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T Isozaki

Publications and source records attributed to T Isozaki.

33 records · Page 2Linked to original sources
PubMed1995

Natriuretic response to acute sodium chloride or sodium bicarbonate infusions in humans.

We compared the natriuretic responses to acute sodium chloride or sodium bicarbonate loading. 2.25 mEq/kg of sodium as sodium chloride, or sodium bicarbonate was infused intravenously in 1 h. Sodium chloride infusion resulted in a gradual increase in urinary sodium excretion (UNaV) for 4 h after starting the infusion, while sodium bicarbonate infusion caused a transient increase in UNaV for the first 2 h followed by a decrease. The amount of sodium excreted over 4 h in the sodium chloride and sodium bicarbonate groups were 20.7 +/- 4.7 and 34.8 +/- 2.3% of the sodium loaded, respectively (p < 0.05). This difference could not be ascribed to divergent responses in glomerular filtration rate, aldosterone, atrial natriuretic peptide, or serum albumin concentration. The difference in UNaV might be caused by the differences in renal tubular handling of chloride and bicarbonate.

Adult↗
PubMed1994

Protein restriction sequentially induces new urea transport processes in rat initial IMCD.

We reported that feeding rats 8% protein for 4 wk induces two new urea transport processes in initial inner medullary collecting ducts (IMCD); neither is present in rats fed 18% protein. In this study, we measured the time course of induction of these transporters in perfused initial IMCD segments from rats fed 8% protein. Net urea flux was induced after 3 wk, whereas vasopressin-stimulated passive urea permeability (P(urea)) was induced after 2 wk. 8-Bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) significantly increased P(urea)); adding vasopressin did not increase P(urea) further. In fact, there was no difference in vasopressin-stimulated cAMP production in initial or terminal IMCD segments from rats fed 18% or 8% protein, suggesting that the adaptive response was not due to increased cAMP production. Glucagon did not change cAMP production or P(urea). Specificity of the response was suggested because neither aldose reductase nor sorbitol dehydrogenase activity changed with feeding 8% protein. Thus 1) in initial IMCD segments, vasopressin-stimulated P(urea) is induced after 2 wk, but net urea flux requires 3 wk of feeding 8% protein; 2) this adaptation is not solely due to a higher rate of cAMP production; and 3) specificity of the adaptive response is suggested because activities of enzymes responding to decreases in concentrating ability are unchanged. These results suggest that two distinct urea transporters may be involved in the adaptation to a low-protein diet.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1994

Sodium-dependent net urea transport in rat initial inner medullary collecting ducts.

We reported that feeding rats 8% protein for 3 wk induces net urea transport and morphologic changes in initial inner medullary collecting ducts (IMCDs) which are not present in rats fed 18% protein. In this study, we measured net urea transport in microperfused initial IMCDs from rats fed 8% protein for > or = 3 wk and tested the effect of inhibiting Na+/K(+)-ATPase activity and found that adding 1 mM ouabain to the bath reversibly inhibited net urea transport from 14 +/- 3 to 6 +/- 2 pmol/mm per min (P < 0.01), and that replacing potassium (with sodium) in the bath reversibly inhibited net urea transport from 18 +/- 3 to 5 +/- 0 pmol/mm per min (P < 0.01). Replacing perfusate sodium with N-methyl-D-glucamine reversibly inhibited net urea transport from 12 +/- 2 to 0 +/- 1 pmol/mm per min (P < 0.01), whereas replacing bath sodium had no significant effect on net urea transport. Adding 10 nM vasopressin to the bath exerted no significant effect on net urea transport. Finally, we measured Na+/K(+)-ATPase activity in initial and terminal IMCDs from rats fed 18% or 8% protein and found no significant difference in either subsegment. Thus, net urea transport in initial IMCDs from rats fed 8% protein for > or = 3 wk requires sodium in the lumen, is reduced by inhibiting Na+/K(+)-ATPase, and is unchanged by vasopressin or phloretin. These results suggest that net urea transport may occur via a novel, secondary active, sodium-urea cotransporter.

Animals↗
PubMed1993

Low protein diet alters urea transport and cell structure in rat initial inner medullary collecting duct.

