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


Aslan N., Goren Z., Onat F., Oktay S.

EUROPEAN JOURNAL OF PHARMACOLOGY, cilt.333, sa.1, ss.63-67, 1997 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 333 Sayı: 1
  • Basım Tarihi: 1997
  • Doi Numarası: 10.1016/s0014-2999(97)01106-0
  • Dergi Adı: EUROPEAN JOURNAL OF PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.63-67
  • Acıbadem Mehmet Ali Aydınlar Üniversitesi Adresli: Hayır

Özet

The type of muscarinic receptor in the central nucleus of the amygdala that mediates the carbachol-evoked presser 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 mmHg 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 presser 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. (C) 1997 Elsevier Science B.V.