Prostaglandins are mediators of vascular tone and salt and water homeostasis in the mammalian kidney; their Following chronic salt depletion, COX-2 expression in regulation of glomerular haemodynamics and distal the macula densa and peri-macula densa region nephron function has been well described. Renin pro-increased significantly [3]. This finding suggested that duction and release is also known to be mediated by prostaglandins generated by macula densa COX-2 prostaglandins generated by afferent arteriole and by might be involved in mediating renin release in prostaglandin-dependent signalling from the macula response to volume depletion. densa [1]. In the mammalian kidney, the macula densa is There are two separate gene products with cyclo-involved in regulating renin release by sensing alteraoxygenase activity, cyclooxygenase-1 (COX-1) and tions in luminal chloride via changes in the rate cyclooxygenase-2 (COX-2). The gene for COX-1, the of Na+/K+/2Cl− cotransport. Inhibition of constitutive prostaglandin G2/H2, encodes a Na+/K+/2Cl− cotransport with loop diuretics results 2.7–2.9 kb transcript, while the gene for COX-2, the in a decrease in chloride reabsorption by the macula ‘inducible’prostaglandin G2/H2 synthase, encodes a densa and an increase in renin secretion [3]. It has 4.2–4.5 kb transcript, which increases in response to long been recognized that non steroidal antiinflammatory or mitogenic stimuli. In the kidney, inflammatory drug (NSAID) administration can elicit constitutive prostaglandin G2/H2 synthase (COX-1) a hyporeninaemic state, and studies using an isolated has been localized to mesangial cells, arteriolar endo-perfused juxtaglomerular preparation indicated that thelial cells, parietal epithelial cells of Bowman’s cap-NSAID administration prevented the increases in renin sule and cortical and medullary collecting ducts [2, 3]. release mediated by macula densa sensing of decreases in luminal NaCl [4]. Immunoreactive COX-1 cannot be detected in cortical thick limb or macula densa.