Effects of Desflurane in Senescent Rat Myocardium

2006 ◽  
Vol 105 (5) ◽  
pp. 961-967 ◽  
Author(s):  
Sandrine Rozenberg ◽  
Sophie Besse ◽  
Julien Amour ◽  
Benoît Vivien ◽  
Benoît Tavernier ◽  
...  
Keyword(s):  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Shortening Velocity ◽  
Adult Rats ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Low Load ◽  
Positive Effect ◽  
Negative Inotropic Effects

Background The myocardial negative inotropic effects of desflurane are less pronounced than those of other halogenated anesthetics, partly because of intramyocardial catecholamine store release. However, the effects of desflurane on aging myocardium are unknown, whereas aging is known to be associated with an attenuation of catecholamine responsiveness. Methods The effects of desflurane (1.9-9.3 vol%) were studied in left ventricular papillary muscle of adult and senescent rats (29 degrees C; 0.5 mm Ca; stimulation frequency 12 pulses/min). The inotropic effects were compared under low and high loads, using the maximum unloaded shortening velocity and maximum isometric active force, and without or with alpha- and beta-adrenoceptor blockade. Results Desflurane induced a moderate positive inotropic effect in adult rats but a negative inotropic effect in senescent rats. After alpha- and beta-adrenoceptor blockade, desflurane induced a comparable negative inotropic effect in adult and senescent rats. No lusitropic effect under low load was observed, whereas desflurane induced a slight but significant positive lusitropic effect under high load similar between the two groups of rats. This positive effect was abolished by adrenoceptor blockade. Conclusion The authors' study suggests that desflurane does not induce significant intramyocardial catecholamine release in senescent myocardium, a result that should be integrated in the well-known alteration in the catecholamine response during aging.

Effects of Desflurane in Rat Myocardium

1997 ◽  
Vol 87 (3) ◽  
pp. 599-609 ◽  
Author(s):  
Pierre-Yves Gueugniaud ◽  
Jean-Luc Hanouz ◽  
Benoit Vivien ◽  
Yves Lecarpentier ◽  
Pierre Coriat ◽  
...  
Keyword(s):  
Negative Inotropic Effect ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Papillary Muscles ◽  
Shortening Velocity ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Low Load

Background The cardiovascular effects of desflurane have been investigated in several in vivo animal and human studies. To determine the possible contributions of myocardial depression, the effects of desflurane on various contractile parameters in isolated cardiac papillary muscles were compared with those of isoflurane and halothane. Methods The effects of desflurane, isoflurane, and halothane (0.5-2.5 minimum alveolar concentration [MAC]) were studied in rat left ventricular papillary muscles (29 degrees C; pH 7.40; stimulation frequency, 12 pulses/min). The inotropic effects were compared under low (isotony) and high (isometry) loads, using the maximum unloaded shortening velocity (Vmax) and maximum isometric active force (AF). The lusitropic effects were compared in isotonic and isometric conditions. Results Desflurane has no significant inotropic effect (AF at 2.5 MAC: 95 +/- 11% of control values; NS) in contrast with halothane and isoflurane (AF at 2.5 MAC: 37 +/- 14 vs. 65 +/- 10%, respectively; P < 0.05). After alpha- and beta-adrenoceptor blockade or pretreatment with reserpine, desflurane induced a negative inotropic effect (AF at 2.5 MAC: 83 +/- 11 vs. 89 +/- 8%, respectively) that was not significantly different from that of isoflurane (AF at 2.5 MAC: 80 +/- 12%). Halothane induced a negative lusitropic effect under low load, which was significantly greater than those of isoflurane and desflurane. In contrast to halothane, isoflurane and desflurane induced no significant lusitropic effect under high load and did not modify postrest potentiation. These results suggest that desflurane did not impair sarcoplasmic reticulum function. Conclusions When compared with isoflurane, desflurane induced a moderate positive inotropic effect related to intramyocardial catecholamine release. After adrenoceptor blockade, desflurane induced a negative inotropic effect comparable with that induced by isoflurane.

