Central mechanism underlying pressor and bradycardic effect of intracerebroventricularly injected XXXX .

@entity2871 @entity19343 @entity2404 @entity1426 @entity13078 @entity35 @entity3352 @entity1168
The aim of the current study was to determine the central cyclooxygenase (COX) pathway and central @entity2871 signaling in the cardiovascular effects evoked by @entity1426 (AA). As a main control for the study, different doses of AA (75, 150, or 300    g) were administered intracerebroventricularly (i.c.v.). Centrally injected AA dose- and time-dependently increased mean arterial pressure and @entity1168 in conscious normotensive @entity35 . The maximal cardiovascular effects of AA were observed at min 10 of the injection and lasted almost 30  min. To investigate the central mechanism of the AA-induced cardiovascular effect in conscious normotensive animals, pretreatment with nonselective COX inhibitor @entity3352 (200    g; i.c.v.), @entity2404 (TXA2) synthesis inhibitor @entity19343 (250 or 500    g; i.c.v.), or TXA2 receptor antagonist @entity13078 (8 or 16    g; i.c.v.) was carried out 15  min before AA (150    g; i.c.v.) injection. While @entity3352 completely prevented the pressor and bradycardic responses to AA, @entity19343 and @entity13078 attenuated these effects in part in awake normotensive @entity35 . In conclusion, these findings suggest that the pressor and bradycardic cardiovascular effects of centrally injected AA are dependent on COX activity being totally central and the TXA2 signaling pathway being subsequently central, at least in part.
