Potential role of purinergic signaling in lithium-induced nephrogenic diabetes insipidus

• Published in: American Journal of Physiology - Renal Physiology Vol. 296; no. 5; pp. F1194 - F1201
• Main Authors: Zhang, Yue, Nelson, Raoul D, Carlson, Noel G, Kamerath, Craig D, Kohan, Donald E, Kishore, Bellamkonda K
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.05.2009
• Subjects: Animals; Antagonist drugs; Diabetes Insipidus, Nephrogenic - chemically induced; Diabetes Insipidus, Nephrogenic - metabolism; Diabetes Insipidus, Nephrogenic - physiopathology; Diet; Dinoprostone - urine; Fluorescent Antibody Technique; Gene expression; Gene Expression - physiology; Kidney Medulla - metabolism; Kidney Tubules, Collecting - metabolism; Kidneys; Lithium; Lithium - toxicity; Male; Polyuria - chemically induced; Polyuria - metabolism; Polyuria - physiopathology; Rats; Rats, Sprague-Dawley; Receptors, Purinergic P2 - genetics; Receptors, Purinergic P2 - metabolism; Receptors, Purinergic P2Y1; Receptors, Purinergic P2Y2; Ribonucleic acid; RNA; Rodents; Signal Transduction - drug effects; Signal Transduction - physiology

Lithium (Li)-induced nephrogenic diabetes insipidus (NDI) has been attributed to the increased production of renal prostaglandin (PG)E(2). Previously we reported that extracellular nucleotides (ATP/UTP), acting through P(2y2) receptor in rat medullary collecting duct (mCD), produce and release PGE(2...