Myocardial Effects of Halothane and Isoflurane in Hamsters with Hypertrophic Cardiomyopathy 

1997 ◽  
Vol 87 (6) ◽  
pp. 1406-1416 ◽  
Author(s):  
Benoit Vivien ◽  
Jean-Luc Hanouz ◽  
Pierre-Yves Gueugniaud ◽  
Yves Lecarpentier ◽  
Pierre Coriat ◽  
...  
Keyword(s):  
Isometric Force ◽  
Negative Inotropic Effect ◽  
Myocardial Contraction ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Low Load ◽  
Cardiomyopathic Hamsters ◽  
Negative Inotropic Effects

Background The effects of halothane and isoflurane on myocardial contraction and relaxation in diseased myocardium are not completely understood. Methods The effects of equianesthetic concentrations of halothane and isoflurane on inotropy and lusitropy in left ventricular papillary muscles of healthy hamsters and those with genetically induced cardiomyopathy (strain BIO 14.6) were investigated in vitro (29 degrees C; pH 7.40; Ca2+ 2.5 mM; stimulation frequency, 3/min) in isotonic and isometric conditions. Results Halothane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (1.5 vol%, active isometric force (AF): 19 +/- 8% vs. 28 +/- 11% of control values; P < 0.05). Isoflurane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (2.0 vol%, AF: 64 +/- 13% vs. 75 +/- 11% of control values; P < 0.01). However, the negative inotropic effects of halothane and isoflurane were not different for cardiomyopathic or healthy hamsters when their concentrations were corrected for minimum alveolar concentration (MAC) values in each strain. Halothane induced a negative lusitropic effect under low load, which was more important in cardiomyopathic hamsters, suggesting a greater impairment in calcium uptake by the sarcoplasmic reticulum. In contrast, isoflurane induced a moderate positive lusitropic effect under low load in healthy but not in cardiomyopathic hamsters. Halothane and isoflurane induced no significant lusitropic effect under high load. Conclusions Halothane and isoflurane had greater negative inotropic effects in cardiomyopathic than in healthy hamsters. Nevertheless, no significant differences in their inotropic effects were noted when concentrations were correlated as a multiple of MAC in each strain.

Myocardial Effects of Halothane and Isoflurane in Senescent Rats

2002 ◽  
Vol 97 (6) ◽  
pp. 1477-1484 ◽  
Author(s):  
Sandrine Rozenberg ◽  
Sophie Besse ◽  
Benoît Vivien ◽  
Pierre Coriat ◽  
Bruno Riou
Keyword(s):  
Negative Inotropic Effect ◽  
Myocardial Contraction ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Shortening Velocity ◽  
Adult Rats ◽  
Inotropic Effects ◽  
Expression Of Genes ◽  
Baseline Values ◽  
Contraction And Relaxation

Background Aging is associated with marked alterations in myocardial contraction and relaxation, whereas halogenated anesthetics depress myocardial contractility. However, their effects on aging myocardium are unknown. Methods Mechanical variables of left ventricular papillary muscles from adult and senescent rats (29 degrees C; pH 7.40; Ca2+ 1.0 or 0.5 mM; stimulation frequency, 12 pulses/min) were studied. The expression of genes coding for the alpha and beta-myosin heavy chain (MHC) and Ca2+ -ATPase of the sarcoplasmic reticulum (SR) were studied. The effects of halothane and isoflurane were studied. The inotropic effects were compared under low and high loads, using the maximum unloaded shortening velocity (Vmax) and maximum isometric active force (AF). The lusitropic effects were compared in isotonic and isometric conditions. Results Senescent rats had a decrease in contraction and relaxation velocities, associated with a reexpression of beta-MHC mRNAs and a decrease in SR Ca2+ -ATPase mRNAs. Halothane induced a lower negative inotropic effect in senescent rats (1.5 vol%, AF: 53 +/- 14% vs. 39 +/- 12% of baseline values; P < 0.01) whereas isoflurane induced a similar negative inotropic effect (1.5 vol%, AF: 81 +/- 7% vs. 87 +/- 7% of baseline values; NS). Halothane induced a negative lusitropic effect in isotonic conditions in adult, but not in senescent, rats. Conclusions The inotropic and lusitropic effects of halothane were less important in senescent than in adult rats, whereas the effects of isoflurane were similar. These differences are probably related to differences in SR function and in the effects of halogenated anesthetics on the SR.

