Vasoactive intestinal peptide has a direct positive inotropic effect on isolated human myocardial trabeculae

2001 ◽  
Vol 101 (6) ◽  
pp. 637-643 ◽  
Author(s):  
Ole SAETRUM OPGAARD ◽  
Mikael KNUTSSON ◽  
René DE VRIES ◽  
Beril TOM ◽  
Pramod R. SAXENA ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Vasoactive Intestinal Peptide ◽  
Right Atrium ◽  
Human Heart ◽  
Positive Inotropic Effect ◽  
Contractile Force ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
The Right ◽  
Ventricular Trabeculae

The aim of the present study was to assess the inotropic effects of vasoactive intestinal peptide (VIP) on isolated myocardial trabeculae from the right atrium and the left ventricle of human hearts. Furthermore, using reverse transcriptase-PCR, we wanted to determine the presence of mRNAs encoding the three cloned human VIP receptors, VPAC1, VPAC2 and PAC1. The trabeculae were paced at 1.0Hz in tissue baths, and changes in isometric contractile force upon exposure to agonist were studied. VIP had a potent positive inotropic effect in some of the atrial and ventricular trabeculae tested. This effect was almost completely blocked by the VIP-receptor antagonist VIP-(6-28). mRNAs encoding the human VPAC1, VPAC2 and PAC1 receptors were detected in human myocardial trabeculae from both the right atrium and the left ventricle. In conclusion, VIP has a direct positive inotropic effect in both the atria and the ventricles of the human heart. The presence of mRNAs for the VPAC1, VPAC2 and PAC1 receptors suggest that VIP may mediate its effect via these receptors.

Contractile effects of cardiac neuropeptides in isolated canine atrial and ventricular muscles

1989 ◽  
Vol 257 (4) ◽  
pp. H1082-H1087 ◽  
Author(s):  
D. F. Rigel ◽  
I. L. Grupp ◽  
A. Balasubramaniam ◽  
G. Grupp
Keyword(s):  
Isometric Force ◽  
Contractile Force ◽  
Adrenergic Blockade ◽  
Canine Heart ◽  
Inotropic Action ◽  
Inotropic Effects ◽  
Calcitonin Gene ◽  
Positive Inotropic Effects ◽  
The Right ◽  
Ventricular Trabeculae

Contractile effects of the cardiac neuropeptides vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), and neurotensin (NT) were compared with those of l-isoproterenol (ISO) in isolated canine atrial and ventricular trabeculae muscles stimulated to contract at 1 Hz. In ventricular muscles, ISO, VIP, and PHI augmented developed isometric force by approximately 100%. VIP and PHI were three times and 1/10, respectively, as potent as ISO. VIP also exhibited positive inotropic effects in atrial trabeculae. The contractile responses to VIP were unchanged after beta-adrenergic blockade with nadolol at a concentration (10 microM) that shifted the ISO dose-response curve two to three orders of magnitude to the right. In atrial and ventricular trabeculae, NPY (1 microM) attenuated contractile force by 36 +/- 8 and 30 +/- 4%, respectively. Each peptide also caused comparable increases or decreases in the rate of development of force and the rate of relaxation. CGRP and NT caused no significant changes in developed force in either atrial or ventricular muscles in concentrations up to 1 microM. Our results indicate a potential positive inotropic action of endogenous VIP and PHI and a cardiodepressant effect of endogenous NPY in the canine heart.

Positive inotropic responses mediated by endothelin ETA and ETB receptors in human myocardial trabeculae

2000 ◽  
Vol 99 (3) ◽  
pp. 161-168 ◽  
Author(s):  
Ole SAETRUM OPGAARD ◽  
Sebastian MÖLLER ◽  
René DE VRIES ◽  
Lars EDVINSSON ◽  
Pramod R. SAXENA
Keyword(s):  
Receptor Antagonist ◽  
Positive Inotropic Effect ◽  
Inotropic Effect ◽  
Maximum Effect ◽  
Inotropic Effects ◽  
Eta Receptor ◽  
Etb Receptor ◽  
Eta Receptor Antagonist ◽  
The Right ◽  
Inotropic Responses

The aim of the present study was to determine possible inotropic effects mediated by endothelin ETA and ETB receptors in human myocardial trabeculae from the right atrium and the left ventricle. Isolated trabeculae from human hearts were paced at 1.0 Hz in tissue baths, and changes in isometric contractile force upon exposure to agonist were studied. Endothelin-1 (ET-1) and ET-3 had a strong positive inotropic effect in all trabeculae. ET-1 was significantly more potent than ET-3 in both atrial (P < 0.001) and ventricular (P < 0.05) trabeculae. Preincubation with the ETA receptor antagonist FR139317 (1 μM) decreased significantly (P < 0.005) the potency of ET-1 in both atrial and ventricular trabeculae, without any significant changes in Emax (maximum effect obtained with an agonist). The ETB receptor agonist IRL 1620 had a positive inotropic effect only in some trabeculae, and the ETB receptor antagonist BQ 788 (1 μM) almost completely blocked this effect. These results suggest that both ETA and ETB receptors mediate positive inotropic responses at both the atrial and ventricular level in the human heart.

