Neural mechanisms accounting for the increase in blood pressure and heart rate during vagino-cervical stimulation

Abstract

The rise in blood pressure and heart rate produced by the mechanical stimulation of the uterine cervix (VS) was examined after adrenalectomy, after pelvic or hypogastric neurectomies or after spinal cord transection in anesthetized rats. Neither adrenalectomy, nor hypogastric neurectomy prevented the rise in heart rate and blood pressure produced by VS. After the spinal cord transection at T6 level, VS was still able to produce the rise in blood pressure. However, the rise in blood pressure was significantly lower than that produced in the same animals before the transection. No changes in heart rate were produced by VS after spinal cord transection. This result can be explained because this level of transection prevents the reach of the afferent inflow to the superior cervical ganglia. Pelvic neurectomy abolished completely the effects of VS on blood pressure and heart rate. Low intensity (1–2 times the threshold) electrical stimulation of the pelvic nerve produced a rise in blood pressure. Even though heart rate increased during electrical stimulation, the change in heart rate was not statistically different from the pre-stimulation value. These results suggest that the changes in blood pressure and heart rate produced by VS represent a neuronal reflex response mediated by the pelvic nerve. The fact that the effects of VS on blood pressure persist in spinal cord-transected animals suggests that the reflex is integrated at the spinal level. However, the cardiovascular responses to VS were significantly lower than before transection, suggesting that supraspinal centers are also involved in the reflex.