Interaction of Halothane with α- and β-Adrenoceptor Stimulations in Rat Myocardium

1997 ◽  
Vol 86 (1) ◽  
pp. 147-159 ◽  
Author(s):  
Jean-Luc Hanouz ◽  
Bruno MD Riou ◽  
Laurent Massias ◽  
Yves Lecarpentier ◽  
Pierre Coriat
Keyword(s):  
Positive Inotropic Effect ◽  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Papillary Muscles ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Low Load ◽  
Positive Inotropic Effects

Background Halothane induces negative inotropic and lusitropic effects in myocardium. It has been suggested that halothane potentiates beta-adrenoceptor stimulation. However, its effects on the inotropic response to alpha-adrenoceptor stimulation and its effects on the lusitropic effects of alpha- and beta-adrenoceptor stimulation are unknown. Methods The effects of halothane (0.5 and 1 minimum alveolar concentration [MAC]) on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) and isoproterenol (10(-8) to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (in Krebs-Henseleit solution at 29 degrees C, pH 7.40, with 0.5 mM calcium and stimulation frequency at 12 pulses/min). The lusitropic effects were studied in isotonic (R1) and isometric (R2) conditions. Results One MAC halothane induced a negative inotropic effect (54 +/- 3%, P < 0.05), increased R1 (109 +/- 3%, P < 0.05), and decreased R2 (88 +/- 2%, P < 0.05). In control groups, phenylephrine (137 +/- 7%, P > 0.05) and isoproterenol (162 +/- 6%, P < 0.05) induced a positive inotropic effect. Halothane did not significantly modify the positive inotropic effect of calcium, suggesting that it did not modify the inotropic reserve of papillary muscles. In contrast, 1 MAC halothane enhanced the positive inotropic effects of phenylephrine (237 +/- 19%, P < 0.05) and isoproterenol (205 +/- 11%, P < 0.05). Halothane did not modify the lusitropic effect of phenylephrine under high or low load. In contrast, 1 MAC halothane impaired the positive lusitropic effect of isoproterenol under low load (P < 0.05), whereas it did not modify the positive lusitropic effect of isoproterenol under high load. Conclusions At clinically relevant concentrations, halothane potentiated the positive inotropic effects of both alpha- and beta-adrenoceptor stimulation. Furthermore, halothane alters the positive lusitropic-effect of beta-adrenoceptor stimulation under low load.

Mechanism of the Negative Inotropic Effect of Thiopental in Isolated Ferret Ventricular Myocardium 

1995 ◽  
Vol 82 (2) ◽  
pp. 436-450 ◽  
Author(s):  
Philippe R. Housmans ◽  
Turkan S. Kudsioglu ◽  
Jonathan Bingham
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Negative Inotropic Effect ◽  
Ventricular Myocardium ◽  
Underlying Mechanism ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Force Peak ◽  
Human Ventricular Myocardium ◽  
Negative Inotropic Effects

