Calcium metabolism and detrusor failure in the aging bladder

Abstract

Bladder smooth muscle contraction depends on a transient rise in cytosolic free calcium that may be achieved by extracellular calcium influx through ion channels in the plasma membrane and by release from intracellular calcium storage sites . The neurotransmitter acetylcholine initiates excitation-contraction coupling. It binds to M3 receptors on the cell membrane and activates phospholipase C, an enzyme that induces the formation of inositol-1,4,5-triphosphate(IP3). IP3 is a second messenger that triggers the release of calcium from the intracellular storage sites . The existence of receptor operated intracellular calcium stores in the bladder was demonstrated by Mostwin (1985). They most likely comprise a heterogeneous group of organelles derived from the endoplasmic reticulum and may be referred to as sarcoplasmic reticulum (SR). A key component of the SR is an energy dependent calcium pump, which serves to drive free calcium out of the cytosol back into the storage sites. It was first described by Maclennan (1970)and is called sarcoplasmic endoplasmic reticulum calcium magnesium- adenosinetriphosphatase (SERCA). SERCA is located on the surface of the SR and it pumps 1 free calcium ion into the SR per molecule of adenosine triphosphate consumed.