Responsiveness of isolated thoracic aorta to norepinephrine and acetylcholine in cold-acclimated rats

We investigated the responses of thoracic aortae to adrenergic contraction and endothelium-dependent relaxation following chronic exposure to cold in rats. Two groups (CA, cold-acclimated for 12 weeks at 5 °C; WA, warm-acclimated for 12 weeks at 24 °C) of 10 male Sprague-Dawley rats were used. After anesthesia, the thoracic aortae (4 mm long) were isolated and the vascular tension was measured with a force transducer. The dose-response relations for aortic responses to norepinephrine (NE), phenylephrine (PE) and acetylcholine (Ach) were determined and compared between the CA and the WA groups. In the CA rats, the thoracic aortae became more sensitive to Ach-induced vasorelaxation. The vascular sensitivities to NE- or PE-induced contraction in the thoracic aortae were lowered. Chronic exposure to cold decreased NE- and PE-induced vasoconstrictive responses and increased Achinduced vasorelaxative response of the isolated thoracic aortae, which were suggested to be due to enhanced release of NE-induced endothelium-derived relaxing factor by up-regulating endothelial α1-adrenoceptors

Increase of norepinephrine-induced endothelium-dependent relaxation of pulmonary artery in rats after chronic exposure to cold

The present study was designed to determine whether norepinephrine (NE) mediate endothelium-dependent relaxations in arteries of the pulmonary vasculature of cold-acclimated rats. Twenty male Sprague-Dawley rats comprising two groups (Cold-acclimated for 12 weeks at 6°C, CA; Warm-acclimated for 12 weeks at 24 °C, WA) were used. After anesthesia, the pulmonary artery (4 mm long) was isolated. Pulmonary artery with and without endothelium were suspended for isometric force measurements in a buffered salt solution. The doseresponse relations for the vascular responses to the isolated pulmonary artery to norepinephrine (NE), phenylephrine (PE) and acetylcholine (Ach) were determined and compared in the CA group and the WA group. In the CA group, the vascular sensitivities to NE and PE-induced contraction in the pulmonary artery was significantly lowered than that in the WA group. NE and PE-induced contractions were significandy greater in endotheliumdenuded compared with endothelium-intact arteries. These differences of contraction responses to NE and PE between arteries with widiout endothelium were significantly greater in the CA group than in the WA group. There was no significant difference between the pulmonary arterial response to Ach in the CA group and that in the WA group. Our data suggest that chronic exposure to cold show decreased NE and PE-induced contraction responses in isolated pulmonary arteries and may decrease NE-induced contraction responses due to enhancing NE-induced endodielium derived relaxing factor release via up-regulating endothelial α-adrenoceptors