Plasma cyclic nucleotides in spontaneously hypertensive rats : Hyper–response to acute hot stress

Abstract

An acute hot stress caused a sharp increase in plasma cyclic AMP and cyclic GMP in both spontaneously hypertensive rats(SHR) and normotensive Wistar-Kyoto rats(WKY). This hot stress-induced increase in plasma cyclic AMP was observed even after chemical sympathectomy elicited by 6-hydroxydopamine or :epleting the catecholamine stores in adrenergic neurons by tyramine or reserpinization, but was no longer observable after β-adrenergic blockade by propranolol, blockade of autonomic ganglia by hexamethonium, adrenodemedullation or anesthesia by pentobarbital. These results indicate that the initial stimulation of the central nervous system evoked the release of catecholamines from the adrenal medulla which could activate adenylate cyclase via the stimulation of β-adrenoceptors on the cell surface. The increment of plasma cyclic GMP was not influenced by prior blockade of the peripheral autonomic nervous system, but was totally abolished by pentobarbital. The plasma cyclic AMP and cyclic GMP responses were greater in adult SHR than in young SHR and young and matured WKY. The predominant response of plasma cyclic AMP might be due to a greater release of catecholamine from the adrenal medulla in matured SHR. The hyperresponse of plasma cyclic GMP in adult SHR remains to be fully elucidated. In conclusion, the hyperresponse of plasma cyclic nucleotides in SHR might be related to a maintenance mechanism of the hypertensive state rather than a trigger mechanism of the syndrome.