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

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

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.

Gs and Gi coupling of adrenomedullin in adult rat ventricular myocytes

2006 ◽  
Vol 290 (5) ◽  
pp. H1842-H1847 ◽  
Author(s):  
Shivani Mittra ◽  
Jean-Pierre Bourreau
Keyword(s):  
Ventricular Myocytes ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Paracrine Factor ◽  
Inotropic Effects ◽  
Prolonged Incubation ◽  
Rat Ventricular Myocytes ◽  
Cell Shortening ◽  
Adult Rat

Adrenomedullin (ADM) acts as an autocrine or a paracrine factor in the regulation of cardiac function. The intracellular mechanisms involved in the direct effect of ADM on adult rat ventricular myocytes (ARVMs) are still to be elucidated. In ARVMs from normal rats, ADM produced an initial (<30 min) increase in cell shortening and Ca2+ transients and a marked decrease in both on prolonged incubation (>1 h). Both effects were sensitive to ADM antagonist ADM-(22–52). Treatment with SQ-22536, an inhibitor of adenylate cyclase, blocked the positive inotropic effect of ADM and potentiated its negative inotropic effect. The negative inotropic effect was sensitive to inhibition by pertussis toxin (PTX), an inhibitor of Gi proteins and KT-5720, an inhibitor of PKA. The observations suggest a switch from Gs-coupled to PTX-sensitive, PKA-dependent Gi coupling by ADM in ARVMs. The ADM-mediated Gi-signaling system involves cAMP-dependent pathways because SQ-22536 further increased the negative inotropic actions of ADM. Also, because ADM is overproduced by ARVMs in our rat model of septic shock, ARVMs from LPS-treated rats were subjected to treatment with ADM-(22–52) and PTX. The decrease in cell shortening and Ca2+ transients in LPS-treated ARVMs could be reversed back with ADM-(22–52) and PTX. This indicates that ADM plays a role in mediating the negative inotropic effect in LPS-treated ARVM through the activation of Gi signaling. This study delineates the intracellular pathways involved in ADM-mediated direct inotropic effects on ARVMs and also suggests a role of ADM in sepsis.

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