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10.1016/j.kint.2016.03.020 http://scihub22266oqcxt.onion/10.1016/j.kint.2016.03.020 27206969!4996630!27206969     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Kidney+Int 2016 ; 90 (3): 555-67 Nephropedia Template TP {{tp|p=27206969|t=2016. beta3 adrenergic receptor in the kidney may be a new player in sympathetic regulation of renal function |pdf=|usr=}}{{27206969}} gab.com Text beta3 adrenergic receptor in the kidney may be a new player in sympathetic regulation of renal function JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=27206969 #FOAvip To date, the study of the sympathetic regulation of renal function has been restricted to the important contribution of beta1- and beta2-adrenergic receptors (ARs). Here we investigate the expression and the possible physiologic role of beta3-adrenergic receptor (beta3-AR) in mouse kidney. The beta3-AR is expressed in most of the nephron segments that also express the type 2 vasopressin receptor (AVPR2), including the thick ascending limb and the cortical and outer medullary collecting duct. Ex vivo experiments in mouse kidney tubules showed that beta3-AR stimulation with the selective agonist BRL37344 increased intracellular cAMP levels and promoted 2 key processes in the urine concentrating mechanism. These are accumulation of the water channel aquaporin 2 at the apical plasma membrane in the collecting duct and activation of the Na-K-2Cl symporter in the thick ascending limb. Both effects were prevented by the beta3-AR antagonist L748,337 or by the protein kinase A inhibitor H89. Interestingly, genetic inactivation of beta3-AR in mice was associated with significantly increased urine excretion of water, sodium, potassium, and chloride. Stimulation of beta3-AR significantly reduced urine excretion of water and the same electrolytes. Moreover, BRL37344 promoted a potent antidiuretic effect in AVPR2-null mice. Thus, our findings are of potential physiologic importance as they uncover the antidiuretic effect of beta3-AR stimulation in the kidney. Hence, beta3-AR agonism might be useful to bypass AVPR2-inactivating mutations. Twit Text FOAVip beta3 adrenergic receptor in the kidney may be a new player in sympathetic regulation of renal function ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=27206969 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27206969 #FOAvip English Wikipedia <ref>{{Cite pmid|27206969}}</ref> beta3 adrenergic receptor in the kidney may be a new player in sympathetic regulation of renal function #MMPMID27206969 Procino G; Carmosino M; Milano S; Dal Monte M; Schena G; Mastrodonato M; Gerbino A; Bagnoli P; Svelto M Kidney Int 2016[Sep]; 90 (3): 555-67 PMID27206969show ga To date, the study of the sympathetic regulation of renal function has been restricted to the important contribution of beta1- and beta2-adrenergic receptors (ARs). Here we investigate the expression and the possible physiologic role of beta3-adrenergic receptor (beta3-AR) in mouse kidney. The beta3-AR is expressed in most of the nephron segments that also express the type 2 vasopressin receptor (AVPR2), including the thick ascending limb and the cortical and outer medullary collecting duct. Ex vivo experiments in mouse kidney tubules showed that beta3-AR stimulation with the selective agonist BRL37344 increased intracellular cAMP levels and promoted 2 key processes in the urine concentrating mechanism. These are accumulation of the water channel aquaporin 2 at the apical plasma membrane in the collecting duct and activation of the Na-K-2Cl symporter in the thick ascending limb. Both effects were prevented by the beta3-AR antagonist L748,337 or by the protein kinase A inhibitor H89. Interestingly, genetic inactivation of beta3-AR in mice was associated with significantly increased urine excretion of water, sodium, potassium, and chloride. Stimulation of beta3-AR significantly reduced urine excretion of water and the same electrolytes. Moreover, BRL37344 promoted a potent antidiuretic effect in AVPR2-null mice. Thus, our findings are of potential physiologic importance as they uncover the antidiuretic effect of beta3-AR stimulation in the kidney. Hence, beta3-AR agonism might be useful to bypass AVPR2-inactivating mutations. |Adrenergic beta-3 Receptor Agonists/pharmacology[MESH] |Adrenergic beta-3 Receptor Antagonists/pharmacology[MESH] |Aminophenols/pharmacology[MESH] |Animals[MESH] |Aquaporin 2/metabolism[MESH] |Cyclic AMP/metabolism[MESH] |Electrolytes/urine[MESH] |Ethanolamines/pharmacology[MESH] |Fluorescent Antibody Technique[MESH] |Glomerular Filtration Rate/physiology[MESH] |Isoquinolines/pharmacology[MESH] |Kidney Tubules/metabolism/*physiology[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Receptors, Adrenergic, beta-3/genetics/*physiology[MESH] |Receptors, Vasopressin/genetics/metabolism[MESH] |Renal Elimination/*physiology[MESH] |Solute Carrier Family 12, Member 1/metabolism[MESH] |Sulfonamides/pharmacology[MESH]beta3 adrenergic receptor in the kidney may be a new player in sympath(epmc).pdf DeepDyve Pubget Overpricing