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in urine concentration
1Institute of Pharmacology and Toxicology, University of Tübingen, 72074 Tübingen; 2Max-Planck-Institute for Experimental Endocrinology, 30625 Hannover, Germany; and 3Departments of Medicine and Pharmacology, University of California, and Veterans Affairs Medical Center, San Diego, California 92161
Submitted 4 August 2003 ; accepted in final form 18 March 2004
In mouse kidney, the conventional protein kinase C (PKC) isoenzyme 
is expressed in glomeruli, the cortical collecting duct (intercalated cells only), and medullary collecting duct. To get insights on its function, PKC- knockout (–/–) and wild-type (+/+) mice were studied. When provided free access to water, PKC- –/– mice showed 
50% greater urine flow rate and lower urinary osmolality in 24-h metabolic cage experiments despite a greater urinary vasopressin-to-creatinine ratio vs. PKC- +/+ mice. Renal albumin excretion was not different. Clearance experiments under inactin/ketamine anesthesia revealed a modestly reduced glomerular filtration rate and showed a reduced absolute and fractional renal fluid reabsorption in PKC- –/– mice. The sodium-restricting response to a low-sodium diet was unaffected in PKC- –/– mice. Urinary osmolality was reduced to similar hypotonic levels in PKC- –/– and +/+ mice during acute oral water loading or application of the vasopressin V2-receptor antagonist SR-121463. In comparison, the lower urinary osmolality observed in PKC- –/– mice vs. wild-type mice under basal conditions persisted during water restriction for 36 h. In conclusion, PKC- appears not to play a major role in renal sodium reabsorption but, consistent with its expression in the medullary collecting duct, contributes to urinary concentration in mice. Considering that PKC-
I and -II are coexpressed with PKC- in mouse medullary collecting duct, the present results indicate that conventional PKC isoenzymes cannot fully compensate for each other.
mouse; collecting duct; knockout
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