Sympathetic mechanisms of increased venomotor tone in chronic angiotensin II hypertension

Chronic infusion of angiotensin II (AngII) activates the sympathetic nervous system (SNS) in rats fed a high salt diet to increase whole body venous tone. Splanchnic veins and venules account for most active capacitance responses in the body, and are richly innervated by the SNS, mostly via the celiac ganglion (CG). We tested the hypothesis that surgical removal of the CG (CGx) will attenuate AngII‐salt mediated increases in venous tone. SHAM operated or CGx male Sprague‐Dawley rats, fed a 0.4% or 2% NaCl diet, were catheterized for repeated measures of mean circulatory filling pressure (MCFP), an index of venous tone. AngII (150ng/kg/min) was delivered by minipump for 14 days. MCFP was measured before and after ganglion blockade with hexamethonium (30mg/kg) on control day 2 and AngII infusion days 1, 3, 7 and 14. Blood volume was also measured on these days and was unaffected by CGx or AngII. In SHAM rats AngII infusion caused a salt sensitive increase in arterial pressure (AP); and a neurogenically mediated increase in venomotor tone in rats on 2% NaCl. In rats fed 2% NaCl CGx significantly attenuated the AngII mediated increase in AP, prevented enhanced depressor responses to hexamethonium and completely abolished the increase in MCFP. CGx had little effect in rats on 0.4% NaCl. We conclude that in the presence of a high salt diet AngII activates the splanchnic SNS to increase venomotor tone and AP. Supported by NIH Grant HL 076312