Background Thiopental's myocardial depressant effects are well known and most likely involve some alteration in intracellular Ca2+ homeostasis. The aim of this study was to investigate the mechanisms of thiopental's negative inotropic effects and its underlying mechanism in isolated ferret ventricular myocardium (which shows physiologic characteristics similar to human ventricular myocardium), and in frog ventricular myocardium, in which Ca2+ ions for myofibrillar activation are derived almost entirely from transsarcolemmal influx. Methods The authors analyzed the effects of thiopental after beta-adrenoceptor blockade on variables of contractility and relaxation, and on the free intracellular Ca2+ transient detected with the Ca(2+)-regulated photoprotein aequorin. Thiopental's effects also were evaluated in ferret right ventricular papillary muscles in which the sarcoplasmic reticulum (SR) function was impaired by ryanodine and in frog ventricular strips with little or no SR function. Results At concentration > or = 10(-4) M, which is in the high range of the clinically encountered free plasma thiopental concentrations, thiopental decreased contractility and the amplitude of the intracellular Ca2+ transient. At equal peak force, peak aequorin luminescence in 10(-4) M thiopental and [Ca2+]0 > 2.25 mM was slightly smaller than that in control conditions at [Ca2+]o = 2.25 mM. This indicates that thiopental causes a small increase in myofibrillar Ca2+ sensitivity. After inactivation of sarcoplasmic reticulum Ca2+ release with 10(-6) M ryanodine, a condition in which myofibrillar activation depends almost exclusively on transsarcolemmal Ca2+ influx, thiopental caused a further decrease in contractility and in the amplitude of the intracellular Ca2+ transient, and thiopental's relative negative inotropic effect was not different from that in control muscles not exposed to ryanodine. Thiopental, > or = 10(-4) M, decreased contractility in frog ventricular myocardium. Conclusions These findings indicate that the direct negative inotropic effect of thiopental results from a decrease in intracellular Ca2+ availability. At least part of thiopental's action is caused by inhibition of transsarcolemmal Ca2+ influx. These effects become apparent at concentrations routinely present during intravenous induction with thiopental.

Interaction of Isoflurane and Sevoflurane with α- and β-adrenoceptor Stimulations in Rat Myocardium 

1998 ◽  
Vol 88 (5) ◽  
pp. 1249-1258 ◽  
Author(s):  
Jean-Luc Hanouz ◽  
Pierre-Yves Gueugniaud ◽  
Yves Lecarpentier ◽  
Pierre Coriat ◽  
Bruno Riou
Keyword(s):  
Positive Inotropic Effect ◽  
Left Ventricular ◽  
Control Groups ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Calcium Stimulation ◽  
Positive Inotropic Effects ◽  
Inotropic Responses ◽  
Negative Inotropic Effects

Background Halothane potentiates the positive inotropic effects of alpha- and beta-adrenoceptor stimulations but impairs the positive lusitropic effect of beta-adrenoceptor stimulations. However, the interactions of isoflurane and sevoflurane with alpha- and beta-adrenoceptor stimulation have not been entirely defined. Methods The effects of 1 minimum alveolar concentration isoflurane and sevoflurane on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) or isoproterenol (10(-8 to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (Krebs-Henseleit solution, 29 degrees C; pH, 7.4; 0.5 mM calcium; stimulation frequency, 12 pulses/min). The positive lusitropic effects of alpha- and beta-adrenoceptor stimulations were studied under isotonic and isometric conditions. Data are mean percentages of baseline +/- SEM. Results In control groups, phenylephrine (134 +/- 8%; P < 0.05) and isoproterenol (171 +/- 7%; P < 0.05) induced a positive inotropic effect. Isoflurane enhanced the positive inotropic effects of phenylephrine (185 +/- 10%; P < 0.05) and of isoproterenol (203 +/- 11%; P < 0.05). Sevoflurane enhanced the positive inotropic effects of phenylephrine (187 +/- 10%; P < 0.05) and of isoproterenol (228 +/- 11%; P < 0.05). These potentiations were similar to those previously reported with halothane. Isoflurane and sevoflurane did not modify the positive lusitropic effects under low and high loads of isoproterenol. Conclusion Although isoflurane and sevoflurane have moderate negative inotropic effects, they potentiated the positive inotropic effects of alpha- and beta-adrenoceptor stimulations but did not modify the positive lusitropic effects of beta-adrenoceptor stimulation.

