Yamamoto R, Takasaki K, Nickols G A
Department of Pharmacology, Miyazaki Medical College, Japan.
J Pharmacol Exp Ther. 1992 Sep;262(3):1133-8.
In the isolated mesenteric vasculature of rats, moderate cooling significantly augments the perfusion pressure responses to transmural field stimulation (TFS), whereas it depresses markedly TFS-induced endogenous norepinephrine (NE) release. Moderate cooling also reduces the perfusion pressure responses to exogenous NE. The present experiments, therefore, were performed to analyze further the mechanism of the augmented pressor responses to TFS during moderate cooling. NE release from the entire mesenteric vasculature was monitored along with the perfusion pressure response to periarterial nerve stimulation (4-14 Hz) at 37 or 24 degrees C. Prazosin (3 x 10(-8) M) abolished the pressor responses to TFS at 37 degrees C but not at 24 degrees C. Furthermore, prazosin abolished the pressor responses to exogenous NE at both temperatures. The TFS-induced pressor responses observed in the presence of prazosin at 24 degrees C were abolished by alpha, beta-methylene adenosine 5'-triphosphate (alpha, beta-Me ATP) (3 x 10(-6) M). alpha, beta-Me ATP significantly decreased the pressor responses to TFS at 24 degrees C but not 37 degrees C. Moderate cooling significantly augmented the vasoconstrictor response to alpha, beta-Me ATP per se. These drugs did not influence the TFS-induced endogenous NE release at either temperature. These results suggest that moderate cooling reveals that ATP or related purines released from sympathetic nerves act as cotransmitters in the isolated mesenteric vasculature of rats. That is, augmented pressor responses to TFS during moderate cooling appeared to be due, at least in part, to a purinergic component.
在大鼠离体肠系膜血管中,适度降温显著增强了对跨壁电场刺激(TFS)的灌注压反应,而显著抑制了TFS诱导的内源性去甲肾上腺素(NE)释放。适度降温还降低了对外源性NE的灌注压反应。因此,进行本实验以进一步分析适度降温期间对TFS升压反应增强的机制。在37℃或24℃下,监测整个肠系膜血管的NE释放以及对动脉周围神经刺激(4 - 14Hz)的灌注压反应。哌唑嗪(3×10⁻⁸M)消除了37℃时对TFS的升压反应,但在24℃时未消除。此外,哌唑嗪在两个温度下均消除了对外源性NE的升压反应。在24℃下,在哌唑嗪存在时观察到的TFS诱导的升压反应被α,β - 亚甲基腺苷5'-三磷酸(α,β - Me ATP)(3×10⁻⁶M)消除。α,β - Me ATP显著降低了24℃时对TFS的升压反应,但在37℃时未降低。适度降温显著增强了对α,β - Me ATP本身的血管收缩反应。这些药物在任一温度下均不影响TFS诱导的内源性NE释放。这些结果表明,适度降温揭示了交感神经释放的ATP或相关嘌呤在大鼠离体肠系膜血管中作为共递质起作用。也就是说,适度降温期间对TFS升压反应增强似乎至少部分归因于嘌呤能成分。