We examined the effect of prostaglandins on the reflex cardiovascular response to bradykinin applied to the abdominal organs of anesthetized cats. Bradykinin (10 μg/ml) was applied to the serosal surface of the stomach, gallbladder, or jejunum before and after injection of indomethacin (2-10 μg/ml iv) and after application of 1 μg/ml of prostaglandins E1, E2, or F(2α) (PGE1, PGE2, PGF(2α)) or prostacyclin (PGI2). In six cats, stimulation of the stomach with bradykinin significantly increased mean arterial pressure (MAP) by 37 ± 5 (SE) mmHg and maximal dP/dt by 633 ± 101 mmHg/s. Following indomethacin the bradykinin-induced increased in MAP and dP/dt were significantly reduced to 19 ± 4 mmHg and 191 ± 58 mmHg/s, respectively. Treatment with PGE1, PGE2, or PGI2, but not PGF(2α), restored the initial bradykinin response. The gallbladder and jejunum responded similarly. Also application of exogenous prostaglandins, PGE2 or PGI2, to the stomach, gallbladder, or jejunum significantly augmented the cardiovascular response to bradykinin. Finally, PGE2 restored a portion of the cardiovascular response to bradykinin following the development of tachyphylaxis. We conclude that prostaglandins are necessary for the full manifestation of the cardiovascular response to bradykinin.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - 1985|
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