Vaginocervical probing elevates blood pressure and induces analgesia by separate mechanisms.

Vaginocervical stimulation (VS) applied as a calibrated mechanical probe force against the cervix produced an increase in blood pressure (BP) of greater than 50 mmHg and an increase in heart rate (HR) of greater than 80 beats per minute (bpm). This response was immediate and reached maximum levels within 5-10 seconds. The magnitude of the response was proportional to the force of the VS over a range of 50-600 grams (g). Administration of propranolol (1 mg/kg, IV), a beta-adrenergic receptor antagonist, attenuated the acceleration of HR in response to VS. Administration of chlorisondamine (5 mg/kg, IV), which eliminates both sympathetic and parasympathetic influences, abolished the increase in BP and HR in response to VS, indicating that VS stimulates autonomic activity involved in the control of these two processes and that the tachycardia resulted from vagal withdrawal as well as sympathetic activation. The analgesic effect of VS, as measured by the VS-produced increase in tail flick latency (TFL), was unaffected by any of the drug treatments that abolished the HR and BP elevating effects of VS. Furthermore, elevation of BP by administration of phenylephrine (5 micrograms/kg, IV), to a level comparable to that produced by VS, did not produce analgesia. These results demonstrate that VS produces a profound increase in BP and HR due primarily to an increase in sympathetic activity. In addition, the increase in HR in response to VS appears to be partly due to a decrease in parasympathetic activity. The analgesia produced by VS is independent of the elevation in BP produced by VS.