Sarcoplasmic reticulum Ca2+ regulatory protein gene expression in human right atrium under hemodynamic overload.

Sarcoplasmic reticulum (SR) Ca2+-adenosine triphosphatase (ATPase) mRNA expression is reduced in the failing human myocardium. However, it is not known whether SR Ca2+-regulatory protein gene expression is altered in human myocardial tissue subjected to pressure overload or volume overload. We sought to determine whether SR Ca2+-regulatory protein gene expression is altered in human atrial tissue subjected to mechanical overload.

Voltage- and time-dependent block of I(f) by Sr2+ in rabbit sino-atrial node cells.

The hyperpolarization-activated cation current (I(f)) was recorded in single myocytes dissociated from the rabbit sino-atrial node and the Sr(2+)-mediated block of I(f) examined. In the presence of 0.1-10 mM Sr2+, the activation phase of I(f) was followed by a slower decay during hyperpolarization.

Cation-dependent gating of the hyperpolarization-activated cation current in the rabbit sino-atrial node cells.

1. The gating properties of the hyperpolarization-activated cation current (I(f) or Ih) were investigated in single pacemaker cells dissociated from the rabbit sino-atrial node. 2.

External K+ increases Na+ conductance of the hyperpolarization-activated current in rabbit cardiac pacemaker cells.

The hyperpolarization-activated current (I(f)) was recorded from single myocytes dissociated from rabbit sinoatrial node. Although I(f) is usually carried by both Na+ and K+, removal of the minor K+ component from physiological saline suppresses inward component. This inward Na+ current through I(f) channel increases on raising the extracellular K+ concentration.

Control of the hyperpolarization-activated cation current by external anions in rabbit sino-atrial node cells.

1. Effects of varying concentrations of anions on the hyperpolarization-activated current (I(f)) were studied in myocytes isolated from the rabbit sino-atrial node. Substituting Cs+ for the intracellular K+ clearly separated I(f) from the delayed rectifier K+ current.