Effect of cooling on cutaneous microvascular adrenoceptors in vivo in the rabbit ear

Abstract

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.

Attenuation of the anti‐contractile effect of cooling in the rat aorta by perivascular adipose tissue

“…This is in agreement with previous reports on this and other vascular smooth muscle preparations in the literature . Several studies have shown that cooling has a variable effect on vascular smooth muscle preparations ranging from relaxation in deep vessels to vasoconstriction in cutaneous arteries . Our present results showed that cooling significantly reduced PE‐induced contractions of aorta segments without PVAT.…”

In vivo reflectance-mode confocal microscopy provides insights in human skin microcirculation and histomorphology

“…Our results evaluated in vivo by RCM are in agreement with previous studies on temperature induced alterations in human skin microcirculation [11][12][13][14]. Recently, Ciplak et al studied the vasodilatory response of skin microcirculation to local heating using laser Doppler imaging [12].…”

“…Based on RCM observations, we are not only able to confirm, but also to quantify this fact in vivo on a histomorphological level, as we assessed cold stress-dependant significant decrease of the capillary size. Moreover, in accordance with previous studies [14] we observed a concomitant decrease of single blood cell flow, induced by local cold stress. In this study, the area of interest was covered prior to contact with water in order not to confound histomorphological data.…”

“…For correlation, confocal images were compared to histological sectioning and a high sensitivity of 82.9% and specificity of 95.7% was found [9,10]. The dynamic effects of temperature changes on the human skin microcirculation are well investigated using non-invasive approaches and also well described in the actual literature [11][12][13][14][15][16]. Temperature-dependent microcirculation changes have been studied, but only at temperatures that damage the skin, using more complex techniques such as fluorescence [17].…”

α2-Adrenergic receptor signalling in hypertension

“…Thus temperature appears to regulate cellular distribution and second messenger coupling of α 2C -AR. Clinical studies in Raynaud's patients have also documented a significant role for α 2 -ARs in the exaggerated cold-induced vasoconstriction typical of this syndrome [40,43,44], although there are other reports that α 2 -AR blockade has little or no effect on cold-induced vasoconstriction [45][46][47]. In addition, the α 2C -ARs appear to contribute to cerebral blood flow by regulating tone in the carotid artery [48,49], and recent studies suggest subtype selective activation of these receptors causes vasoconstriction which may be a beneficial therapy for migraine [38,49].…”