TY - JOUR
T1 - Heat stress induces ultrastructural changes in cutaneous capillary wall of heat-acclimated rock pigeon
AU - Arieli, Yehuda
AU - Feinstein, Neomi
AU - Raber, Pnina
AU - Horowitz, Michal
AU - Marder, Jacob
PY - 1999/10
Y1 - 1999/10
N2 - In heat-acclimated rock pigeons, cutaneous water evaporation is the major cooling mechanism when exposed at rest to an extremely hot environment of 50-60°C. This evaporative pathway is also activated in room temperature by a β-adrenergic antagonist (propranolol) or an α-adrenergic agonist (clonidine) and inhibited by a β-adrenergic agonist (isoproterenol). In contrast, neither heat exposure nor drug administration activates cutaneous evaporation in cold-acclimated pigeons. To elucidate the mechanisms underlying this phenomenon, we studied the role of the ultrastructure and permeability of the cutaneous vasculature. During both heat stress and the administration of propranolol and clonidine, we observed increased capillary fenestration and endothelial gaps. Similarly, propranolol increased the extravasation of Evans blue-labeled albumin in the skin tissue. We concluded that heat acclimation reinforces a mechanism by which the activation of adrenergic signal transduction pathways alters microvessel permeability during heat stress. Consequently the flux of plasma proteins and water into the interstitial space is accelerated, providing an interstitial source of water for sustained cutaneous evaporative cooling.
AB - In heat-acclimated rock pigeons, cutaneous water evaporation is the major cooling mechanism when exposed at rest to an extremely hot environment of 50-60°C. This evaporative pathway is also activated in room temperature by a β-adrenergic antagonist (propranolol) or an α-adrenergic agonist (clonidine) and inhibited by a β-adrenergic agonist (isoproterenol). In contrast, neither heat exposure nor drug administration activates cutaneous evaporation in cold-acclimated pigeons. To elucidate the mechanisms underlying this phenomenon, we studied the role of the ultrastructure and permeability of the cutaneous vasculature. During both heat stress and the administration of propranolol and clonidine, we observed increased capillary fenestration and endothelial gaps. Similarly, propranolol increased the extravasation of Evans blue-labeled albumin in the skin tissue. We concluded that heat acclimation reinforces a mechanism by which the activation of adrenergic signal transduction pathways alters microvessel permeability during heat stress. Consequently the flux of plasma proteins and water into the interstitial space is accelerated, providing an interstitial source of water for sustained cutaneous evaporative cooling.
KW - Adrenergic receptor
KW - Cutaneous water evaporation
KW - Endothelial gap
KW - Fenestrated capillary
KW - Plasma protein extravasation
UR - http://www.scopus.com/inward/record.url?scp=0032720687&partnerID=8YFLogxK
U2 - 10.1152/ajpregu.1999.277.4.r967
DO - 10.1152/ajpregu.1999.277.4.r967
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C2 - 10516233
AN - SCOPUS:0032720687
SN - 0363-6119
VL - 277
SP - R967-R974
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 4 46-4
ER -