These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Influence of extracellular potassium on energetics of resting heart muscle. Author: Ponce-Hornos JE, Márquez MT, Bonazzola P. Journal: Am J Physiol; 1992 Apr; 262(4 Pt 2):H1081-7. PubMed ID: 1566890. Abstract: The effects of various extracellular K concentrations ([K]e) on energy expenditure and their relationship to ionic exchange mechanisms under quiescent conditions were investigated in the arterially perfused rat heart. The increase in [K]e (from 6 to 12, 24, or 50 mM K) leads to a rapid increase (results are given per gram dry weight) in resting energy expenditure (+5.9 +/- 0.9, +13.6 +/- 1.1, and +30.0 +/- 2.0 mW/g, respectively) followed by a slow decrease toward a new steady rate of heat production but higher (+2.8 +/- 0.7, +6.3 +/- 0.6, and +10.5 +/- 1.1 mW/g) than that observed under control conditions (21.1 +/- 0.7 mW/g). The increase in [K]e from 6 to 50 mM also induced an increase in K influx (calculated from 86Rb uptake and efflux experiments) of approximately 0.25 mumol.g-1.s-1. If this increased K influx is driven by the Na-K pump, an increase in steady resting heat production of approximately 10 mW/g would be expected. This represents 95% of the increase in steady heat production measured for 50 mM K intervention. The simultaneous increase in the cellular Ca flux (+0.1 mumol.g-1.min-1) can only explain (if driven by the sarcolemmal Ca pump) less than 1% of the steady increase in heat production. The work also shows that the initial, transitory increase in resting heat production induced by increasing [K]e is caffeine sensitive and may be at least partially attributable to a transitory enhanced activity of the sarcoplasmic reticulum.[Abstract] [Full Text] [Related] [New Search]