Interaction of Halogenated Anesthetics with α- and β-Adrenoceptor Stimulations in Diabetic Rat Myocardium

2004 ◽  
Vol 101 (5) ◽  
pp. 1145-1152 ◽  
Author(s):  
Julien Amour ◽  
Jean-Stéphane David ◽  
Benoît Vivien ◽  
Pierre Coriat ◽  
Bruno Riou
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Positive Inotropic Effect ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Diabetic Rat ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Positive Inotropic Effects

Background Halogenated anesthetics potentiate the positive inotropic effects of alpha- and beta-adrenoceptor stimulations. Although diabetes mellitus induces significant myocardial abnormalities, the interaction of halogenated anesthetics and adrenoceptor stimulation in diabetic myocardium remains unknown. Methods Left ventricular papillary muscles were provided from healthy and streptozotocin-induced diabetic rats. Effects of 1 minimum alveolar concentration halothane, isoflurane, and sevoflurane on the inotropic and lusitropic responses of alpha (phenylephrine)- and beta (isoproterenol)-adrenoceptor stimulations were studied at 29 degrees C with 12 pulses/min. Data shown are mean percentage of baseline active force +/- SD. Results Phenylephrine induced comparable positive inotropic effects in healthy and diabetic rats (143 +/- 8 vs. 136 +/- 18%; not significant), but the potentiation by halogenated anesthetics was abolished in the diabetic rats (121 +/- 20, 130 +/- 20, and 123 +/- 20% for halothane, isoflurane, and sevoflurane, respectively; not significant). In diabetic rats, the positive inotropic effect of isoproterenol was markedly diminished (109 +/- 9 vs. 190 +/- 18%; P < 0.05), but its potentiation was preserved with isoflurane (148 +/- 21%; P < 0.05) and sevoflurane (161 +/- 40%; P < 0.05) but not with halothane (126 +/- 16%; not significant). Halothane induced a deleterious effect on the sarcoplasmic reticulum, as shown by its impairment in the lusitropic effect of isoproterenol, compared with isoflurane and sevoflurane. Conclusion Potentiation of the positive inotropic effect of alpha-adrenoceptor stimulation by halogenated anesthetics is abolished in diabetic rats. In contrast, potentiation of beta-adrenoceptor stimulation is preserved with isoflurane and sevoflurane but not with halothane, probably because of its deleterious effects on sarcoplasmic reticulum.

Abstract 1469: Diastolic dysfunction induced by Flecainide but not Amiodarone

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Egbert Bisping ◽  
Christian Pagel ◽  
Andre Wilken ◽  
Karl Toischer ◽  
Burkert Pieske
Keyword(s):  
Atrial Fibrillation ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Negative Inotropic Effect ◽  
Human Myocardium ◽  
Inotropic Effect ◽  
Force Frequency ◽  
Inotropic Effects ◽  
Rabbit Myocardium ◽  
Negative Inotropic Effects

