Takesako T, Takeda K, Kuwahara T, Takenaka K, Tanaka M, Itoh H, Nakata T, Sasaki S, Nakagawa M
Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Hypertension. 1994 Jan;23(1 Suppl):I93-6. doi: 10.1161/01.hyp.23.1_suppl.i93.
In normotensive rats, microinjections of neuropeptide Y (2.5 to 25 pmol) into the unilateral nucleus tractus solitarius elicited dose-dependent vasodepressor and bradycardiac responses accompanied by an inhibition of sympathetic nerve firing. After microinjections of the alpha 2-adrenergic receptor antagonist yohimbine (100 ng) into the nucleus tractus solitarius, the depressor and bradycardic responses to the injection of neuropeptide Y (25 pmol) into the nucleus tractus solitarius were significantly attenuated. In contrast, pretreatment with the alpha 1-adrenergic receptor antagonist doxazosin (200 ng) injected into the nucleus tractus solitarius did not alter these responses. In spontaneously hypertensive rats, microinjections of neuropeptide Y (25 pmol) into the nucleus tractus solitarius also elicited depressor and bradycardic responses that were significantly less than those of normotensive Wistar-Kyoto rats. However, pretreatment with yohimbine (100 ng) in the nucleus tractus solitarius did not diminish these depressor responses in spontaneously hypertensive rats. Depressor responses to neuropeptide Y, which was administered after yohimbine pretreatment, were also less in Wistar-Kyoto rats than in spontaneously hypertensive rats. The results suggest that the depressor and bradycardic responses elicited by neuropeptide Y were accompanied by the inhibition of sympathetic nerve activity. These responses may be mediated in part by alpha 2-adrenergic receptor in the nucleus tractus solitarius. The impairment of alpha 2-adrenergic receptor-mediated responses to neuropeptide Y in spontaneously hypertensive rats may contribute to the development of hypertension.
在血压正常的大鼠中，向单侧孤束核微量注射神经肽Y（2.5至25皮摩尔）可引发剂量依赖性的血管减压和心动过缓反应，并伴有交感神经放电的抑制。向孤束核微量注射α2肾上腺素能受体拮抗剂育亨宾（100纳克）后，向孤束核注射神经肽Y（25皮摩尔）所引起的降压和心动过缓反应显著减弱。相比之下，向孤束核注射α1肾上腺素能受体拮抗剂多沙唑嗪（200纳克）进行预处理并未改变这些反应。在自发性高血压大鼠中，向孤束核微量注射神经肽Y（25皮摩尔）也引发了降压和心动过缓反应，但其反应明显小于血压正常的Wistar-Kyoto大鼠。然而，在孤束核中用育亨宾（100纳克）进行预处理并没有减弱自发性高血压大鼠的这些降压反应。在Wistar-Kyoto大鼠中，育亨宾预处理后给予神经肽Y所引起的降压反应也比自发性高血压大鼠小。结果表明，神经肽Y引发的降压和心动过缓反应伴有交感神经活动的抑制。这些反应可能部分由孤束核中的α2肾上腺素能受体介导。自发性高血压大鼠中α2肾上腺素能受体介导的对神经肽Y的反应受损可能有助于高血压的发展。
