1 The nature of the muscarinic receptor involved in mediating cardiovascular changes caused by unilateral microinjection of carbachol (5 nmol) into, and electrical stimulation (200 ± 300 mA) of, the amygdaloid complex was investigated in conscious, unrestrained female Sprague-Dawley rats. 2 Unilateral microinjection of carbachol (5 nmol; n=6) and electrical stimulation (200 ± 300 mA, 80 Hz, 30 s; n=4) caused a signi®cant rise in blood pressure of 21+4 mmHg and 25+5 mmHg, respectively. These changes were associated with no overall e ect on heart rate. The e ects of electrical stimulation were found to be repeatable. 3 Pretreatment i.c.v. with pirenzepine (5 ± 20 nmol; n=6 ± 7 for each dose), dose-dependently inhibited the rise in blood pressure induced by carbachol, whereas AF-DX 116 (100 nmol; n=6) failed to have any e ect on the carbachol-induced pressure response. Neither antagonist alone had any e ect on resting baseline variables. 4 Unilateral microinjections of atropine sulphate (1 ± 100 nmol; n=4 ± 6 for each dose), pirenzepine (0.03 ± 10 nmol; n=4 for each dose) or AF-DX 116 (10 ± 60 nmol; n=4 ± 5 for each dose), into the amygdala, dose-dependently inhibited the rise in blood pressure caused by electrical stimulation (200 ± 300 mA). The ID 50 values were 1.05, 0.23 and 39.5 nmol, respectively. Although pirenzepine seemed to be more potent than atropine, this di erence was not signi®cant. 5 It is concluded that the rise in blood pressure elicited by unilateral microinjection of carbachol into, or electrical stimulation of, the amygdaloid complex is mediated by M 1 -muscarinic receptors.