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The role of extracellular Na⁺ and Ca⁺⁺ in cooling-induced contraction (CIC) was studied in guinea pig trachealis muscle. Tracheal preparations were tested in Krebs-Ringer bicarbonate (KRB) solution and then in either: (1) a low Na⁺ sucrose KRB, (2) KRB plus amiloride, a sodium channel blocker, or (3) KRB plus nifedipine, a calcium channel blocker. When the trachealis muscle was cooled from 37 to 20 °C in KRB, the value of the isometric tension increased on average by 25% of the maximal tension induced by acetylcholine; however, when the tissue was tested in the low Na⁺ sucrose KRB or the KRB containing amiloride, CIC was totally prevented. In the presence of nifedipine the mean value of CIC was only 10% of the acetylcholine-induced contraction, which was also observed not to be affected by extracellular Na⁺ or Ca⁺⁺; whereas the KCl-induced contraction was affected by Ca⁺⁺ but not by Na⁺. The results suggest that rapid cooling of the smooth muscle cells causes an increase in sodium conductance and a decrease in the activity of the Na⁺-K⁺ pump, resulting in membrane depolarization. During depolarization a significant quantity of Ca⁺⁺ enters the cell, contributing to the magnitude of CIC.

Background: The exposure of the airways to low temperature (LT) is a well-known trigger of bronchoconstriction and asthma. However, the mechanisms involved in this response are not well understood. In particular, the specific role of the airway epithelium in the response to LT has not been well established. Objective: The purpose of this work is to study the regulatory role of the airway epithelium in the contractile response of the rat trachea under conditions of LT. Methods: Isolated rat tracheas were stimulated with acetylcholine (ACH) at 37 and 18°C, and dose-response curves were generated in epithelium-intact or epithelium-denuded conditions. EC₅₀ and E_max were determined under these conditions. Results: Epithelium denudation at 37°C, increases the tracheal sensitivity to ACH, (EC₅₀ from 5.9 to 2.6 µM, p = 0.003). The effects of denudation were even more pronounced at 18°C. E_max was significantly decreased under these conditions. Exposure of intact tracheas to 18°C also produced a significant increase in tracheal sensitivity (EC₅₀ from 5.9 to 1.5 µM, p = 0.0004), although no changes in E_max were noted. Conclusions: These results strongly suggest that the airway epithelium diminishes the sensitivity of the airway smooth muscle to ACH at 37 and 18°C, and that it is also needed to observe the maximal contractile response under LT conditions. Therefore, the spasmogenic effect of low temperature is significantly potentiated by the absence of airway epithelium.

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Background-Coronary vasospasms have been reported in the early stages of cardiomyopathy in the Syrian cardiomyopathic hamster (CM, BIO-TO2 strain). It has been proposed these alterations could lead to ischemic heart disease and heart failure. However, the cause of these coronary abnormalities has not been established. In this study, we evaluated coronary hemodynamic to assess the role of Ang-II, ROS, and NO in the development of these alterations in CM of 1, 2, and 6 months of age.