?-adrenoceptors mediating the positive inotropic effect of phenylephrine in the right ventricular muscle of the monkey (Macaca fuscata)

1982 ◽  
Vol 318 (4) ◽  
pp. 370-373 ◽  
Author(s):  
Masao Endoh ◽  
Keisuke Satoh ◽  
Norio Taira
Keyword(s):  
Right Ventricular ◽  
Macaca Fuscata ◽  
Positive Inotropic Effect ◽  
Inotropic Effect ◽  
Ventricular Muscle ◽  
The Right

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.

Changes in mitochondrial energy-producing ability in the right ventricular muscle of monocrotaline-induced pulmonary hypertensive rats

2008 ◽  
Vol 45 (4) ◽  
pp. S21-S22
Author(s):  
Takuya Daicho ◽  
Tatsuya Yagi ◽  
Yohei Abe ◽  
Meiko Ohara ◽  
Yoriko Daisho ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Ventricular Muscle ◽  
Hypertensive Rats ◽  
The Right

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.

Membrane depolarization as a cause of tension development in mammalian ventricular muscle

1959 ◽  
Vol 197 (5) ◽  
pp. 968-970 ◽  
Author(s):  
Frederic Kavaler
Keyword(s):  
Action Potential ◽  
Right Ventricular ◽  
Fiber Bundle ◽  
Small Area ◽  
Short Interval ◽  
Ventricular Muscle ◽  
Tension Development ◽  
External Voltage ◽  
Ventricular Cavity ◽  
The Right

A method was devised which made it possible to depolarize ventricular muscle, over a short interval of length, by applying an external voltage and to record, from the same segment, the developed tension. A fiber bundle, 0.5–1.0 mm in diameter, from the right ventricular cavity of the sheep or calf, was inserted into a close-fitting hole in a plastic block, contained in a Tyrode bath. The fibers were depolarized where they exited from the block. The muscle was held, by suction, at two surface points of very small area, 0.4 mm apart. Measurements with microelectrodes showed that the depolarization was roughly uniform over the length of muscle segment from which tension was recorded. By this means, the action potential (normally lasting about 1/2 sec.) could be prolonged to a duration of 2 seconds. This caused tension to be maintained at near-peak levels; relaxation occurred only when the fibers were allowed to repolarize. Evidence was thus adduced in support of the view that the contractile mechanism is continuously responsive to depolarization.

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