[Mechanisms of action of hypersodium medium on contractile activity of isolated rat heart].
Despite the high efficiency of elevated concentrations of sodium ions during myocardial ischemia and calcium paradox, the molecular mechanism of action of hypersodium media on heart contractions remains unknown. The purpose of the investigation was to study mechanisms by which raised concentrations of sodium ions alter cardiac contractility. Subsequent to initially developed reduced pressure in the left ventricle, elevated concentrations of sodium ions (200 mM instead of 140 mM NaCl, 3 mM KCl) produced an increased force of contractions of about 50%. The first stage of decrease in developed pressure did not relate to elevated tonicity of extracellular ionic millieu because lithium chloride (60 mM) did not produce the same effect. This action of elevated concentrations of sodium ions has been shown to be independent of blockers of ion-transporting systems (caffeine, verapamile, ethmozine, HMA or lidocaine). Raising the contractions by elevating the concentration of sodium ions (second stage) has been shown to be susceptible to sodium channel blockers (6-IA, benzamil, of phenamil) and to caffeine. Decreasing of potassium concentration (from 3 mM to 1-2 mM amplified, and increasing of K+ level (from 3 mM to 6 mM) attenuated the positive inotropic action of the elevated concentration of sodium ions. The positive inotropic effect due to elevated concentrations of sodium ions remains even after heart arrest by high concentrations of verapamile (2 mcM). Lithium chloride (60 mM) failed to elevate left ventricle developed pressure which was raised by elevated concentrations of sodium ions. These data suggest that the elevated concentration of sodium ions could effect Na+/Ca2+ exchange and provoke Ca2+ release from sarcoplasmic reticulum by changing the sodium gradient and resulting in Ca2+ entry via Na+/Ca2+ exchange. These observations are consistent with the hypothesis of Leblanc N., Hume J.R. (1990) regarding sodium-induced calcium ion release from sarcoplasmic reticulum.
Alabovskii
V V
VV
Department of Biochemistry, Voronezh State Medical Academy, Russia.
Cragoe
E J
EJ
Vinokurov
A A
AA
D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D005110:Extracellular Space / Q000737:chemistry; D066298:In Vitro Techniques; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D010477:Perfusion; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism; D026941:Sodium Channel Blockers / Q000494:pharmacology; D012965:Sodium Chloride / Q000494:pharmacology*; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013268:Stimulation, Chemical
D026941:Sodium Channel Blockers; D017923:Sodium-Hydrogen Exchangers; D002110:Caffeine; D012965:Sodium Chloride; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium