Carbachol-induced pressor responses and muscarinic M 1 receptors in the central nucleus of amygdala in conscious rats

Abstract

The type of muscarinic receptor in the central nucleus of the amygdala that mediates the carbachol-evoked pressor responses was investigated in conscious unrestraint Sprague–Dawley rats. Carbachol (100 ng) injected into the lateral cerebral ventricle caused a significant rise in blood pressure of 31.8±4.5 mm Hg and a decrease in heart rate of 80.0±12.2 beats/min. Pirenzepine (10–75 nmol) injected into the central nucleus of the amygdala inhibited carbachol-induced pressor responses dose-dependently. The bradycardic response to carbachol was also inhibited by pirenzepine, but no dose-dependency was observed. Injection of pirenzepine into the basolateral amygdala at a dose (50 nmol) that inhibited carbachol-induced changes in mean arterial pressure and heart rate when injected into the central nucleus of the amygdala failed to exert any inhibition. Methoctramine at a dose of 50 nmol injected into both the central nucleus of the amygdala and the basolateral amygdala did not cause any significant alteration in the responses. These results indicate that muscarinic M 1 receptors in the central nucleus of the amygdala are involved in cardiovascular regulation mediated by central cholinergic pathways.