The effect of hyperosmolality on the rate of heat production of quiescent trabeculae isolated from the rat heart
| Autor: | J Daut, C. van Hardeveld, Denis S. Loiselle, G I Zahalak, E. T. van der Meulen, G. Elzinga, Ger J.M. Stienen |
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| Rok vydání: | 1996 |
| Předmět: |
Male
Hot Temperature Physiology chemistry.chemical_element Calorimetry In Vitro Techniques Calcium Calcium in biology Ouabain Procaine Isometric Contraction medicine Animals Osmotic pressure Osmotic concentration Chemistry Myocardium Histological Techniques Osmolar Concentration Heart Intracellular Membranes Articles Rats Oxygen Biochemistry Renal physiology Biophysics Verapamil medicine.drug |
| Zdroj: | The Journal of General Physiology Scopus-Elsevier |
| ISSN: | 1540-7748 0022-1295 |
| DOI: | 10.1085/jgp.108.6.497 |
| Popis: | We have measured the rate of heat production of isolated, quiescent, right ventricular trabeculae of the rat under isosmotic and hyperosmotic conditions, using a microcalorimetric technique. In parallel experiments, we measured force production and intracellular calcium concentration ([Ca2+]i). The rate of resting heat production under isosmotic conditions (mean +/- SEM, n = 32) was 100 +/- 7 mW (g dry wt)-1; it increased sigmoidally with osmolality, reaching a peak that was about four times the isosmotic value at about twice normal osmotic pressure. The hyperosmotic thermal response was: (a) abolished by anoxia, (b) attenuated by procaine, (c) insensitive to verapamil, ouabain, and external calcium concentration, and (d) absent in chemically skinned trabeculae bathed in low-Ca2+ "relaxing solution." Active force production was inhibited at all osmolalities above isosmotic. Passive (tonic) force increased to, at most, 15% of the peak active force developed under isosmotic conditions while [Ca2+]i increased, at most, 30% above its isosmotic value. We infer that hyperosmotic stimulation of resting cardiac heat production reflects, in large part, greatly increased activity of the sarcoplasmic reticular Ca2+ ATPase in the face of increased efflux via a procaine-inhibitable Ca(2+)-release channel. |
| Databáze: | OpenAIRE |
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