Features of GABAergic Cardiovascular Control Provided by Medullary Neurons in Rats

Abstract

In acute experiments on rats anesthetized with urethane, features of the involvement of GABA in medullary cardiovascular control were studied. It was found that microinjections of GABA (10–8 or 10–10 M) into the medullary nuclei (paramedian reticular nucleus, PMn, lateral reticular nucleus, LRN, and nucl. ambiguous, AMB) were accompanied by the development of either hypo- or hypertensive responses in a dose-dependent manner. There were some differences in the structure of GABA-induced hemodynamic responses. In particular, the cardiac and vascular components contributed about equally to the development of the hypotensive responses caused by GABA injections into the PMn (with significant inhibition of the heart’s chronotropic function). However, GABA-induced hypotensive responses evoked from the LRN were mainly based on the vascular component, with the a less pronounced cardiac component. GABA injections into the AMB resulted in significant decreases in the diastolic blood pressure and the heart rate. As for GABA-induced hypertensive responses originated from PMn and LRN neurons, the vascular component was predominant in their development, and chronotropic effects on the cardiac function were less pronounced. Injections of bicuculline (10–7 M), a competitive antagonist of GABAA receptors, into the medullary nuclei under investigation were accompanied by increases in both the systolic and diastolic blood pressure and heart rate. Therefore, bicuculline-sensitive GABAA receptors are involved in GABA-induced hypotensive effects. After inhibition of neuronal NO synthase, injections of GABA into the medullary nuclei did not cause the development of hypotensive responses, and GABA-induced hypertensive responses were weakened, indicating the possibility for GABA interaction with nitric oxide in nervous control of the cardiovascular system. It was also found that the effects of GABA injected into the medullary nuclei depended on the activity of Na+,K+-ATPase, the enzyme of the plasma membrane of cardiovascular neurons.