AJP - Heart and Circulatory Physiology, Vol 251, Issue 1 176-H181, Copyright © 1986 by American Physiological Society
Cold-induced vasodilatation in isolated, perfused rat tail artery
C. A. Gardner and R. C. Webb
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.
