β₃-Adrenergic regulation of L-type Ca²⁺ current and force of contraction in human ventricle.

β3-Adrenergic receptor (β3-AR) is expressed in human atrial and ventricular tissues. Recently, we have demonstrated that it was involved in the activation of L-type Ca(2+) current (I(Ca,L)) in human atrial myocytes and the force of contraction of human atrial trabeculae. In the present study, we examined the effect of β3-AR agonist CGP12177 which also is a β1-AR/β2-AR antagonist on I(Ca,L) in human ventricular myocytes (HVMs) and the force of contraction of human ventricular trabeculae.

Characterization of Mg²⁺-regulated TRPM7-like current in human atrial myocytes.

Background: TRPM7 (Transient Receptor Potential of the Melastatin subfamily) proteins are highly expressed in the heart, however, electrophysiological studies, demonstrating and characterizing these channels in human cardiomyocytes, are missing.

Methods: We have used the patch clamp technique to characterize the biophysical properties of TRPM7 channel in human myocytes isolated from right atria small chunks obtained from 116 patients in sinus rhythm during coronary artery and valvular surgery. Under whole-cell voltage-clamp, with Ca²⁺ and K⁺ channels blocked, currents were generated by symmetrical voltage ramp commands to potentials between -120 and +80 mV, from a holding potential of -80 mV.

Effect of inhibitors of mitochondrial respiratory chain complexes on the electromechanical activity in human myocardium.

Unlabelled: THE AIM OF THE STUDY was to investigate the effect of inhibitors of mitochondrial respiratory chain complexes I, III, and IV on the electromechanical activity in human myocardium.

Material And Methods: The experiments were performed on the human myocardial strips obtained from patients with heart failure (NYHA class III or IV) using a conventional method of registration of myocardial electromechanical activity. Under the perfusion with physiological Tyrode solution (control), contraction force (P) was 0.

[I(KACh) inhibitor 2-[(4-methylphenyl)sulfonylcarbamido]-1-(4-nitrobenzyl)pyridinium bromide (2-AP27) is a muscarinic M(2) receptor antagonist].

Aminopyridines are known to inhibit acetylcholine-activated K(+) current (I(KACh)) in cardiac myocytes. The aim of this study was to examine the effect of 2-aminopyridine sulfonylcarbamide derivative 2-AP27 on isoprenaline-stimulated L-type Ca(2+) current (I(CaL)) and to identify whether 2-AP27 acts via blocking of muscarinic M(2)-receptors in frog cardiomyocytes. The whole-cell configuration of the patch-clamp technique was used to record I(CaL) in enzymatically isolated cardiac myocytes.

beta3-adrenergic receptor activation increases human atrial tissue contractility and stimulates the L-type Ca2+ current.

beta3-adrenergic receptor (beta3-AR) activation produces a negative inotropic effect in human ventricles. Here we explored the role of beta3-AR in the human atrium. Unexpectedly, beta3-AR activation increased human atrial tissue contractility and stimulated the L-type Ca2+ channel current (I Ca,L) in isolated human atrial myocytes (HAMs).