The effect of shear stress on the basolateral membrane potential of proximal convoluted tubule of the rat kidney
- PMID: 17219192
- DOI: 10.1007/s00424-006-0198-7
The effect of shear stress on the basolateral membrane potential of proximal convoluted tubule of the rat kidney
Abstract
As consequence of glomerular filtration the viscosity of blood flowing through the efferent arteriole increases. Recently, we found that shear stress modulates proximal bicarbonate reabsorption and nitric oxide (NO.) was the chemical mediator of this effect. In the present work, we found that agonists of NO. production affected basolateral membrane potential (V (blm)) of the proximal convoluted tubule (PCT) epithelium. Using paired micropuncture experiments, we perfused peritubular capillaries with solutions with different viscosity while registering the V (blm). Our results showed that a 50% increment in the viscosity, or the addition of bradykinin (10(-5) M) to the peritubular perfusion solution, induced a significant and similar hyperpolarization of the V (blm) at the PCT epithelium of 6 +/- 0.7 mV (p < 0.05). Both hyperpolarizations were reverted by L-NAME (10(-4) M). Addition of 2,2'-(hydroxynitrosohydrazino) bis-ethanamine (NOC-18) 3 x 10(-4) M to the peritubular perfusion solution induced a hyperpolarization of the same magnitude of that high viscosity or bradykinin. These results strongly suggest the involvement of NO. in the effect of high viscosity solutions. This effect seems to be mediated by activation of K+(ATP) channels as glybenclamide (5 x 10(-5) M) added to peritubular solutions induced a larger depolarization of the V (blm) with high viscosity solutions. Acetazolamide (5 x 10(-5) M) added to high viscosity solutions induced a larger hyperpolarization (8 +/- 1 mV; p < 0.05), suggesting that depolarizing current due to HCO(-)3 exit across the basolateral membrane damps the hyperpolarizing effect of high viscosity. Considering that Na(+) and consequently water reabsorption is highly dependent on electrical gradient, the present data suggest that the endothelium of kidney vascular bed interacts in paracrine fashion with the epithelia, affecting V (blm) and thus modulating PCT reabsorption.
Similar articles
-
Control of proximal tubule acidification by the endothelium of the peritubular capillaries.Am J Physiol. 1997 Feb;272(2 Pt 2):R691-4. doi: 10.1152/ajpregu.1997.272.2.R691. Am J Physiol. 1997. PMID: 9124496
-
Peritubular fluid viscosity modulates H+ flux in proximal tubules through NO release.Am J Physiol Renal Physiol. 2001 Feb;280(2):F239-43. doi: 10.1152/ajprenal.2001.280.2.F239. Am J Physiol Renal Physiol. 2001. PMID: 11208599
-
Regulation of an inwardly rectifying K+ channel by nitric oxide in cultured human proximal tubule cells.Am J Physiol Renal Physiol. 2004 Sep;287(3):F411-7. doi: 10.1152/ajprenal.00014.2004. Epub 2004 May 12. Am J Physiol Renal Physiol. 2004. PMID: 15140759
-
Electrophysiology of basolateral bicarbonate transport in the rabbit proximal tubule.Am J Physiol. 1986 Feb;250(2 Pt 2):F267-72. doi: 10.1152/ajprenal.1986.250.2.F267. Am J Physiol. 1986. PMID: 3946604
-
Shear-stress-responsive signal transduction mechanisms in renal proximal tubule cells.Curr Opin Nephrol Hypertens. 2003 Jan;12(1):31-4. doi: 10.1097/00041552-200301000-00006. Curr Opin Nephrol Hypertens. 2003. PMID: 12496663 Review.
Cited by
-
Real-time monitoring of angiotensin II-induced contractile response and cytoskeleton remodeling in individual cells by atomic force microscopy.Pflugers Arch. 2009 Apr;457(6):1361-72. doi: 10.1007/s00424-008-0596-0. Epub 2008 Oct 25. Pflugers Arch. 2009. PMID: 18953565
-
Surface Plasmon Resonance Monitoring of Cell Monolayer Integrity: Implication of Signaling Pathways Involved in Actin-Driven Morphological Remodeling.Cell Mol Bioeng. 2008 Dec 1;1(4):229-239. doi: 10.1007/s12195-008-0028-4. Cell Mol Bioeng. 2008. PMID: 21052479 Free PMC article.
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials
Miscellaneous