Effects of arginine vasopressin and extracellular osmolarity on atrial natriuretic peptide release by superfused rat atria.

This study investigated the characteristics of atrial natriuretic peptide (ANP) release from superfused sliced atria and ventricles of rats. Right atria spontaneously released more immunoreactive ANP (Ir-ANP: pg/min per mg tissue) (32 +/- 3) than did left atria (11 +/- 2) or right ventricles (1.5 +/- 0.5). Addition of 10(-9) to 10(-5) M of arginine vasopressin (AVP) to the superfusing fluid or increasing its osmolarity (290 to 490 mOsM) resulted in a significant increase of the Ir-ANP outflow from right atria. The effect of AVP was prevented by a specific V1 receptor antagonist, ([d(ch2)5Tyr(Me)]AVP). Superfusion with indomethacin (10(-5) M) did not alter spontaneous release but inhibited the peak levels of Ir-ANP induced by AVP (10(-5) M). Moreover, DDAVP, a specific V2 receptor agonist, did not induce Ir-ANP release. Ca(2+)-free medium alone or plus 1 mM EGTA induced a significant increase in basal Ir-ANP outflow. The Ir-ANP released chromatographed similarly to the standard alpha-rANP. These results suggest a specific stimulatory effect of AVP and osmolarity and a negative influence of extracellular Ca2+ on atrial spontaneous Ir-ANP release. It appears that the effect of AVP could be mediated by prostaglandin synthesis.