@entity23189 -induced @entity551 in conscious @entity95 involves XXXX -preferring receptors.

@entity23189 @entity101 @entity95 @entity591 @entity9006 @entity12833 @entity601 @entity23190 @entity551 @entity1168 @entity947
The relative contributions of @entity947 -preferring receptors (IPR) and alpha 2-adrenoceptors to @entity551 and bradycardic effects of intracisternal (i.c.) @entity23189 were investigated in conscious @entity95 . We compared the antagonist potencies of two alpha 2-adrenoceptor antagonists, @entity23190 (0.001-10 micrograms/kg i.c.), which has very low affinity for IPR, and @entity9006 (0.003-30 micrograms/kg i.c.), which has high affinity for blocking IPR. We also compared the i.c. effects of the antagonists on responses to @entity12833 (alpha- @entity601 ), a drug with centrally acting alpha 2-adrenoceptor agonist metabolites that have no affinity for IPR. @entity23189 (22 micrograms/kg i.c.) and alpha- @entity601 (400 micrograms/kg i.c.) produced similar decreases in mean arterial pressure (MAP) (delta MAP = -23 +/- 2 and -24 +/- 2%, respectively) and in heart rate (HR) (delta HR = -11 +/- 1 and -9 +/- 2%, respectively, n = 30). The @entity551 and @entity1168 produced by alpha- @entity601 and @entity23189 were completely reversed by @entity23190 , but @entity23190 was 16 and 9 times more potent at restoring MAP and HR, respectively, after alpha- @entity601 than after @entity23189 . In contrast, @entity9006 was more potent in reversing the @entity551 elicited by i.c. injections of @entity23189 than that elicited by alpha- @entity601 . @entity9006 , however, had no effect on @entity23189 -induced @entity1168 , but did dose-dependently reverse the decrease in HR produced by alpha- @entity601 . In separate experiments, we observed that the doses of each antagonist drug in themselves did not modify MAP nor HR significantly, but a 10-fold higher dose of @entity9006 (300 micrograms/kg) caused immediate although brief @entity101 and @entity591 .(ABSTRACT TRUNCATED AT 250 WORDS)
