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

• Published in: Journal of hypertension Vol. 9; no. 12; p. 1177
• Main Authors: Oparil, S, Chen, Y F, Wang, R P
• Format: Journal Article
• Language: English
• Published: England 01.12.1991
• Subjects: Animals; Atrial Natriuretic Factor - physiology; Blood Pressure - physiology; Heart Rate - physiology; Hypertension - genetics; Hypertension - physiopathology; Male; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Sodium, Dietary - pharmacology; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - physiology
• ISSN: 0263-6352

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.