scholarly journals IL-13 Has a Positive Inotropic Effect Associated with an Increase of Membrane Excitability on Healthy Rat Heart but not in Septic Rat Heart

2019 ◽  
pp. 1-9
Author(s):  
Jude B ◽  
Vermeersch V ◽  
Vetel S ◽  
Léon K ◽  
Droguet M ◽  
...  
Keyword(s):  
Rat Heart ◽  
Positive Inotropic Effect ◽  
Ex Vivo ◽  
Sodium Current ◽  
Contractile Force ◽  
Inotropic Effect ◽  
Membrane Excitability ◽  
Perfused Heart ◽  
Inotropic Effects ◽  
The Impact

Introduction: Interleukin 13 (IL-13) is a cytokine produced during sepsis. The pro- and/or anti-inflammatory effects of IL-13 still remain not clearly stated, especially at the heart level. In this study, we evidenced the impact of IL-13 on (i) the heart contraction; and on (ii) the voltage-dependent Na+ channels, NaV1.4 and NaV1.5, which are responsible for the membrane excitability, are essential for the excitation/contraction coupling. Methods: Rat hearts were perfused ex vivo with IL-13 at 10ng/ml. The contractile force, heart frequency and coronary flow were recorded. The expression and translocation of NaV1.4 and NaV1.5 were analyzed by western blot after extraction of membrane and cytosol proteins from ventricular cardiomyocytes. Results: Results showed that IL-13 induced an increase of the contractile force (+28.3%), as well as of both maximal speeds of contraction (+35.5%) and relaxation (+38.9%). We also demonstrated that IL-13 was acting via a pathway involving β1-adrenergic - adenylyl cyclase - PKA activation. An increase in sodium current was also shown to be regulated by the same pathway. The hearts perfused with IL-13 showed increased number of NaV1.4 (+37.4%) and NaV1.5 (+52.2%) at the membrane level, and the ratios of membrane/cytosol channels proteins were also increased after IL-13 perfusion for NaV1.4 (+281.4%) and NaV1.5 (+214.4%). Conclusion: This study shows that IL-13 has a positive inotropic effect on perfused heart and that IL-13 can also increase NaV1.4 and NaV1.5 membrane targeting, therefore increasing the membrane excitability of the cardiomyocytes. However, IL-13 was shown to lose its inotropic effects in chronic septic hearts.

5-Hydroxytryptamine increases contractile force in porcine right atrium but not in left ventricle

1992 ◽  
Vol 346 (5) ◽  
Author(s):  
RegienG. Schoemaker ◽  
XiaoY. Du ◽  
WillemA. Bax ◽  
PramodR. Saxena
Keyword(s):  
Left Ventricle ◽  
Right Atrium ◽  
Contractile Force

Positive inotropic effects of low concentrations of leukotrienes C4 and D4 in rat heart

1990 ◽  
Vol 259 (4) ◽  
pp. H1239-H1246 ◽  
Author(s):  
M. Karmazyn ◽  
M. P. Moffat
Keyword(s):  
Calcium Channel ◽  
Positive Inotropic Effect ◽  
Negative Inotropic Effect ◽  
Bay K 8644 ◽  
Inotropic Effect ◽  
Receptor Interaction ◽  
Inotropic Effects ◽  
Coronary Pressure ◽  
Low Concentrations ◽  
Rat Hearts

We examined the effects of leukotrienes (LT) B4, C4, D4, and E4 (0.010-2.5 ng/ml) on contractile and coronary function in isolated rat hearts. Concentration-dependent effects were examined either by the cumulative addition of LTs or by addition of specific concentrations to individual preparations. Neither LTB4 nor LTE4 produced myocardial or coronary effects at any concentration, irrespective of addition protocol. At 0.010 ng/ml, both LTC4 and LTD4 produced an increase in force that was associated with a 30% elevation in coronary pressure. Further cumulative addition of either leukotriene resulted in a negative inotropic effect and a further increase in coronary pressure. In contrast, following single additions of LTC4 or LTD4 (0.01-0.50 ng/ml) a positive inotropic effect and an increased coronary pressure were observed. LTC4 or LTD4 at 0.5 ng/ml produced a negative inotropic effect in hearts pretreated with 0.01 ng/ml of LTD4 or LTC4, respectively. Reversal of this addition protocol resulted in a negative inotropic effect of either 0.01 ng/ml LTD4 or LTC4. Verapamil and nifedipine significantly attenuated the positive inotropic and coronary constricting effect of 0.5 ng/ml LTC4 and LTD4. The addition of either LT following BAY K 8644 resulted in a negative inotropic effect, in contrast to the positive inotropic influence seen with leukotriene alone. Our results demonstrate a positive inotropic effect of low concentrations of LTC4 and LTD4 concomitant with coronary artery constriction, a phenomenon determined by leukotriene addition protocols and suggestive of LTC4/LTD4 receptor interaction. The effects of calcium channel antagonists and BAY K 8644 on the inotropic response suggest a leukotriene-mediated activation of the calcium channel resulting in increased intracellular calcium concentrations.

