| First Author | Yao L | Year | 2004 |
| Journal | Am J Physiol Renal Physiol | Volume | 287 |
| Issue | 2 | Pages | F299-304 |
| PubMed ID | 15039142 | Mgi Jnum | J:95426 |
| Mgi Id | MGI:3525975 | Doi | 10.1152/ajprenal.00274.2003 |
| Citation | Yao L, et al. (2004) Evidence for a role of protein kinase C-alpha in urine concentration. Am J Physiol Renal Physiol 287(2):F299-304 |
| abstractText | In mouse kidney, the conventional protein kinase C (PKC) isoenzyme alpha is expressed in glomeruli, the cortical collecting duct (intercalated cells only), and medullary collecting duct. To get insights on its function, PKC-alpha knockout (-/-) and wild-type (+/+) mice were studied. When provided free access to water, PKC-alpha -/- mice showed approximately 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-alpha +/+ 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-alpha -/- mice. The sodium-restricting response to a low-sodium diet was unaffected in PKC-alpha -/- mice. Urinary osmolality was reduced to similar hypotonic levels in PKC-alpha -/- and +/+ mice during acute oral water loading or application of the vasopressin V(2)-receptor antagonist SR-121463. In comparison, the lower urinary osmolality observed in PKC-alpha -/- mice vs. wild-type mice under basal conditions persisted during water restriction for 36 h. In conclusion, PKC-alpha 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-beta I and -beta II are coexpressed with PKC-alpha in mouse medullary collecting duct, the present results indicate that conventional PKC isoenzymes cannot fully compensate for each other. |
