Biomedical subjects

Shinichi Uchida

Publications and source records attributed to Shinichi Uchida.

39 records · Page 3Linked to original sources

PubMed2002

Analysis of NaCl transport in thin ascending limb of Henle's loop in CLC-K1 null mice.

To characterize the nature of NaCl transport in the thin ascending limb (tAL), we examined the transport properties of Na(+) and Cl(-) using in vitro microperfusion of the tAL in CLC-K1 null mice. In the presence of a transmural NaCl concentration gradient (100 mM higher in the lumen), the transepithelial diffusion voltage (V(d)) was 15.5 +/- 1.0 and -7.6 +/- 1.4 mV in CLC-K1(+/+) and CLC-K1(-/-) mice, respectively. Neither Cl(-) transport inhibitor 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) nor acidification of the bathing fluid changed the V(d) values in CLC-K1(-/-) mice. The addition of 300 microg/ml protamine, a selective blocker of paracellular conductance, to the bath increased the V(d) values by 5.6 +/- 0.7 and 12.6 +/- 1.5 mV (P < 0.001) in CLC-K1(+/+) and CLC-K1(-/-) mice, respectively. Although efflux coefficients of (36)Cl were significantly decreased in CLC-K1(-/-) mice (188.3 +/- 25.6 in 4 tubules vs. 17.2 +/- 7.0 x 10(-5) cm/s in 6 tubules), those of (22)Na were not different between CLC-K1(+/+) and CLC-K1(-/-) mice. These results clearly indicate that the major component of Cl(-) transport sensitive to NPPB or pH is mediated by CLC-K1 in the tAL.

Angiogenesis Inhibitors↗

PubMed2002

Water intake and 24-hour blood pressure monitoring in a patient with nephrogenic diabetes insipidus caused by a novel mutation of the vasopressin V2R gene.

A 47-year-old man presented with polydipsia, which had had since childhood, and recent onset of hypertension. Genetic analysis proved that he had nephrogenic diabetes insipidus caused by a novel mutation (deletion of 6 amino acids between G107 and C112) in the vasopressin V2 receptor gene. Results of 24-hour blood pressure monitoring disclosed a greater dipping pattern and greater blood pressure variability during waking hours than in male patients with only essential hypertension. This characteristic blood pressure profile may result from daily occurrence of free water depletion, as further observation indicated that water deprivation was associated with a reduction in blood pressure.

Arginine Vasopressin↗

PubMed2001

Intrarenal and cellular localization of CLC-K2 protein in the mouse kidney.

CLC-K2, a kidney-specific member of the CLC chloride channel family, is thought to play an important role in the transepithelial Cl(-) transport in the kidney. This consensus was first reached shortly after it was demonstrated that the mutations of the human CLCNKB gene resulted in Bartter's syndrome type III. To clarify the pathogenesis, the exact intrarenal and cellular localization of CLC-K2 by immunohistochemistry of the Clcnk1-/- mouse kidney were investigated by use of an anti-CLC-K antibody that recognized both CLC-K1 and CLC-K2. CLC-K2 is expressed in the thick ascending limb of Henle's loop and distal tubules, where it is localized to the basolateral membranes. The localization of CLC-K2 to these nephron segments strongly implies that CLC-K2 confers the basolateral chloride conductance in the thick ascending limb of Henle's loop and distal tubules, where Cl(-) is taken up by the bumetanide-sensitive Na-K-2Cl cotransporter or the thiazide-sensitive Na-Cl cotransporter at the apical membranes. CLC-K2 expression was also shown to extend into the connecting tubule in the basolateral membrane. CLC-K2 was found in basolateral membranes of the type A intercalated cells residing along the collecting duct. This localization strongly suggests that CLC-K2 confers the basolateral conductance in the type A intercalated cells where Cl(-) is taken up by the anion exchanger in exchange for HCO(3)(-) at the basolateral membranes. These aspects of CLC-K2 localization suggest that CLC-K2 is important in Cl(-) transport in the distal nephron segments.

Animals↗