The present study was performed to investigate the mechanism of heat-induced vasoconstriction (HIVC) in human fingers. The left fingers of five male subjects were immersed in water controlled at an initial temperature of 35.0 degrees C. The blood flows (BF) of the left index and fourth fingers were measured continuously with laser-Doppler flowmeter probes, and the temperatures of the middle finger and water bath were also monitored continuously using thermistor probes. Arterial blood pressure and heart rate were measured every minute before and during local finger warming. A local anesthetic (0.5% bupivacaine hydrochloride) or saline at a volume of 5.0-8.0 ml was aseptically injected into the base of the fourth or index finger, respectively. After finger BFs had been stabilized for > or = 10 min, the fingers were warmed by raising the water bath temperature from 35.0 to 41.5 degrees C in 14 min. The BF of the index finger fell significantly for 6 min after local warming was commenced (at water bath temperatures between 35.5 and 37.5 degrees C) without associated changes in mean arterial blood pressure, indicating the occurrence of HIVC. Then BF increased toward prewarming levels. The local anesthetic injection, however, completely abolished HIVC in the fourth finger. These results suggest that, in humans, innervation to finger vessels is indispensable for producing HIVC and hence that a local mechanism, such as myogenic vascular response to high temperature, may not be involved in the induction of HIVC.