Ganglion atrial natriuretic peptide in nacl sensitive spontaneously hypertensive rats

Academic Article


  • Reports from other laboratories have shown that atrial natriuretic peptide (ANP) stores in sympathetic ganglia are increased during dietary NaCl supplementation in normotensive rats. We have previously demonstrated that dietary NaCl supplementation in NaCl sensitive spontaneously hypertensive rats (SHR-S) exacerbates hypertension and enhances peripheral sympathetic nervous system activity, while NaCl resistant Wistar-Kyoto (WKY) rats show neither response. Since endogenous ANP may inhibit ganglion transmission, an inability of SHR-S to increase ganglion ANP appropriately in response to high NaCl feeding could contribute to the NaCl induced increase in sympathetic nervous system activity and blood pressure in this model, while an increase in ganglion ANP in NaCl supplemented WKY would tend to prevent sympathetic activity and blood pressure from rising. The current study tested the hypothesis that ganglion ANP levels increase in WKY but not in SHR-S during dietary NaCl supplementation. Male SHR-S and WKY rats were placed on 1% or 8% NaCl diets at 7 weeks of age. The rats were decapitated Without prior anesthesia 3 weeks later, and the superior cervical and celiac ganglia were removed for the measurement of ANP by radioimmunoassay. Dietary NaCl supplementation produced significant increases in blood pressure in SHR-S, but not in WKY rats; the high NaCl diet was associated with significant increases in the ANP content of superioi cervical and celiac ganglia in WKY rats, but not in SHR-S. These results are consistent with the interpretation that failure of SHR-S to increase ANP in sympathetic ganglia appropriately in response to dietary NaCl supplementation may contribute to increased sympathetic activity and NaCl sensitive hypertension in this model. Am J Hypertens. © 1992 by the American Journal of Hypertension, Inc.
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    Author List

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

  • 806
  • End Page

  • 810
  • Volume

  • 5
  • Issue

  • 11