Cilostamide potentiates more the positive inotropic effects of (−)-adrenaline through β2-adrenoceptors than the effects of (−)-noradrenaline through β1-adrenoceptors in human atrial myocardium

@article{Christ2006CilostamidePM,
  title={Cilostamide potentiates more the positive inotropic effects of (−)-adrenaline through $\beta$2-adrenoceptors than the effects of (−)-noradrenaline through $\beta$1-adrenoceptors in human atrial myocardium},
  author={Torsten Christ and Andreas Engel and Ursula Ravens and Alberto Julio Kaumann},
  journal={Naunyn-Schmiedeberg's Archives of Pharmacology},
  year={2006},
  volume={374},
  pages={249-253}
}
Activation of both β1- and β2-adrenoceptors increases the contractility of human atrial myocardium through cyclic AMP-dependent pathways. Cyclic AMP is hydrolised by phosphodiesterases, but little is known about which isoenzymes catalyse inotropically relevant cyclic AMP accumulated upon stimulation of β-adrenoceptor subtypes. We have compared the positive inotropic effects of (−)-noradrenaline and (−)-adrenaline, mediated through β1- and β2-adrenoceptors, respectively, in the absence and… Expand
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(-)-Adrenaline elicits positive inotropic, lusitropic, and biochemical effects through β2-adrenoceptors in human atrial myocardium from nonfailing and failing hearts, consistent with Gs coupling but not with Gi coupling
TLDR
The hastening of relaxation caused by (-)-adrenaline together with the PKA-catalyzed phosphorylation of the three proteins involved in relaxation, indicate coupling of β2-adrenoceptors to Gs protein. Expand
The effects of both noradrenaline and CGP12177, mediated through human β1-adrenoceptors, are reduced by PDE3 in human atrium but PDE4 in CHO cells
TLDR
The role of PDE3 and PDE4 on signals through the H and L sites in human myocardium was sought to unravel and cilostamide, but not rolipram, increased the positive inotropic effects and abolished the time dependent fade of both agonists. Expand
Carvedilol induces greater control of β2- than β1-adrenoceptor-mediated inotropic and lusitropic effects by PDE3, while PDE4 has no effect in human failing myocardium
TLDR
The β2-adrenoceptor-selectivity of carvedilol may provide protection against β1- and β2 -adrenOceptor-mediated ventricular overstimulation in PDE3 inhibitor-treated patients. Expand
Phosphodiesterases PDE3 and PDE4 jointly control the inotropic effects but not chronotropic effects of (−)-CGP12177 despite PDE4-evoked sinoatrial bradycardia in rat atrium
TLDR
These isoenzymes jointly reduce (−)-CGP12177-evoked increases of left atrial contractility through β1LAR and Cyclic AMP appears to maintain sinoatrial rate and PDE4 elicits bradycardia through hydrolysis of cAMP in a compartment distinct from the β1-adrenoceptor-induced cAMP compartment through which cAMP causes tachycardia. Expand
Phosphodiesterases do not limit β1-adrenoceptor-mediated sinoatrial tachycardia: evidence with PDE3 and PDE4 in rabbits and PDE1–5 in rats
TLDR
The mammalian heart expresses at least five phosphodiesterases (PDE1–5) and rabbit sinoatrial cells are an important model for pacemaker research, and whether the positive chronotropic effects of (−)-noradrenaline on spontaneously beating right atria of the rabbit are potentiated by inhibition of PDE3 with cilostamide (300 nM) is investigated. Expand
AkrinorTM, a Cafedrine/ Theodrenaline Mixture (20:1), Increases Force of Contraction of Human Atrial Myocardium But Does Not Constrict Internal Mammary Artery In Vitro
TLDR
AkinorTM increased cardiac contractile force by direct sympathomimetic actions and PDE inhibition, did not constrict A. mammaria interna rings, but shifted the noradrenaline curve rightward from -logEC50 6.18 ±0.08 to 5.23 ± 0.05 M.mam maria rings, compatible with an α-AR antagonistic effect or PDE inhibited. Expand
HUMAN HEART β‐ADRENOCEPTORS: β1‐ADRENOCEPTOR DIVERSIFICATION THROUGH ‘AFFINITY STATES’ AND POLYMORPHISM
TLDR
Investigation of the effect of long‐term maximally tolerated carvedilol administration on left ventricular ejection fraction (LVEF) in patients with non‐ischaemic cardiomyopathy and segregation of patients into Arg389Gly‐β1‐adrenoceptors found that carveilol caused a greater increase in left vent cardiac ejection faction in patients carrying the Arg389 allele. Expand
Atropine augments cardiac contractility by inhibiting cAMP-specific phosphodiesterase type 4
TLDR
It is proposed that inhibition of PDE4 by atropine accounts, at least in part, for the induction of tachycardia and the arrhythmogenic potency of this drug. Expand
The low-affinity site of the beta1-adrenoceptor and its relevance to cardiovascular pharmacology.
TLDR
Non-conventional partial agonists may be beneficial for the treatment of peripheral autonomic neuropathy but probably due to their arrhythmic propensities, may be harmful for the Treatment of chronic heart failure. Expand
Phosphodiesterase‐4 blunts inotropism and arrhythmias but not sinoatrial tachycardia of (−)‐adrenaline mediated through mouse cardiac β1‐adrenoceptors
TLDR
This work investigated the influence of the PDE3 inhibitor cilostamide and PDE4 inhibitor rolipram on the effects of (−)‐adrenaline in three regions of murine heart. Expand
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