Dilator effect of bradykinin and acetylcholine in cerebral vessels after brain lesion

Vasodilation elicited by bradykinin (BK) or acetylcholine (Ach) (10 nM-10 microM) in isolated rat cerebral arteries was studied under control conditions, after sham treatment, and after cold lesion (placing a cooled metal probe on the exposed dura) of the cortex. After 24 or 48 hours, isometric force was measured in ring segments of basilar (BA) and middle cerebral arteries (MCA). Concentration-effect curves were constructed after precontraction with 100 microM uridine triphosphate (MCA) or 1 microM serotonin (BA). In MCA and BA, BK elicited similar relative relaxations with maxima of 40.9 +/- 1.5% and 40.7 +/- 3.1%, respectively, at 1 microM. Ach-induced relaxation in BA was much stronger with 82.0 +/- 5.8% at 1 microM. MCA did not relax consistently to Ach. Relaxation to BK in MCA segments was not different between sham-treated and untreated animals. After cold lesion, the dilation to BK (1 microM) was significantly reduced at 24 hours from 0.7 +/- 0.06 to 0.4 +/- 0.06 mN. At 48 hours, this decrease was partly reversed (to 0.5 +/- 0.07 mN). In BA, there was no difference in Ach-induced relaxation between cold-lesioned or sham-treated animals. In summary, the nitric oxide (NO)-mediated response to BK in MCA is attenuated 24 hours after cold lesion. This damage to the BK/NO system is partly reversed 48 hours after the lesion.