Atrial natriuretic peptide inhibits sympathetic outflow in NaCl-sensitive spontaneously hypertensive rats

    loading  Checking for direct PDF access through Ovid


The current study tested the hypothesis that circulating atrial natriuretic peptide (ANP) inhibits sympathetic outflow, as reflected in lumbar sympathetic nerve activity (LSNA), in NaCl-sensitive spontaneously hypertensive rats (SHR-S) and that this effect is exaggerated by high NaCl feeding. NaCl-resistant SHR (SHR-R) and Wistar-Kyoto (WKY) rats maintained on basal and high-NaCl diets were used as controls. Intravenous administration of ANP to conscious, freely moving rats with intact baroreflexes decreased blood pressure and LSNA in SHR-S, SHR-R and WKY rats maintained on basal or high-NaCl diets for 2-3 weeks. The depressor response to intravenous ANP was greater in 8% NaCl-fed SHR-S than in any other group; the LSNA response was greater in SHR-S on either diet than in any other group. Intracerebroventricular administration of ANP evoked small, transient sympatholytic responses in SHR-S on both diets and minimal responses in SHR-R and WKY rats; these responses could not be attributed to leakage of ANP into the peripheral circulation. Thus, circulating ANP has a sympatholytic effect in SHR-S that is not amplified by high-NaCl feeding and can be only partially accounted for by a central action

    loading  Loading Related Articles