Cat heart acetylcholine: structural proof and distribution

1976 ◽  
Vol 231 (3) ◽  
pp. 781-785 ◽  
Author(s):  
OM Brown
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Left Atrium ◽  
Right Atrium ◽  
Interventricular Septum ◽  
Pyrolysis Product ◽  
Heart Tissue ◽  
Choline Esters ◽  
The Right ◽  
Cat Heart

The distribution of acetylcholine (ACh) in the cat heart was investigated by a pyrolysis-gas chromatography (PGC) method. The hearts were dissected into various regions and homogenized in acetonitrile in the presence of propionylcholine, internal standard. Following extraction with toluene and hexane, the choline esters were precipitated as the enneaiodide complex. The isolated choline esters were analyzed by PGC, and the peak corresponding to ACh was quantified. The compound extracted from heart tissue that eluted with the retention time of authentic ACh was identified by mass spectrometry as dimethylaminoethylacetate, the pyrolysis product of ACh. ACh concentrations were found to be higher in the atria than the ventricles. In both the atria and the ventricles, a higher content of ACh was found in the right than the left portions: right ventricle, 5.0 compared to left ventricle, 2.0 nmol/g; and right atrium, 16.8 compared to left atrium, 11.3 nmol/g. Some cats were subjected to a bilateral cervical vagotomy 3 wk before removal and analysis of heart tissue. Hearts from vagotomized cats contained less ACh than controls in the right ventricle (-31%), right atrium (-54%), SA node (-42%), and papillary muscle (-53%), but no decreases were found in the left ventricle, left atrium, or interventricular septum.

Positive Inotropic Effect of Prostaglandin F2α in Rat Ventricular Trabeculae

2016 ◽  
Vol 68 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Xin Shen ◽  
Sarbjot Kaur ◽  
Amelia Power ◽  
Logan Z. J. Williams ◽  
Marie-Louise Ward
Keyword(s):  
Positive Inotropic Effect ◽  
Prostaglandin F2α ◽  
Inotropic Effect ◽  
Ventricular Trabeculae

Further characterization of the receptors involved in the positive inotropic effect of histamine on rabbit papillary muscle

1986 ◽  
Vol 64 (12) ◽  
pp. 1484-1488 ◽  
Author(s):  
Alejandro Elizalde ◽  
Jesús Perez-Chavez ◽  
José Sánchez-Chapula
Keyword(s):  
Action Potentials ◽  
Positive Inotropic Effect ◽  
Phosphodiesterase Inhibitor ◽  
Adenosine Monophosphate ◽  
Inotropic Effect ◽  
Slow Inward Current ◽  
Force Of Contraction ◽  
Inotropic Effects ◽  
Slow Action Potentials ◽  
Stimulation Of

The effects of histamine on the force of contraction and calcium-dependent action potentials were studied in rabbit ventricular papillary muscles. The positive inotropic effect of histamine seems to be dependent on stimulation of H1 and H2 receptors. The H1 antagonist chlorpheniramine produced a competitive blockade of the positive inotropic effects of histamine. Cimetidine produced a competitive blockade, which was apparent only after blockade of H1 receptors. Histamine increased the maximum upstroke velocity of slow action potentials. This effect can be entirely accounted for by stimulation of H2 receptors. The phosphodiesterase inhibitor 3-isobutyl-methyl-xanthine potentiated the H2 receptor mediated effects of histamine on the force of contraction and slow action potentials. We conclude that rabbit ventricular muscle possesses both H1 and H2 receptors that mediate the positive inotropic effect of histamine. The H2-mediated effect seems to be causally related to an increase in the calcium slow inward current and is probably linked to an enhanced cellular cyclic adenosine monophosphate content. The mechanism of the H1-mediated positive inotropic effect remains unknown.

Constitutional Anatomy of the Right Atrium of the Human Heart

2016 ◽  
Vol 5 (3) ◽  
pp. 42-49
Author(s):  
N. A. Kornienko ◽  
◽  
E. V. Chaplygina ◽  
A. A. Kornienko ◽  
◽  
...  
Keyword(s):  
Right Atrium ◽  
Human Heart ◽  
The Right

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 &lt; 0.05), but its potentiation was preserved with isoflurane (148 +/- 21%; P &lt; 0.05) and sevoflurane (161 +/- 40%; P &lt; 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.

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