Effect of cooling on cutaneous microvascular adrenoceptors in vivo in the rabbit ear.
Previous studies have suggested that moderate cooling increases the responsiveness of vascular alpha2-adrenoceptors. However, limited information is available documenting the influence of temperature changes on adrenoceptor responses in the microvasculature of thermoregulatory organs (e.g., the human digit and the rabbit ear) subjected to a wide range of temperatures. In the present study, the effect of local cooling (24 degrees C) on cutaneous microvascular adrenoceptors in the ear was observed in vivo in male New Zealand White rabbits (total: 66 ears). The rabbit ear was studied in a temperature-controlled tissue bath; the ear preparation was pretreated with terazosin (an alpha1-adrenoceptor antagonist) (10(-5) M) or a combination of terazosin (10(-5) M) and propranolol (a beta-adrenoceptor antagonist) (10(-6) M). The microvascular diameter responses of the ear to norepinephrine (10(-11)-10(-4) M) then were determined at 24 or 34 degrees C, respectively, to determine the influences of low temperature on adrenoceptor responses to norepinephrine stimulation. The results demonstrated that low concentrations of norepinephrine induced vasodilation in arterioles and arteriovenous anastomoses. This vasodilation was followed by vasoconstriction with an increased concentration of norepinephrine in animals with alpha1-adrenergic blockade at 34 degrees C. Moderate tissue cooling increased the microvascular maximal response of the rabbit ear to norepinephrine and abolished the vasodilatation induced by a low concentration of norepinephrine. There was no significant difference in the microvascular response to norepinephrine between the two temperature conditions after simultaneous blockade of alpha1-adrenoceptors and beta-adrenoceptors. Data from the present study indicate that moderate cooling does not enhance the responsiveness of alpha2-adrenoceptors to norepinephrine. In contrast, cooling reduced the beta-adrenergic activity of arterioles and arteriovenous anastomoses after norepinephrine stimulation.
Li
Z
Z
Department of Orthopaedic Surgery, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA.
Koman
L A
LA
Rosencrance
E
E
Pollock
D C
DC
Smith
B P
BP
Strandhoy
J W
JW
Smith
T L
TL
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000502:physiology; D003080:Cold Temperature; D004305:Dose-Response Relationship, Drug; D004423:Ear / Q000098:blood supply / Q000294:innervation; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D010525:Peripheral Nerves / Q000737:chemistry / Q000502:physiology; D011224:Prazosin / Q000031:analogs & derivatives / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011817:Rabbits; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012867:Skin / Q000098:blood supply* / Q000294:innervation; D014661:Vasoconstriction / Q000502:physiology*; D014699:Venules / Q000502:physiology
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D018340:Receptors, Adrenergic, alpha-1; D011943:Receptors, Adrenergic, beta; C041226:Terazosin; D011433:Propranolol; D009638:Norepinephrine; D011224:Prazosin