Low protein diets reverse the urea concentration gradient in the renal inner medulla. To investigate the mechanism(s) for this change, we studied urea transport and cell ultrastructure in initial and terminal inner medullary collecting ducts (IMCD) from rats fed 18% protein or an isocaloric, 8% protein diet for 4 wk. Serum urea, aldosterone, and albumin were significantly lower in rats fed 8% protein, but total protein and potassium were unchanged. Vasopressin stimulated passive urea permeability (Purea) threefold (P < 0.05) in initial IMCDs from rats fed 8% protein, but not from rats fed 18% protein. Luminal phloretin reversibly inhibited vasopressin-stimulated Purea. However, in terminal IMCDs from rats fed either diet, vasopressin stimulated Purea. Net transepithelial urea flux (measured with identical perfusate and bath solutions) was found only in initial IMCDs from rats fed 8% protein. Reducing the temperature reversibly inhibited it, but phloretin did not. Electron microscopy of initial IMCD principal cells from rats fed 8% protein showed expanded Golgi bodies and prominent autophagic vacuoles, and morphometric analysis demonstrated a marked increase in the surface density and boundary length of the basolateral plasma membrane. These ultrastructural changes were not observed in the terminal IMCD. Thus, 8% dietary protein causes two new urea transport processes to appear in initial but not terminal IMCDs. This is the first demonstration that "active" urea transport can be induced in a mammalian collecting duct segment.

Animals↗
PubMed1992

Bucillamine (a new therapeutic agent for rheumatoid arthritis) induced nephrotic syndrome: a report of two cases and review of the literature.

Two cases of nephrotic syndrome during bucillamine treatment were encountered in 1989 in our hospital; both patients had suffered from rheumatoid arthritis for 2 years. They had received 200 mg bucillamine orally per day for 3-4 months before the onset of the nephrotic syndrome. Discontinuation of bucillamine led to complete remission of the nephrotic syndrome within 1 year. Bucillamine is a new therapeutic agent for rheumatoid arthritis developed in 1982 in Japan. Since 1985, 14 cases of nephrotic syndrome, including the two cases reported here have been reported. We review these cases and discuss the pathogenesis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Selectivity of ion permeability across ascending thin limb of Henle's loop: interaction of Cl- and other halogens with anion transport system.

In hamster ascending thin limb of Henle's loop (ATL) perfused in vitro, we examined halogen selective permeability and effects on Cl- transport. Relative permeabilities for halogens to sodium (PX/PNa) were determined by single salt dilution voltage. (PF/PNA, PCl/PNa, PBr/PNa and PI/PNa were 0.47 +/- 0.09, 3.23 +/- 0.22, 3.23 +/- 0.26, and 0.47 +/- 0.09, respectively. Simultaneous determination of 36Cl and 125I fluxes confirmed that addition of 10(-4) M 5-nitro-2-(3-phenyl-propylamino)-benzoate (NPPB), a Cl- channel blocker, to the bath decreased the flux coefficient for 36Cl (10(-7) cm2/s) from 67.0 +/- 11.7 to 29.5 +/- 7.9 without affecting that for 125I. NPPB also reduced both PCl/PNa and PBr/PNa from 2.67 +/- 0.20 to 0.95 +/- 0.12 and from 2.33 +/- 0.24 to 1.32 +/- 0.12, respectively. Addition of 100 mM Cl- or I- decreased 36Cl flux coefficient from 124.8 +/- 14.3 to 87.7 +/- 13.0 or to 41.0 +/- 11.6 without affecting that for 125I. All other halogens and SCN- also exhibited inhibitory effects on 36Cl flux. These findings support the hypothesis that the putative Cl- channel in the ATL is highly permeable to both Cl- and Br- but less permeable to I-, F-, and SCN-. They suggest that there are at least two functionally distinct components in the process of Cl- transport across the ATL, the binding site and the selective barrier. All halogens may compete against Cl- at the binding site.

Animals↗
PubMed1989

Effects of Cl- transport inhibitors on Cl- permeability across hamster ascending thin limb.

