| First Author | Smith-White MA | Year | 2002 |
| Journal | Regul Pept | Volume | 103 |
| Issue | 2-3 | Pages | 105-11 |
| PubMed ID | 11786149 | Mgi Jnum | J:102623 |
| Mgi Id | MGI:3607845 | Doi | 10.1016/s0167-0115(01)00368-8 |
| Citation | Smith-White MA, et al. (2002) Role of neuropeptide Y Y(2) receptors in modulation of cardiac parasympathetic neurotransmission. Regul Pept 103(2-3):105-11 |
| abstractText | The aim of the study was to clarify the role of the Y(2) receptor in regulation of vagal control of the heart, using Y(2)((-/-)) receptor-knockout mice. Adult Y(2)((+/+),(-/-)) mice (50% C57BL/6-50% 129/SvJ background) were anaesthetised and artificially ventilated. Arterial blood pressure and pulse interval was recorded and both vagus nerves were cut. The cardiac end of the right vagus nerve was stimulated supra-maximally every 30 s (7 V, 2-2.5 Hz, 5 s). Neuropeptide Y (NPY) and a Y(2) receptor agonist, N-acetyl [Leu(28, 31)]NPY 24-36, were injected intravenously in both groups of mice. N-acetyl [Leu(28, 31)] NPY 24-36 was also administered to control mice in the presence of a Y(2) receptor antagonist, BIIE0246. Stimulation of the vagus nerve increased pulse interval (PI) by approximately 100 ms. NPY and N-acetyl [Leu(28, 31)] NPY 24-36 attenuated the increase in PI evoked by vagal stimulation in control mice only. The attenuation was reduced in the presence of BIIE0246. The results presented here show in Y(2)((-/-)) receptor-knockout mice that NPY and N-acetyl [Leu(28, 31)] NPY 24-36 have no effect on PI evoked by vagal stimulation. These findings demonstrate that NPY attenuates parasympathetic activity to the heart via the Y(2) receptor. |
