Galanin modulates cholinergic neurotransmission in the heart

The role of galanin (Gal) in the modulation of cholinergic neurotransmission in the heart in wild-type (129 SvJ), and GALR1 knockout mice has been studied. The mice were anaesthetised and ventilated. Blood pressure (BP) and the increase in pulse interval evoked by stimulation of the vagus nerve (ΔPI) were recorded. Resting BP and PI were not different in control and GALR1-KO mice. In control mice an intravenous, bolus injection of Gal (0.8-13 nmol/kg; n = 4-6) attenuated the ΔPI, dose dependently from 33 ± 7% to 78 ± 9.5%. In GALR1-KO mice, Gal (0.8-13 nmol/kg) did not attenuate ΔPI at any dose (n = 3-4). In control mice intravenous, bolus injection of neuropeptide Y (NPY; 0.5-10 nmol/kg, n = 5-7) attenuated the ΔPI by 13 ± 10% to 67 ± 7% with a half time to recovery of 0.5-5 ± 1 min. In control mice, following activation of the cardiac sympathetic nerve (10 Hz for 2 min; n = 3) the ΔPI was attenuated by 92 ± 2% with a half time to recovery of 7 ± 1 min. In control mice in the presence of the β-adrenoceptor antagonist propranolol (1 mg/kg), and 1 μmol/kg BIIE0426 (an NPY Y2 receptor antagonist) the ΔPI was 57 ± 3% with a half time to recovery of 2.5 ± 0.5 min. In GALR1-KO mice, in the presence of propranolol and BIIE0426 there was no inhibition of ΔPI. In mice, it is proposed that both Gal and NPY contribute to the prolonged attenuation of parasympathetic slowing of the heart following activation of the cardiac sympathetic nerve.