal or lumbar sympathetic nerve activity to hypoglycemia in rats

Abstract Blockade of angiotensin II (ANGII) receptors or converting enzyme inhibition attenuates reflex increases in epinephrine during insulin-induced hypoglycemia. Because ANGII receptors are found in several sites within the central nervous system, the aim of this study was to examine whether acute captopril attenuates the reflex increase in adrenal preganglionic sympathetic nerve activity (SNA) induced by hypoglycemia. We infused vehicle (control) or insulin (30 U/kg IV) in anesthetized rats or in rats pretreated with captopril (Cap-insulin; 2.5 mg/kg, then 1 mg/kg per hour IV) while measuring hemodynamics and SNA from adrenal preganglionic, adrenal postganglionic, and lumbar sympathetic nerves. Hypoglycemia elicited similar adrenal preganglionic SNA increases in insulin-treated (260% ± 31% from 100% baseline) and Cap-insulin–treated (255% ± 34%) rats. Likewise, increases in adrenal postganglionic SNA and lumbar SNA were equivalent in the insulin and Cap-insulin groups. Hypoglycemia also elicited a tachycardia in insulin-treated rats that was attenuated in Cap-insulin–treated rats, and corresponding blood pressure decreases in insulin rats were enhanced in Cap-insulin–treated rats. Thus, blockade of ANGII formation by captopril did not affect hypoglycemia-induced activation of adrenal preganglionic SNA, indicating that the renin-angiotensin systems in the brain and spinal cord do not modulate increases in adrenal SNA during hypoglycemia.