[Phenothiazine derivatives, chlorpromazine and triflupromazine, produce different effects on sympathetic nerve activity in urethane-anesthetized rabbits].

UNLABELLED

This study was designed to evaluate effects of chlorpromazine (CPZ) or triflupromazine (TPZ) on renal sympathetic nerve activity and hemodynamics in urethane-anesthetized rabbits.

METHODS

Thirty-five rabbits were divided into the following two groups: CPZ group (N = 10) and TPZ group (N = 25), challenged by an intravenous injection of either CPZ (0.4 mg.kg-1) or TPZ (0.2 mg.kg-1), respectively. Each experimental group was further divided into the following groups. CPZ group was divided into CPZ-INTACT group of animals with neuraxis intact (N = 6) and CPZ-SAD group of animals with combined denervation of the carotid sinus and aortic nerves (N = 4). TPZ group was divided into TPZ-INTACT group of rabbits with neuraxis intact (N = 8), TPZ-VAGOTOMY group of only cervical vagotomy (N = 6), TPZ-SADV group with combined denervation of the carotid sinus and aortic nerves with cervical vagotomy (N = 5) and TPZ-VI group with right cervical vagotomy but having the intact left vagus (N = 6). In the last group, right afferent vagal nerve activity was measured simultaneously. Mean blood pressure, central venous pressure, heart rate and renal sympathetic nerve activity were measured at the same time.

RESULTS

In the CPZ-INTACT group, the agent caused a decrease in mean blood pressure and significant increases in sympathetic nerve activity and heart rate, but no significant change in central venous pressure. This increase in sympathetic nerve activity and heart rate disappeared in the SAD animals in spite of hypotension. Animals of the TPZ-INTACT group showed an abrupt decrease in sympathetic nerve activity in response to hypotension, but did not exhibit a remarkable change in heart rate and central venous pressure. However, in contrast, animals with severed cervical vagi showed a sympathetic augmentation after the TPZ injection. These sympathetic changes were abolished in the SADV animals. In the TPZ-VI group, TPZ elicited a decline in sympathetic nerve activity similar to that observed in INTACT animals, but afferent vagal nerve activity increaed simultaneously with sympathetic depression.

CONCLUSION

These results indicate that a reflex increase in sympathetic nerve activity which occurred during hypotension after CPZ injection may have been mediated by the arterial baroreceptor reflex and that a sympathetic reduction after TPZ administration may have resulted from a reciprocal interaction between an excitation through the sino-aortic nerves and an inhibition via the vagal nerves.