scholarly journals Mechanism underlying the negative inotropic effect in rat left ventricle in hyperthermia: the role of TRPV1

2020 ◽  
Vol 70 (1) ◽  
Author(s):  
Koji Obata ◽  
Hironobu Morita ◽  
Miyako Takaki
Keyword(s):  
Left Ventricle ◽  
Negative Inotropic Effect ◽  
Inotropic Effect

Crucial role of cytoskeleton reorganization in the negative inotropic effect of chromogranin A-derived peptides in eel and frog hearts

2007 ◽  
Vol 138 (2-3) ◽  
pp. 145-151 ◽  
Author(s):  
Rosa Mazza ◽  
Cinzia Mannarino ◽  
Sandra Imbrogno ◽  
Sandra Francesca Barbieri ◽  
Cristina Adamo ◽  
...  
Keyword(s):  
Crucial Role ◽  
Chromogranin A ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Cytoskeleton Reorganization

Negative inotropic effect of bradykinin in porcine isolated atrial trabeculae: role of nitric oxide

2001 ◽  
Vol 19 (7) ◽  
pp. 1289-1293 ◽  
Author(s):  
Beril Tom ◽  
René de Vries ◽  
Pramod R. Saxena ◽  
A. H. Jan Danser
Keyword(s):  
Nitric Oxide ◽  
Negative Inotropic Effect ◽  
Inotropic Effect

Halothane Inhibits Contraction and Action Potential Duration to a Greater Extent in Subendocardial than Subepicardial Myocytes from the Rat Left Ventricle

2001 ◽  
Vol 95 (5) ◽  
pp. 1213-1219 ◽  
Author(s):  
Amber Rithalia ◽  
Clare N. Gibson ◽  
Philip M. Hopkins ◽  
Simon M. Harrison
Keyword(s):  
Left Ventricle ◽  
Action Potential ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Minimum Alveolar Concentration ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Control Action ◽  
Differential Effects ◽  
K Current

Background Halothane inhibits the 4-aminopyridine-sensitive transient outward K(+) current (I(to)) which in many species, including humans, plays an important role in determining action potential duration. As I(to) is greater in the ventricular subepicardium than subendocardium, halothane may have differential effects on action potential duration and, therefore, contraction in cells isolated from these two regions. Methods Myocytes were isolated from the subendocardium and subepicardium of the rat left ventricle. Myocytes from each region were electrically stimulated at 1 Hz to measure contractions and action potentials and exposed to 0.6 mm halothane (approximately 2 x minimum alveolar concentration(50) for the rat) for 1 min. The time from the peak of the action potential to repolarization at 0 and -50 mV was measured to assess the effects of halothane on action potential duration. Results Halothane inhibited contraction to a significantly (P = 0.002) greater extent in subendocardial myocytes than in subepicardial myocytes: the amplitude of contraction during control conditions was 3.6 +/- 0.4 microm and 3.2 +/- 0.7 microm in subendocardial and subepicardial cells, respectively, and this was reduced to 1.1 +/- 0.2 microm (29 +/- 2% of control, P < 0.0001, n = 10) and 1.4 +/- 0.3 microm (46 +/- 3% of control, P = 0.007, n = 7), respectively, after a 1-min exposure to 0.6 mm halothane. Control action potential duration (at -50 mV) was 67 +/- 10 and 28 +/- 4 ms in subendocardial and subepicardial myocytes, respectively, and these values were reduced to 39 +/- 6 ms (58 +/- 3% of control, P < 0.001) and 20 +/- 3 ms (73 +/- 5% of control, P = 0.009) by halothane, respectively. Conclusions Action potential duration was reduced to a greater extent in subendocardial than subepicardial myocytes, which would contribute to the greater negative inotropic effect of halothane in the subendocardium. Furthermore, the transmural difference in action potential duration was reduced by halothane, which could contribute to its arrhythmogenic properties.

The role of calcium in the negative inotropic effect of lanthanum

1976 ◽  
Vol 32 (10) ◽  
pp. 1317-1318 ◽  
Author(s):  
F. Villani ◽  
F. Piccinini ◽  
L. Favalli
Keyword(s):  
Negative Inotropic Effect ◽  
Inotropic Effect

Protein kinase C is not involved in alpha 1-adrenoceptor-mediated positive inotropic effect

1991 ◽  
Vol 260 (1) ◽  
pp. H27-H36 ◽  
Author(s):  
M. Endou ◽  
Y. Hattori ◽  
N. Tohse ◽  
M. Kanno
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Positive Inotropic Effect ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Kinase C ◽  
Protein Kinase C Inhibitor ◽  
Prolongation Of Action Potential ◽  
Electrophysiological Effects

This study was performed to determine whether activation of protein kinase C is responsible for the positive inotropic effect of alpha 1-adrenoceptor stimulation in rat papillary muscle. In the presence of 1 microM propranolol, phenylephrine (10 microM) produced triphasic inotropic response that was accompanied by prolongation of action potential duration (APD) and hyperpolarization of membrane potential. Phorbol 12,13-dibutyrate (PDBu, 0.1 microM) abolished the negative inotropic effect of phenylephrine and apparently resulted in enhancement of the positive inotropic effect. PDBu also attenuated the phenylephrine-induced hyperpolarization without affecting the APD prolongation. However, such changes were not observed with 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.1 microM). Neither PDBu nor TPA increased the force of contraction or prolonged APD similar to phenylephrine. The protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine (H 7, 10 microM) did not suppress the changes induced by PDBu, and more importantly H 7 did not affect the inotropic and electrophysiological effects of phenylephrine. Both TPA and PDBu significantly inhibited the phenylephrine-induced phosphoinositide hydrolysis as measured by [3H]inositol monophosphate, and these inhibitory effects were eliminated in the presence of H 7. Our results provide an argument against a role of protein kinase C activation in the alpha 1-adrenoceptor-mediated inotropic and electrophysiological effects.

Responses of contractile function to ruthenium red in rat heart

1988 ◽  
Vol 255 (6) ◽  
pp. H1413-H1420 ◽  
Author(s):  
M. P. Gupta ◽  
I. R. Innes ◽  
N. S. Dhalla
Keyword(s):  
Rat Heart ◽  
Contractile Function ◽  
Negative Inotropic Effect ◽  
Ruthenium Red ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Rat Hearts ◽  
Positive Inotropic Effects ◽  
High Concentrations

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.

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