Developmental increase in the inotropic and cyclic AMP response to isoproterenol in embryonic and newly hatched chicks

1989 ◽  
Vol 67 (9) ◽  
pp. 1109-1111 ◽  
Author(s):  
Ken Nakazawa ◽  
Yutaka Kusuya ◽  
Koki Shigenobu
Keyword(s):  
Cyclic Amp ◽  
Positive Inotropic Effect ◽  
Developmental Stages ◽  
Sympathetic Innervation ◽  
Contractile Force ◽  
Inotropic Effect ◽  
Chick Embryos

The cyclic adenosine 3′,5′-monophosphate (cyclic AMP) levels of ventricles isolated from 15- to 20-day-old chick embryos and 0- to 3-day-old hatched chicks were compared to clarify the mechanism underlying the change in sensitivity to isoproterenol during perinatal developmental stages when the functional sympathetic innervation has been completely achieved. Isoproterenol produced a positive inotropic effect on ventricles isolated from both embryonic and hatched chicks, but the ventricles from the hatched chicks were more sensitive. At both developmental stages sotalol was an equipotent antagonist of isoproterenol. 3-Isobutyl-1-methylxanthine (IBMX) produced an increment in the contractile force of the ventricles at both stages, but the ventricles from the hatched chicks responded to lower doses of IBMX. The reactivity to isoproterenol in increasing cyclic AMP level was significantly higher in the hatched ventricles than in the embryonic ventricles. The results suggest that the different sensitivities to isoproterenol between embryonic and newly hatched chick ventricles may be due to some changes in the process for cyclic AMP production.Key words: chick ventricle, development, β-adrenergic sensitivity, cyclic AMP.

Cyclic AMP and the positive inotropic effect of norepinephrine and phenylephrine

1977 ◽  
Vol 55 (2) ◽  
pp. 279-287 ◽  
Author(s):  
T. T. Martinez ◽  
J. H. McNeill
Keyword(s):  
Cyclic Amp ◽  
Cell Membrane ◽  
Time Course ◽  
Positive Inotropic Effect ◽  
Contractile Response ◽  
Contractile Force ◽  
Time Response ◽  
Inotropic Effect ◽  
Chronotropic Response ◽  
Right Atria

Time-response studies of the effects of norepinephrine and phenylephrine revealed that both agonists caused an increase in cyclic AMP levels before increases in contractile force in either the electrically stimulated left atria or spontaneously beating right atria of the rat. Norepinephrine caused a nearly sixfold increase in cyclic AMP, whereas phenylephrine produced only a 50% increase in the nucleotide. Pretreatment with reserpine did not affect the norepinephrine cyclic AMP response; however, the phenylephrine cyclic AMP response was abolished. Reserpine pretreatment did not significantly affect the contractile responses of either amine. In the presence of propranolol, norepinephrine was found to have the ability to produce an increase in contractile force in which cyclic AMP was apparently not involved. The time course of the contractile response induced by adrenergic amines was found to be remarkably influenced by the chronotropic response in spontaneously beating preparations while the cyclic AMP response was not greatly affected. This difference in the contractile response may be due to the ability of the chronotropic response to influence the flux of calcium through the cell membrane.

The effect of calcium on cardiac phosphorylase activation, contractile force and cyclic AMP in euthyroid and hyperthyroid rat hearts

1976 ◽  
Vol 54 (4) ◽  
pp. 590-595 ◽  
Author(s):  
Elizabeth J. Hartley ◽  
John H. McNeill
Keyword(s):  
Enzyme Activity ◽  
Thyroid Hormone ◽  
Cyclic Amp ◽  
Positive Inotropic Effect ◽  
Contractile Force ◽  
Inotropic Effect ◽  
Chronotropic Effect ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Isolated Perfused Rat Hearts

Calcium chloride injected into isolated perfused rat hearts produced a positive inotropic effect and increased the levels of phosphorylase a (EC 2.4.1.1). The increase in enzyme activity lagged behind the inotropic effect. Pretreatment of animals with thyroid hormone enhanced the ability of noradrenaline to activate phosphorylase but did not affect the inotropic or phosphorylase activating effect of calcium. Thyroid hormone pretreatment did enhance the chronotropic effect of calcium. Calcium did not affect the cardiac levels of cyclic AMP. It is concluded that calcium can activate phosphorylase by a mechanism other than cyclic AMP and that the enhancement of adrenergic amine-induced phosphorylase activation by thyroid hormone is not a calcium mediated event.

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.

scholarly journals Adenosine inhibits the positive inotropic effect of 3-isobutyl-1-methylxanthine in papillary muscles without effect on cyclic AMP or cyclic GMP

1988 ◽  
Vol 93 (4) ◽  
pp. 729-738 ◽  
Author(s):  
Michael Böhm ◽  
Reinhard Brückner ◽  
Joachim Neumann ◽  
Monika Nose ◽  
Wilhelm Schmitz ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Positive Inotropic Effect ◽  
Inotropic Effect ◽  
Papillary Muscles

Hypothermia modifies anesthetic effect on contractile force and Ca2+ transients in cardiac Purkinje fibers

1994 ◽  
Vol 267 (2) ◽  
pp. H725-H733 ◽  
Author(s):  
J. Sprung ◽  
D. F. Stowe ◽  
J. P. Kampine ◽  
Z. J. Bosnjak
Keyword(s):  
Positive Inotropic Effect ◽  
Mild Hypothermia ◽  
Cardiac Contractility ◽  
Volatile Anesthetics ◽  
Contractile Force ◽  
Isometric Tension ◽  
Inotropic Effect ◽  
Purkinje Fibers ◽  
Peak Tension ◽  
Cardiac Purkinje Fibers

Mild hypothermia enhances cardiac contractility, and volatile anesthetics depress contractility. Contractile force (tension) and Ca2+ transients were measured in canine Purkinje fibers at 35 and 25 degrees C with and without halothane and isoflurane to examine how anesthetics attenuate the positive inotropic effect of mild hypothermia. Isometric tension and light emitted from the photoprotein aequorin were used to assess contractility and intracellular Ca2+ transients in fibers stimulated at 40–60 pulses/min. At 35 degrees C, each anesthetic depressed peak tension and peak Ca2+ transients and decreased contractile force duration but, for halothane, increased Ca2+ transient duration. Decreases in tension by both anesthetics at 35 degrees C were converted to marked increases in tension at 25 degrees C, whereas Ca2+ transients were little changed. Removal of anesthetics at 25 degrees C greatly increased tension with a small increase in Ca2+ transients that was much lower than that at 35 degrees C. The curve relating peak contractile force as a function of Ca2+ transients at 25 degrees C during stepwise increases in extracellular CaCl2 was shifted steeper and leftward of the curve at 35 degrees C. These studies suggest that the positive inotropic effect of mild hypothermia is due primarily to increased myofibrillar Ca2+ sensitivity and that anesthetics decrease tension during hypothermia by decreasing myofibrillar Ca2+ sensitivity. Reduced influx of transsarcolemmal or sarcoplasmic reticular Ca2+ may also play a role during mild hypothermia.

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