Effect of sodium azide on catecholamine release from isolated adrenal gland and on guanylate cyclase.
Sodium azide and other compounds which activate guanylate cyclase could stimulate catecholamine (CA) release from perfused dog adrenals. Verapamil reduced the secretory effect of sodium azide, but atropine and hexamethonium did not affect it while isobutyl methylxanthine potentiated it. Ca2+ deprivation abolished the stimulating effect of sodium azide on CA release and cyclic AMP output but the increased output of cyclic GMP remained. These results suggest the involvement of the Ca2+ influx mechanism in the secretory action of sodium azide.
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000313:Adrenal Medulla / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D001386:Azides / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D002395:Catecholamines / Q000378:metabolism*; D002417:Cattle; D000242:Cyclic AMP / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D004285:Dogs; D006162:Guanylate Cyclase / Q000378:metabolism*; D066298:In Vitro Techniques; D019810:Sodium Azide
D001386:Azides; D002395:Catecholamines; D019810:Sodium Azide; D000242:Cyclic AMP; D006162:Guanylate Cyclase; D006152:Cyclic GMP; D002118:Calcium