In-vivo and in-vitro studies on the effects of chronic dexamethasone treatment on cardiovascular responses to sympathetic stimulation.

Rats treated with dexamethasone, 1.5 mg/kg s.c. weekly for 3 weeks exhibited significantly greater increases in mean arterial pressure than their controls, following either sympathetic nerve stimulation or noradrenaline administration. The atria from dexamethasone-treated rats showed greater chronotropic activity in response to noradrenaline but not to field stimulation, whereas the force of contraction was significantly less than that of the controls after either field or noradrenaline stimulation. Isolated rat tail artery preparations from dexamethasone-treated rats were found to be twice more sensitive to noradrenaline than the controls. Prazosin antagonised the noradrenaline-induced pressor response to the same extent in control and dexamethasone-treated rats. Dexamethasone treatment did not significantly increase the sensitivity to KCl or the angiotensin-potentiated pressor response to noradrenaline. This study shows that dexamethasone treatment increases postsynaptic sensitivity of the cardiovascular system to noradrenaline in rats.