The highly conductive Cl- transport pathway exists in the ascending thin limb (ATL) of Henle's loop. To characterize the mechanism of the Cl- conductance across the ATL, we examined effects on Cl- permeability across hamster ATL of Cl- transport inhibitors, including 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), diphenylamine carboxylate (DPC), and anthracene-9-carboxylic acid (9-AC), by the in vitro microperfusion technique. NPPB added to the bath caused reversible suppression of the relative permeability of Cl- to Na+ (PCl/PNa), as estimated from the NaCl diffusion voltage in a dose-dependent manner in a range from 3 x 10(-6) to 10(-3) M. The concentration of NPPB that inhibited PCl/PNa by 50% (ID50) was approximately 3 X 10(-5) M. When 3 X 10(-5) M NPPB was added to the bath, the lumen-to-bath flux coefficient for 36Cl (Kl----b,Cl- 10(-7) cm2/s) was decreased from 130.7 +/- 7.3 to 52.2 +/- 11.6 (n = 7, P less than 0.01). Application of NPPB in the lumen also caused reversible suppression of PCl/PNa, but this effect was less potent compared with the application of the drug via the bath. Whereas 10(-3) M 9-AC or 10(-3) M DPC decreased PCl/PNa by 6.5 +/- 1.2 and 10.2 +/- 2.6%, respectively, 3 X 10(-4) M NPPB decreased PCl/PNa by 69.7 +/- 3.8%. In maleimide-treated tubules, addition of 10(-3) M N-ethylmaleimide (NEM) increased PCl/PNa from 1.0 +/- 0.1 to 1.8 +/- 0.1 (n = 7, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Urine beta-core fragment, a potential screening test for ectopic pregnancy and spontaneous abortion.

The incidence of ectopic pregnancy in the United States has risen 6-fold in the last three decades. It now accounts for about 2% of reported pregnancies. Tests are now needed to identify ectopic pregnancy before it is clinically evident. We evaluated human chorionic gonadotropin beta-core fragment as a test to predict ectopic pregnancy and spontaneous abortion. Urine samples were collected from women with in vitro fertilized pregnancies, 2 1/2-5 weeks after embryo transfer. Fifty samples were collected from those later shown to have normal intrauterine pregnancies, samples from 13 women subsequently found (at 5-9.3 weeks) to have ectopic gestations, and 15 from those with impending spontaneous abortion. Beta-Core fragment levels were determined by immunoassay, and results normalized to creatinine concentration. Median beta-core fragment levels at 2 1/2-3, 3-4, and 4-5 weeks after embryo transfer, were 6.7, 91 and 737 microg/g for unaffected pregnancies, 1.0, 5.9 and 0.6 microg/g for impending ectopic pregnancies (0.15, 0.065 and 0.0008, multiples of the unaffected pregnancy median, MoM), and 0.75, 6.8 and 12 microg/g for impending spontaneous abortions (0.11, 0.07 and 0.016 MoM). A gestation-linked curve was modeled to discriminate unaffected pregnancy from impending ectopic gestation or spontaneous abortion. Plotted beta-core fragment levels were below this curve in 12 of 13 (92%) women with impending ectopic pregnancy, in 10 of 15 (67%) with spontaneous abortion outcome, and in 2 of 50 (4%) with intrauterine pregnancy and term outcome. Measurement of urine beta-core fragment at 2 1/2-5 weeks after embryo transfer (4 1/2-7 weeks after last menstrual period) might be useful for identifying failing pregnancies. Over three quarters (predictive value positive 76%) of those with low beta-core fragment levels have ectopic pregnancy or spontaneous abortion. On the contrary, 95% (predictive value negative) of those with normal range test values may be predicted to have a nonfailing term pregnancy. Diagnosis of ectopic pregnancy could be confirmed by transvaginal ultrasound, and ectopic pregnancy terminated early by nonsurgical methods, with minimal mortality or fertility loss. Major fetal defects that cause spontaneous abort pregnancies may also be recognized by transvaginal ultrasound. In such cases, chorionic villous sampling or possibly termination may be considered.

Abortion, Spontaneous↗