This study characterizes an in vitro model of the "hunting response" (cold-induced vasoconstriction and vasodilatation). Two-centimeter segments of rat tail arteries (n = 15) were placed in a muscle bath (37 degrees C) and perfused (37 degrees C) at constant pressure (50 mmHg; flow = 14.5 +/- 0.8 ml/min) with physiological salt solution. Arteries constricted (23.7 +/- 2.8% decrease in flow) in response to activation of adrenergic nerves by electrical stimulation (9 V, 0.1-1.0 Hz, 0.1-4 ms). Cooling the bath to 4-12 degrees C (perfusate = 37 degrees C) caused further flow reduction (0-0.5 ml/min) in 14 arteries. After 20-40 min, 12 arteries dilated (7.4 +/- 1.2 ml/min) followed by constriction in 5-10 min. Typically, flow oscillated between periods of prolonged low flow and brief periods of high flow. Phentolamine (10(-6) M in bath) and acute adrenergic denervation blocked flow changes caused by decreased bath temperature. In unstimulated arteries, exogenous norepinephrine (6 X 10(-8) M in bath) decreased flow by 20%. On cooling (7-10 degrees C) flow decreased to zero, but did not oscillate. These results are consistent with the hypothesis that cold-induced vasoconstriction is caused by augmented smooth muscle responsiveness to norepinephrine, whereas cold-induced vasodilatation is caused by a cessation of transmitter release from adrenergic nerve endings.