Central adenosine signaling plays a key role in centrally mediated hypotension in conscious aortic barodenervated rats.

摘要: We tested the hypothesis that clonidine-evoked hypotension is dependent on central adenosinergic pathways. Five groups of male, conscious, aortic baroreceptor-denervated (ABD) rats received clonidine (10 microg/kg i.v.) 30 min after i.v. 1) saline, 2) theophylline mg/kg), or 3) 8-(p-sulfophenyl)theophylline (8-SPT) (2.5 mg/kg) 1 h i.p. 4) dipyridamole (5 5) an equal volume sesame oil. Blockade (theophylline) but not peripheral adenosine receptors abolished hypotension. In contrast, substantially enhanced bradycardic response to clonidine. additional groups, intracisternal (i.c.) (150 microg) and 8-SPT abolished, respectively, (0.6 microg i.c.)-evoked Because a mixed I1/alpha2 agonist, we also investigated whether signaling linked I1 alpha2A receptor by administering selective (rilmenidine, 25 [alpha-methylnorepinephrine (alpha-MNE), 4 microg] agonist blockade (8-SPT; 10 i.c.) artificial cerebrospinal fluid. The hypotensive elicited rilmenidine alpha-MNE was in 8-SPT-pretreated rats. To delineate role A2A hypotension, i.c. administered [5-amino-7-(2-phenylethyl)-2-(2-furyl)-pyrazolo[4,3-epsilon]-1,2,4-triazolo[1,5-c]-pyrimidine (SCH58261); 150 i.c.]. latter virtually responses conclusion, plays key conscious barodenervated