ADRENAL-CORTEX CONTRIBUTES TO THE REGULATION OF NACL-STIMULATED ANP RELEASE IN THE RAT

The present study documents the effects of hypophysectomy and the effects of dexamethasone substitution on the NaCl-stimulated release and on the basal secretion rates of ANP from the rat atria in vitro. We also measured the concentration of mRNA in the atria after hypophysectomy. Rats (n = 12) were subjected to hypophysectomy by a parapharyngeal approach. One group of rats (n = 6) received dexamethasone 0.2 mg s.c. daily for 4 weeks, while the other group was left unsubstituted. After 4 weeks, the atrial block (n = 10) was excised, placed in an organ bath (field stimulation 4 s-1, 20 V, 1 ms; resting tension = 5 mN) and superfused (7 ml min-1) either with a physiological buffer solution (295 mosmol kg-1) or with a hyperosmotic NaCl solution (330 mosmol kg-1). The atria from the hypophysectomized rats did not respond to the stimulus: the concentration of ANP in the 1-min samples of the perfusate was under 100 pg ml-1. Dexamethasone treatment significantly (P < 0.05) increased the ANP concentration to a maximum of 165 ± 17 (mean ± SEM) pg ml-1 during the superfusion while the control concentration was 110 ± 19 pg ml-1. The ANP mRNA/18 S RNA ratios did not differ between the atria of hypophysectomized and control rats. In conclusion, glucocorticoids are required in the stimulus-induced release of ANP and the impaired release of ANP after hypophysectomy does not depend on an impaired synthesis of ANP.