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CT Harker and PM Vanhoutte
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota.
Experiments were designed to determine the effects of acute cooling (from 37-24 degrees C) on responses to alpha-1 and alpha-2 adrenergic activation in the central ear artery of the rabbit. Rings were suspended in physiological salt solution for recording of isometric force. Cooling quiescent vessels resulted in an increase in force. This myogenic response was sensitive to depletion of either intra- or extracellular calcium, as well as treatment with the calcium antagonists verapamil and diltiazem. Cooling did not significantly alter contractile responses to norepinephrine in ear arteries under control conditions or under alpha-2 adrenergic blockade (rauwolscine). Cooling arteries under alpha-1 adrenergic blockade (prazosin) caused augmentations which were not significantly different in magnitude from the myogenic responses to cooling exhibited by the same rings when unstimulated. The alpha-1 adrenergic agonist phenylephrine caused concentration-dependent contractions which were not altered by cooling. The alpha-2 adrenergic agonist UK 14,304 evoked only weak contractions; cooling rings exposed to UK 14,304 caused further increases in tension but no more so than when quiescent. A similar pattern was seen to hold for contractions elicited by electrical stimulation. Thus, in the central ear artery of the rabbit cooling appears to have very little effect on adrenergically induced contractions but does cause the development of myogenic tone.
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