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

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.

1988 ◽  
Vol 255 (6) ◽  
pp. H1413-H1420 ◽  
Author(s):  
M. P. Gupta ◽  
I. R. Innes ◽  
N. S. Dhalla

Isolated rat hearts exhibited a biphasic contractile response to varying concentrations of ruthenium red. A negative inotropic effect was observed with concentrations of 0.025–0.5 microM, whereas a reversal of these initial changes toward control or even exceeding the predrug values was obtained as ruthenium red concentration was increased to 2.5 or 5.0 microM. High concentrations (12.5–25.0 microM) of ruthenium red caused a sustained contracture. In contrast, isolated frog hearts exhibited only a sustained negative inotropic effect at 0.25–12.5 microM ruthenium red. In studies with rat heart, both negative and positive inotropic effects of 2.5 microM ruthenium red were blocked either by increasing the concentration of Ca2+ (from 1.25 to 5.0 mM) or by decreasing the concentration of Na+ (from 140 to 35 mM) in the perfusion medium. The contracture induced by 12.5 microM ruthenium red was markedly inhibited when Ca2+ in the medium was lowered. The positive inotropic effect and contracture due to ruthenium red were also blocked by 1 microM of verapamil and 1.5 mM of amiloride; however, these interventions did not prevent the initial negative inotropic effect of ruthenium red. These experiments suggest the role of extracellular Ca2+ in the dose- and time-dependent effects of ruthenium red on contractile function of the rat heart. Furthermore, the positive inotropic response to ruthenium red may be related to its actions on the Na+-dependent Ca2+ movements in the cardiac cell.


Cytokine ◽  
2018 ◽  
Vol 107 ◽  
pp. 65-69 ◽  
Author(s):  
B. Jude ◽  
S. Vetel ◽  
M.A. Giroux-Metges ◽  
J.P. Pennec

1982 ◽  
Vol 242 (1) ◽  
pp. H89-H93
Author(s):  
M. M. Bersohn ◽  
K. I. Shine ◽  
W. D. Sterman

Perfusates containing high magnesium concentrations have been suggested to have a protective effect for ischemic myocardium, but the mechanism for such an effect is unclear. We investigated the recovery of isolated perfused rabbit and rat hearts from ischemia under varied conditions of increased Mg. Hearts were made ischemic in the presence of normal 1.2 mM Mg or elevated 15 mM Mg. Rabbit hearts, which show minimal alteration in contractility in the presence of 15 mM Mg, were not protected from ischemia by high Mg perfusate. Rat hearts, which have a large negative inotropic response to 15 mM Mg, exhibited significantly better recovery of mechanical function following ischemia in the presence of high Mg than following ischemia with normal Mg. This protective effect was abolished by increasing both Ca and Mg in the perfusate to prevent the decline in contractility that normally occurred with Mg. Reperfusion with 15 mM Mg after ischemia also had no protective effect if the rat heart had been made ischemic in the presence of normal Mg. We conclude that elevated Mg protects ischemic myocardium only under circumstances in which it has a negative inotropic effect before the onset of ischemia, i.e., in the rat heart perfused with normal Ca. These results suggest that the mechanism of protection by high Mg involves sparing of ATP. However, the different responses to Mg of the species studied in these experiments should be a caution against extrapolating such results from rat hearts to other species.


2021 ◽  
Vol 4 (3) ◽  
pp. 01-05
Author(s):  
Inoyat Jumayev

In studies, the alkaloid 1-(2-Chloro-4,5-methylenedioxyphenyl)-2-hydroxyethyl-6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline (N-14) had a negative inotropic effect on the activity of the papillary muscle contraction of the rat heart detected. Ca2+ ions from SR play an important role in the process of contraction of the heart muscle. With this in mind, the negative inotropic effect of the N-14 alkaloid was investigated with the modification of the accumulation processes of Ca2+ ions to SR. To clarify this, we examined the effects of the alkaloid being studied on SERCA2a and RyR2. To do this, the inhibitor of SERCA2a - cyclopiazonic acid (CPA) and RyR activator caffeine, which provide the accumulation of Ca2+ ions in SR, were used.


2014 ◽  
Vol 728 ◽  
pp. 119-127 ◽  
Author(s):  
Grégoire Carré ◽  
Hélène Carreyre ◽  
Maurice Ouedraogo ◽  
Frédéric Becq ◽  
Patrick Bois ◽  
...  

1986 ◽  
Vol 250 (6) ◽  
pp. H923-H931 ◽  
Author(s):  
L. G. Lelievre ◽  
J. M. Maixent ◽  
P. Lorente ◽  
C. Mouas ◽  
D. Charlemagne ◽  
...  

The inotropic effect of ouabain on cardiac hypertrophy was evaluated on an isolated Langendorff rat heart preparation with performances registrated by means of an intraventricular balloon. These effects were compared with the drug action on the sarcolemma-bound Na+-K+-ATPase activity. On both normal and pressure-overload induced hypertrophied rat hearts (ventricular wt-to-body wt ratios of 2.1 and 3.3, respectively) the inotropic effect of ouabain (10(-9)-10(-4) M) was evaluated at 0.25 mM external Ca2+. Compared with normal hearts, the recovery of a normal contractile function after the inotropic response was significantly slower in hypertrophied hearts. This was valid with the two protocols applied. During a 30-min washout period, the inotropic response remained nearly unchanged in hypertrophied hearts, whereas it was almost completely reversed in control groups. Sarcolemmal vesicles from both heart groups exhibited high Na+-K+-ATPase activities (sp. act.: 105 +/- 16 mumol X h-1 X mg-1). In both normal and hypertrophied cardiac sarcolemmal preparations, the Na+-K+-ATPase was heterogeneous, with high- and low-sensitivity forms. Their relative proportion was two-to-one. In both heart groups, their respective apparent affinities for ouabain were similar (inhibitory concentration of 50% = 10(-8) and 10(-6) M, respectively). The release of ouabain from these two sites was measured, in washout experiments, by the rates of enzyme relief from inhibition. High- and low-sensitivity forms in hypertrophied heart preparations released ouabain at seven- and threefold lower rates, respectively, than the corresponding forms present in normal cardiac sarcolemmal vesicles.(ABSTRACT TRUNCATED AT 250 WORDS)


2003 ◽  
Vol 66 (1) ◽  
pp. 157-161 ◽  
Author(s):  
Gustavo Guevara-Balcázar ◽  
Enrique Querejeta-Villagómez ◽  
Oskar Nuevo-Adalla ◽  
Alejandra Orozco-Guillen ◽  
Ivan Rubio-Gayosso ◽  
...  

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