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 degrees 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.
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