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J. Biol. Chem., Vol. 275, Issue 34, 25892-25899, August 25, 2000

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Activation of the Particulate and Not the Soluble Guanylate Cyclase Leads to the Inhibition of Ca²⁺ Extrusion through Localized Elevation of cGMP^*

Olga Zolle, Alison M. Lawrie, and Alec W. M. Simpson^§

From the Department of Human Anatomy and Cell Biology, University of Liverpool, New Medical School, Ashton St., Liverpool L69 3GE, United Kingdom and  Biomedical Sciences, IMS, University of Aberdeen, Foresterhill, Aberdeen AB25 2DZ, United Kingdom

We examined whether localized increases in cytosolic cGMP have distinct regulatory effects on the concentration of cytosolic free Ca²⁺ in ECV304 cells. Stimulation of the particulate guanylate cyclase by brain-type natriuretic peptide in fura-2-loaded cells caused a profound potentiation of the ATP-stimulated and thapsigargin-stimulated rise in cytosolic free Ca²⁺. This effect is mediated by the inhibition of Ca²⁺ extrusion via the plasma membrane Ca²⁺-ATPase pump. Furthermore, the addition of brain-type natriuretic peptide caused the partial inhibition of cation influx in ATP-stimulated cells. In contrast, elevation of cytosolic cGMP by activation of the soluble guanylate cyclase induced by the addition of sodium nitroprusside causes an increased reuptake of Ca²⁺ into the intracellular stores without affecting cation influx or Ca²⁺ efflux. Thus, localized pools of cGMP play distinct regulatory roles in the regulation of Ca²⁺ homeostasis within individual cells. We define a new role for natriuretic peptides in the inhibition of Ca²⁺ efflux that leads to the potentiation of agonist-evoked increases in cytosolic free Ca²⁺.

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