Calcium: a mediator of the cellular response to chronic Na+/K(+)-ATPase inhibition.

Chronic reduction of Na+/K(+)-ATPase activity has been demonstrated in a number of cell systems to elicit a cellular homeostatic response. Over the course of this response, there is initially a transient stimulation of synthesis of new Na+/K(+)-ATPase molecules, followed by a delayed decrease in its degradation rate, eliciting an effective increase in the number of active pumps in the membrane. The resultant enhancement of pumping capacity promotes the extrusion of accumulated Na+ ions and restores the intracellular electrolyte milieu to preinsult conditions.

Juxtaglomerular cells cultured on a reconstituted basement membrane.

Circulating renin levels are regulated by release from juxtaglomerular (JG) cells. Here, for the first time, we describe the primary culture of rat juxtaglomerular cells on a reconstituted basement membrane. In addition, primary cultures were transformed with a temperature-sensitive SV40 large T antigen gene to promote the development of a continuous JG cell line.

[Ca2+]i regulates transcription rate of the Na+/K(+)-ATPase alpha 1 subunit.

The Na+/K(+)-ATPase enzyme is a pivotal regulator of intracellular electrolyte levels in animal cells. Changes in the rate of its synthesis have been demonstrated to mediate a number of physiological responses. The cellular mechanisms implicated in such regulatory responses though remain poorly defined.

Rates of synthesis and degradation of Na+-K+-ATPase during chronic ouabain treatment.

Chronic inhibition of Na+-K+-ATPase activity in outer medullary kidney tubules has previously been demonstrated to elicit a 60% increase in activity, measured under maximal velocity (Vmax) conditions (J. Biol. Chem.