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Previous studies from our laboratories have demonstrated a selective increase in stores of atrial natriuretic peptide (ANP) in the anterior hypothalamus of NaCl-sensitive spontaneously hypertensive rats (SHR-S) compared to NaCl-resistant Wistar-Kyoto (WKY) controls and have suggested that anterior hypothalamic ANP contributes to the pathogenesis of NaCl-sensitive hypertension in SHR-S by local inhibition of norepinephrine release. We have also observed blunting of cardiopulmonary and arterial baroreflex function in SHR-S compared to WKY. In the current study, ANP stores in 12 brain nuclei thought to participate in the pathogenesis of hypertension, including locus coeruleus (LC), A1/C1 area (A1/C1), nucleus tractus solitarii (NTS), medial preoptic nucleus (MPON), suprachiasmatic nucleus (SCN), supraoptic nucleus (SON), anterior hypothalamic area (AHA), paraventricular hypothalamic nucleus (PVN), ventromedial hypothalamic nucleus (VMN), dorsomedial hypothalamic nucleus (DMN), lateral hypothalamic nucleus (LN), and posterior hypothalamic area (PHA), were compared in 10-week-old male SHR-S and WKY rats following 3 weeks of 1% v 8% NaCl feeding. Individual brain nuclei were obtained by the micropunch technique and ANP content of bilateral brain nuclei from individual rats was measured by radioimmunoassay. ANP content was significantly decreased in NTS and LC and elevated in AHA of SHR-S compared to WKY rats on either diet. Dietary NaCl supplementation was associated with increased ANP content in PVN of both strains. These alterations in ANP content in SHR-S may be related to the reduced release of norepinephrine from nerve terminals in AHA and to the presumed central defect in baroreceptor function.

Altered Stores of Atrial Natriuretic Peptide in Specific Brain Nuclei of NaCl-Sensitive Spontaneously Hypertensive Rats