Extracellular sodium and chloride depletion enhances nonexocytotic noradrenaline release induced by energy deficiency in rat heart

1989 ◽  
Vol 340 (3) ◽  
Author(s):  
Thomas Kurz ◽  
Albert Sch�mig
Keyword(s):  
Noradrenaline Release ◽  
Rat Heart ◽  
Energy Deficiency ◽  
Chloride Depletion ◽  
Extracellular Sodium

Inotropic effect of low extracellular sodium on perfused perinatal rat heart

1995 ◽  
Vol 73 (1) ◽  
pp. 50-54 ◽  
Author(s):  
Ivana Oštádalová ◽  
František Kolář ◽  
Bohuslav Oštádal
Keyword(s):  
Rat Heart ◽  
Contractile Function ◽  
Severe Depression ◽  
Negative Inotropic Effect ◽  
Perinatal Period ◽  
Inotropic Effect ◽  
Initial Increase ◽  
Cardiac Contractile ◽  
Extracellular Sodium ◽  
Day By Day

The purpose of the present study was to estimate the development of the inotropic response to low extracellular sodium (LES) during the perinatal period. The effect of LES (35 mmol∙L−1) was measured in isolated perfused control and ryanodine-pretreated rat hearts on prenatal day 20 and postnatal days 1, 2, 4, and 7. The effect of LES on the developed force (DF) of control hearts changes significantly day by day: whereas a persisting increase of magnitude of contractions was recorded in the prenatal hearts, this increase was only transient on postnatal day 1 and 2. Starting from day 4, the initial signs of a triphasic response, typical for adult hearts, appeared (an initial increase of DF, followed by a decrease of DF and a rise of resting force, and finally a delayed increase of DF); this trend was more pronounced on day 7. The LES-induced increase of resting force was recorded only in 2-, 4-, and 7-day-old hearts. The negative inotropic effect of ryanodine (10−6 mol∙L−1) was observed already prenatally (60% of the controls) and continued during the whole period of investigation; in contrast, a ryanodine-induced increase of resting force was recorded only postnatally. However, pretreatment with ryanodine abolished the day-by-day changes in the response to LES: in all the hearts studied, the first phase (initial increase of DF) was followed by a severe depression of the magnitude of contractions, together with increased resting force. Our data show significant age-dependent differences in the cardiac contractile response to LES. This response changes rapidly during the perinatal development, and it attains the adult pattern by the end of the 1st postnatal week in rats.Key words: low extracellular sodium, ryanodine, inotropic effect, contractile function, perinatal ontogeny, rat heart, Na+–Ca2+ exchange.

Transient inotropic effects of low extracellular sodium in perfused rat heart

1990 ◽  
Vol 259 (3) ◽  
pp. H712-H719 ◽  
Author(s):  
F. Kolar ◽  
W. C. Cole ◽  
B. Ostadal ◽  
N. S. Dhalla
Keyword(s):  
Rat Heart ◽  
Positive Inotropic Effect ◽  
Minor Role ◽  
Inotropic Response ◽  
Inotropic Effects ◽  
Low Concentrations ◽  
Rat Hearts ◽  
Rapid Loading ◽  
Perfused Rat Hearts ◽  
Extracellular Sodium

The inotropic effects of low concentrations of extracellular Na+ (35-110 mM) were studied using Langendorff-perfused rat hearts. Low Na+ induced an initial positive inotropic response proportional to the decrease of transsarcolemmal Na+ gradient. At 35 mM Na+, this effect was followed by a secondary fall in contractility and rise of resting force (RF) and then by a delayed positive inotropic effect and recovery of RF. The magnitude of these low Na(+)-induced transient changes was dependent on the extracellular Ca2+ concentration and was altered by amiloride (6 x 10(-4) and 2.5 x 10(-3) M), ouabain (5 x 10(-5) and 5 x 10(-4) M), ryanodine (2 x 10(-8), 1 x 10(-7) and 1 x 10(-6) M), and sodium azide (1 x 10(-3) and 5 x 10(-3) M) but not by verapamil (2 x 10(-8) and 1 x 10(-7) M) or vanadate (4 x 10(-6) M). The data indicate the initial positive inotropic response of the rat heart to low Na+ may be due to rapid loading of myocytes with Ca2+ through the Na(+)-Ca2+ exchange mechanism. The secondary depression of contractility and the rise of RF appear to be the consequence of the short-lived intracellular Ca2+ overload. Furthermore, the recovery of contractions and the delayed positive inotropic response may be the result of the intracellular redistribution of excessive Ca2+ into the sarcoplasmic reticulum with mitochondria and increased transsarcolemmal Ca2+ efflux apparently playing a more minor role.

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