To determine whether bradykinin, an algesic substance produced in certain inflammatory states, can stimulate gallbladder receptors to cause significant cardiovascular reflexes, we applied this agent to the serosal surface of the gallbladder in cats anesthetized with methoxyflurane. As a control, bradykinin was also applied to the serosal surface of the liver surrounding the gallbladder. Significant cardiovascular reflexes were obtained from the gallbladder in an increasing, dose related fashion over a range of concentrations from 50 pg/ml to 100 micrograms/ml of bradykinin. The cardiovascular responses occurred after a latency of 13 +/- 0.92 seconds (mean +/- SE) and included increases in mean arterial pressure, systemic vascular resistance, heart rate and myocardial contractility (dP/dt at 40 mmHg developed pressure). There was also a small but significant increase in left ventricular end-diastolic pressure, but no change in aortic flow. Application of bradykinin to the liver did not evoke any cardiovascular responses. Bilateral vagus nerve transection just above the diaphragm did not alter the cardiovascular responses to application of bradykinin on the gallbladder. However, the hemodynamic responses were partially diminished by right splanchnic nerve transection and were completely eliminated by bilateral splanchnic nerve transection. We conclude that bradykinin, a substance that is formed within the gastrointestinal tract and possibly in bile, can stimulate gallbladder receptors to induce significant reflex activation of the cardiovascular system.
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