[Active calcium and sodium transport by cardiac plasma membranes in the genetically hypertensive rat]

Arch Mal Coeur Vaiss. 1984 Oct;77(11):1261-5.
[Article in French]

Abstract

Active Na+ and Ca2+ transports by sarcolemmal vesicles from young spontaneously hypertensive rats (SHR) and their normotensive controls (WKY) were compared. The effects of the calmodulin and the calcium antagonist nifedipine on Ca2+ binding ATP-dependent accumulation of Ca2+ were studied at free Ca2+ concentrations of 2.10(-8)M and 4.10(-7)M. 2.10(-7)M calmodulin stimulated Ca2+ binding to SHR membranes up to a level equivalent to that in WKY, whereas it enhanced active Ca2+ transport more in WKY than in SHR, thus suppressing the difference between the two substrains. At a 2.10(-8)M free Ca2+ concentration low concentrations of nifedipine (10(-7) to 10(-6)M) induced an increases in ATP-dependent Ca2+ transport by SHR vesicles. Inhibition of NA+, K+-adenosine triphosphatase activity by ouabain was also studied. Na+, K+ATPase activity in SHR membranes was double that in membranes from WKY (22.1 +/- 2.8 v.s. 11.3 +/- 1.1. mumole Pi/h/mg protein). These differences, observed on 3 week-old rats, before a significant rise blood pressure, may reflect genetic characteristics of these hypertensive-prone rats.

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calmodulin / pharmacology
  • Cell Membrane / metabolism
  • Hypertension / metabolism*
  • In Vitro Techniques
  • Ion Channels / drug effects
  • Ion Channels / metabolism*
  • Male
  • Myocardium / metabolism*
  • Myocardium / ultrastructure
  • Nifedipine / pharmacology
  • Ouabain / pharmacology
  • Rats
  • Rats, Inbred SHR
  • Rats, Inbred Strains
  • Sodium / metabolism*
  • Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors

Substances

  • Calmodulin
  • Ion Channels
  • Ouabain
  • Sodium
  • Sodium-Potassium-Exchanging ATPase
  • Nifedipine
  • Calcium