Pharmacological evidence for the existance of different subtypes of muscarinic acetylcholine receptors for phosphoinositide hydrolysis in neonatal versus adult rat atria

JoséCamusso, Juan; Sterin‐Borda, Leonor; Rodríguez, M.; Bacman, Sandra R.; Borda, Enri

doi:10.1016/0929-7855(95)00003-9

Cited by 15 publications

(4 citation statements)

References 15 publications

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“…Recently in late 1990s, pharmacological data from radioligand binding studies have provided more favourable evidence in support of the view of the functional M 3 subtypes in hearts (Camusso et al , 1995; Dhein et al , 2001). Moreover, combined functional and molecular studies further support the presence of the cardiac M 3 receptors, with data indicating expression of the M 3 transcript and protein in the hearts of various species including mouse, rat, guinea‐pig, cat, canine and man (Yang et al.…”

Section: Historic Remarks In the Identification Of The M3‐machr In Thmentioning

confidence: 96%

Function of cardiac M₃ receptors

Wang

2006

Auton Autocoid Pharmacol

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1. Since the initial identification of the M3 subtype of muscarinic acetylcholine receptors (M3-mAChR) in the heart, there have been increasing interest and advances in studies on the pathophysiological roles of M3-mAChR in the heart. Recent studies from several laboratories have provided compelling and solid evidence in support of the important roles of M3-mAChR in regulation and maintenance of cardiac function and in generation and progression of heart disease as well. 2. The functions of the cardiac M3-mAChR revealed thus far include (i) M3-mAChR regulation of heart rate and cardiac repolarization, (ii) modulation of inotropic effects, (iii) cytoprotection against ischaemic injuries of myocardium, (iv) regulation of cell-to-cell communication, and (v) participation in generation and maintenance of atrial fibrillation. 3. Signal transduction mechanisms underlying these pathophysiological functions have also been studied, which have allowed us to get insight into the following mechanistic aspects. (i) M3-mAChR activates a delayed rectifying K+ current I(KM3) to participate in cardiac repolarization, negative chronotropic actions, and anti-dysrhythmic (suppresses ischaemic dysrhythmias) as well as pro-dysrhythmic (facilitates atrial fibrillation) actions. (ii) M3-mAChR interacts with gap-junctional channel connexin 43 to maintain cell-cell communication and excitation propagation. (iii) M3-mAChR regulates intracellular phosphoinositide hydrolysis to improve cardiac contraction and haemodynamic function. (iv) M3-mAChR activate anti-apoptotic signalling molecules, enhances endogenous antioxidant capacity, and diminishes intracellular Ca2+ overload, all of which contribute to protecting the heart against ischaemic injuries. 4. This article provides an overview of the potential roles of the M3-mAChR in parasympathetic control of heart function under normal physiological conditions and in the setting of a variety of pathological processes including heart failure, myocardial ischaemia and dysrhythmias.

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Section: Historic Remarks In the Identification Of The M3‐machr In Thmentioning

confidence: 96%

Function of cardiac M₃ receptors

Wang

2006

Auton Autocoid Pharmacol

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“…For example, heart atria of rats expresses M 1 and M 2 receptors in newborn, while only M 2 are expressed in adults [102,103]. The production of IP 3 (as consequence of the odd-numbered muscarinic subtypes activation) decreases from fetal period to adulthood in sheep [85].…”

Section: Ontogenetic Changes In Muscarinic Receptor Expression and Sementioning

confidence: 99%

Receptor Subtype Abundance as a Tool for Effective Intracellular Signalling

Mysliveček

Nováková²,

Klein³

2008

CHDDT

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The regulation of heart function is one of the essentials for the survival of organism. Therefore, the effective mechanisms of regulation can minimize the energy requirements and improve the ability to react to different needs on time and appropriately. Two receptor types, beta-adrenoceptors and muscarinic receptors, with almost antagonistic function, are "basic regulators" of the heart parameters. It is relevant to mention that beside the main adrenoceptors and muscarinic receptors subtypes (beta(1)- and M(2)-subtype), other minor subtypes that regulate heart function, i.e. beta-, beta-adrenoceptors, alpha(1)-adrenoceptors and minor subtypes of muscarinic receptors (M(1), M(3) and M(5)) are present in the heart. In this regard is intriguing that just two catecholamines (adrenaline, noradrenaline) have many "targets"--receptors that differ so much in the functional consequences of their activation: while beta(1)- and beta(2)-adrenoceptors cause cardiostimulation, beta(3)-adrenoceptors are responsible for cardioinhibition and alpha(1)-adrenoceptors contribute to enhanced inotropy. Similarly, some data show that other muscarinic receptors than M(2) muscarinic subtype, are expressed in the heart and these minor subtype(s) can contribute to the heart regulation in similar way as beta(3)-adrenoceptors to the catecholamine action. Taken together, regulation of heart function through different receptor subtypes and using homologous and heterologous regulation can represent an effective tool for coping with permanently changing environmental conditions.

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“…Fractions of 1 ml were recovered and radioactivity was determined by scintillation counting. Results are expressed as the absolute values of area under the curve following the criteria of Simpson's equation [15].…”

Section: Inositol Phosphate Measurementmentioning

confidence: 99%

IgA from HIV+ haemophilic patients triggers intracellular signals coupled to the cholinergic system of the intestine

Sales

Sterin‐Borda

Bracco

et al. 1997

Clinical and Experimental Immunology

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SUMMARYIgA was obtained from HIV-infected haemophilic patients and the intracellular signals triggered by its reaction with isolated rat intestinal strips were studied. HIV+IgA stained intestinal microvilli with a granular immunofluorescence pattern and bound to the muscarinic acetylcholine receptor (mAChR), displacing the specific muscarinic cholinergic antagonist QNB in a non-competitive manner. It triggered the signals that are the consequence of mAChR stimulation in the intestine. Thus, it decreased CAMP synthesis and increased guanosine 3':5'-cyclic monophosphate (cGMP) formation and phosphoinositide (PI) turnover of the intestine. In addition, it stimulated prostaglandin E2 (PGE2) synthesis by intestinal strips. Through its effect on PGE2 synthesis, HIVfIgA could have a dual action. On the one hand, it could enhance immunosuppression at a local level, favouring pathogen growth and subsequent intestinal dysfunction. On the other hand, PGE2 could directly increase intestinal motility and electrolyte/fluid loss. Both effects could be involved in intestinal damage in AIDS.

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Pharmacological evidence for the existance of different subtypes of muscarinic acetylcholine receptors for phosphoinositide hydrolysis in neonatal versus adult rat atria

Cited by 15 publications

References 15 publications

Function of cardiac M₃ receptors

Function of cardiac M₃ receptors

Receptor Subtype Abundance as a Tool for Effective Intracellular Signalling

IgA from HIV+ haemophilic patients triggers intracellular signals coupled to the cholinergic system of the intestine

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Pharmacological evidence for the existance of different subtypes of muscarinic acetylcholine receptors for phosphoinositide hydrolysis in neonatal versus adult rat atria

Cited by 15 publications

References 15 publications

Function of cardiac M3 receptors

Function of cardiac M3 receptors

Receptor Subtype Abundance as a Tool for Effective Intracellular Signalling

IgA from HIV+ haemophilic patients triggers intracellular signals coupled to the cholinergic system of the intestine

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Product

Resources

About

Function of cardiac M₃ receptors

Function of cardiac M₃ receptors