Evidence for increased in vivoN a –H antiporter activity and an altered skeletal muscle contractile response in the spontaneously hypertensive rat

Autor: Syme, Paul D., Arnolda, Leonard, Green, Yvonne, Aronson, Jeffrey K., Grahame-Smith, David G., Radda, George K.
Zdroj: Journal of Hypertension; November 1990, Vol. 8 Issue: 11 p1027-1036, 10p
Abstrakt: We have assessed the in vivo activity of the Na–Hantiporter skeletal muscle in spontaneously hypertensive rats (SHR) and Wistar–Kyoto (WKY) controls using phosphorus (31P) nuclear magnetic resonance spectroscopy to measure changes in cytosolic acid concentrations during isometric contraction. During contraction there was a smaller rate of rise in skeletal muscle cytosolic acid concentration to a smaller maximum concentration in SHR. This difference in acid response was removed by amiloride and was not attributable to differences in cell buffering or the rate of production of lactic acid, suggesting that the difference in acid response in SHR skeletal muscle is due to increased in vivo Na–Hantiporter activity. Amiloride reduced resting muscle glycogen concentration and increased muscle lactate concentration in the SHR. This could be related to altered in vivo calcium metabolism. The maximum tension produced by skeletal muscle during contraction in SHR was less than in WKY rats, and relaxation between twitches was significantly greater, consistent with the finding of increased vascular smooth muscle relaxation in essential hypertension. Since increased Na–Hantiporter activity occurs in association with increased relaxation of both skeletal and vascular smooth muscle, these data are not consistent with a relationship between increased Na– Hantiporter activity and increased maximal muscle tension development. However, they show that increased Na–Hantiporter activity is associated with increased muscle relaxation.
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