[Bradykinin inhibits carotid sinus baroreflex in anesthetized rats]

The effects of bradykinin (BK) on the carotid baroreflex were examined in 36 anesthetized rats with isolated carotid sinus perfusion. The results obtained are as follows. (1) By perfusing the isolated carotid sinus with BK (1.0 mumol/L), the functional curve of baroreflex was shifted to the right and upward, its peak slope (PS) decreasing from 0.44 +/- 0.14 to 0.31 +/- 0.01 kPa (P < 0.01) and the reflex decrease in mean arterial pressure (RD) was lowered from 6.85 +/- 0.18 to 4.46 +/- 0.16 kPa (P < 0.05), while the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were significantly enhanced from 7.76 +/- 0.20 to 10.04 +/- 0.09 kPa (P < 0.001), 12.72 +/- 0.29 to 13.74 +/- 0.31 kPa (P < 0.05) and 23.28 +/- 0.24 to 25.31 +/- 0.20 kPa (P < 0.01), respectively. Among the functional parameters of carotid baroreflex, the changes in RD, PS and TP induced by BK were dose-dependent. (2) By pretreatment with indomethacin (10 mumol/L), an inhibitor of prostaglandin synthesis, the above-mentioned effects of BK on carotid baroreflex were not affected. (3) Preperfusion with an inhibitor of NO synthase L-NAME (100 mumol/L) could completely eliminate the effects of BK. (4) Pretreatment with angiotensin-converting enzyme inhibitor captopril (20 mumol/L) could potentiate the effects of BK. Taken together, it is indicated that BK may cause vascular endothelium to release NO, thereby inhibiting the carotid baroreflex.