Altered stores of atrial natriuretic peptide in specific brain nuclei of nacl-sensitive spontaneously hypertensive rats

Academic Article

Abstract

  • 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 bj 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), Al/Cl area (Al/Cl), 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. Am J Hypertens 1991;4:449-455. © 1991 American Journal of Hypertension, Inc.
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    Author List

  • Jin H; Yang R; Chen YF; Wyss JM; Oparil S
  • Start Page

  • 449
  • End Page

  • 455
  • Volume

  • 4
  • Issue

  • 5