Purinergic vasoconstrictor component revealed by moderate cooling in the isolated mesenteric vasculature of Sprague-Dawley rats.

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.