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Temperature dependence of Na+ transport in the isolated toad bladder
Affiliation:1. School of New Technologies, Iran University of Science and Technology, Tehran 1684613114, Iran;2. Research Laboratory of Real Samples Analysis, Faculty of Chemistry, Iran University of Science and Technology, Tehran 1684613114, Iran;3. Electroanalytical Chemistry Research Center, Iran University of Science and Technology, Tehran 1684613114, Iran;4. School of Chemical, Petroleum and Gas Engineering, Iran University of Science and Technology, Narmak, Tehran 1684613114, Iran;1. Department of Materials Science and Technology, Nagaoka University of Technology, Kamitomioka 1603-1, Nagaoka, Niigata 940-2188, Japan;2. CIC nanoGUNE Consolider, Avenida Tolosa 76, E-20018 Donostita-San Sebastian, Spain;3. IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Basque Country, Spain;4. Department of System Safety, Nagaoka University of Technology, 1603-1 Kamitomioka, Nagaoka, Niigata 940-2188, Japan;5. Department of Bioengineering, Nagaoka University of Technology, 1603-1 Kamitomioka, Nagaoka, Niigata 940-2188, Japan;1. Department of Chemistry Education and Institute of Fusion Science, Chonbuk National University, Jeonju, 561-756, Republic of Korea;2. Department of Bioactive Material Sciences and Research Center of Bioactive Materials, Chonbuk National University, Jeonju, 561-756, Republic of Korea;3. Department of Physics Education and Institute of Fusion Science, Chonbuk National University, Jeonbuk, 561-756, Republic of Korea;4. Institute of Advanced Composite Materials, Korea Institute of Science and Technology, Chudong-ro 92, Bongdong-eup, Wanju-gun, Jeonbuk, 565-950, Republic of Korea;5. Department of Chemistry and Institute of Nano Science and Technology, Hanyang University, 17 Haengdang-dong, Seongdong-gu, Seoul, 133-791, Republic of Korea
Abstract:
  • 1.1. Na+ transport, measured in the urinary bladder of the toad, was positively dependent on temperature over the range 18–27° and negatively dependent over the range 27–36°. At all temperatures, there was a 1:1 correspondence between radio-isotopically measured net Na+ flux and short-circuit current (s.c.c.).
  • 2.2. Three possible mechanisms for the positive temperature dependence, i.e. (1) thermal activation of Na+ pump, (2) thermal enhancement of metabolism, and (3) thermal facilitation of Na+ entry across the apical membrane, were explored by a one-step rapid change in temperature from 18–25° (the temperature-jump method).
  • 3.3. In the presence of ouabain, an inhibitor of ATPase, the response to the temperature jump was more impaired than the response to vasopressin, suggesting that thermal activation of the Na+ pump may be involved. Metabolic interference with iodoacetate, rotenone or antimycin A abolished the s.c.c. response to the temperature jump, while considerable responsiveness to the stimulating actions of vasopressin and amphotericin B was preserved in the presence of these inhibitors. These results suggest a role for metabolic pathways in mediating thermal activation of Na+ transport.
  • 4.4. Reduction of the inward Na+ gradient significantly reduced the response to the temperature jump, whereas pretreatment with vasopressin or amphotericin B, presumed activators of apical conductance, enhanced the subsequent response to the temperature jump. Thus, heat does not appear to act on the same Na+ conductance pathway as do vasopressin or amphotericin B.
  • 5.5. These studies indicate that thermal activation of Na+ transport does not involve a single unique rate-limiting step, a conclusion consistent with the nonlinear character of the Arrhenius plot.
  • 6.6. Owing to the complex character of the temperature dependence of active Na+ transport, the response to increments in temperature does not provide useful information on the mechanism of action of mineralocorticoids as implied in an earlier study.
Keywords:
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