Diastolic dysfunction is a significant risk factor for the development and progression of atrial fibrillation. Flecainide (Flec) and Amiodarone (AM) are frequently used in patients with atrial fibrillation but their impact on diastolic function has not been evaluated yet. We tested the effect of Flec and AM on systolic and diastolic performance in isolated muscle strips from failing human and nonfailing rabbit myocardium. Isolated ventricular trabeculae contracted isometrically at 1 Hz, Ca2+ 2.5 mmol/L, 37°C. Flec (0.01 – 100 μmol/L, dissolved in water) showed a concentration dependent negative inotropic effect in human myocardium (13 ± 2 vs. 3 ± 0.5 mN/mm 2 at base vs. 100 μmol/L; p< 0.05). This was associated with a significant prolongation of the relaxation time RT95 and an increase of diastolic tension (Dias) by 35 ± 9 % (at 100 μmol/L; p< 0.05). Water alone had no effect. Calcium transients measured by Aequorin technique declined proportionally to developed force after Flec. In contrast, AM (0.01 – 100 μmol/L, dissolved in 2% benzyl alcohol and 10% polsorbate) showed identical negative inotropic effects to solvent alone (maximally by 16 ± 8 %), and neither AM nor its solvent affected diastolic tension or relaxation times. Flec (3 μmol/L) resulted in a significant impairment of the Force frequency relationship (FFR) at 0.5–3.0 Hz in human myocardium. This was related to a decline in systolic force and a rise in Dias at high frequencies (at 3 Hz by 32 ± 12 % in control and 87 ± 25 % after Flec, p < 0.05 vs. control). In nonfailing rabbit myocardium (1.0–5.0 Hz) Dias decreased by 11 ± 10 % (n.s.) in control but raised by 65 ± 25 % after Flec, p < 0.05). AM (100 μmol/L) had no significant effect on FFR, whereas its solvent tended to impair the FFR by a decline in systolic performance. Conclusion: Flec exerts calcium dependent negative inotropic effects in human myocardium and significantly impairs diastolic function. The latter is observable not only in human failing myocardium with preexisting diastolic dysfunction but also in nonfailing animal myocardium. In contrast AM shows no compound specific negative inotropic effect and no change in diastolic function. In patients treated with Flec attention should be turned to the potential of the drug to deteriorate diastolic function.

scholarly journals Evaluation of Negative Inotropic Effects of a Isoquinoline Alkaloid N-14

2021 ◽  
Vol 4 (3) ◽  
pp. 01-05
Author(s):  
Inoyat Jumayev
Keyword(s):  
Muscle Contraction ◽  
Papillary Muscle ◽  
Heart Muscle ◽  
Rat Heart ◽  
Cyclopiazonic Acid ◽  
Negative Inotropic Effect ◽  
Isoquinoline Alkaloid ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Negative Inotropic Effects

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.

Mechanism of the negative inotropic effects of α1-adrenoceptor agonists on mouse myocardium

2003 ◽  
Vol 81 (8) ◽  
pp. 783-789 ◽  
Author(s):  
Daya R Varma ◽  
Hansjorg Rindt ◽  
Sylvain Chemtob ◽  
Shree Mulay
Keyword(s):  
Adult Mouse ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Adult Mice ◽  
Pkc Isoforms ◽  
Adrenoceptor Agonists ◽  
Inotropic Responses ◽  
Negative Inotropic Effects

This study was done to identify the mechanism of the α1-adrenoceptor (AR) mediated negative inotropic effects of phenylephrine (PE) on adult mouse myocardium. As reported by others, we also found that the nonselective α1AR agonist PE produced a negative inotropic effect on ventricular strips from adult mice that was inhibited by the α1AAR antagonist 5-methylurapidil (5MU) but not by the α1BAR antagonist chloroethylclonidine (CEC) or the α1DAR antagonist BMY 7378. The selective α1AAR agonist A61603 also produced a negative inotropic effect, which was antagonized by 5MU. Phorbol 12,13-dibutyrate (activator of all PKC isoforms) mimicked the negative inotropic responses to PE and A61603. The negative inotropic effects of PE were inhibited by bisindolylmaleimide (inhibitor of all PKC isoforms) but not by Gö 6976 (inhibitor of Ca2+-dependant PKC). Rottlerin, an inhibitor of Ca2+-independent PKCδ, antagonized the negative inotropic effects of PE and A61603. PE and A61603 increased the translocation of PKCδ, which was prevented by rottlerin. These data suggest that the α1AR-mediated negative inotropy on adult mouse myocardium is signaled by Ca2+-independent PKCδ.Key words: phorbol 12,13-dibutyrate, 5-methylurapidil, BMY 7378, chloroethylclolidine, Ca2+-dependant PKC isoforms, α1A-adrenoceptor.

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