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Biomedical subjects

T Shiigai

Publications and source records attributed to T Shiigai.

At least 73 records · Page 4Linked to original sources
PubMed1989

Leukotriene D4 inhibits atrial natriuretic factor-dependent cGMP production in rat glomerulus.

The effects of leukotriene D4 (LTD4) on guanosine 3',5'-cyclic monophosphate (cGMP) production induced by atrial natriuretic factor (ANF) or sodium nitroprusside (SNP) were investigated in isolated rat glomeruli. First, the isolated glomeruli were preincubated in Krebs-Ringer buffer containing 3-isobutyl-1-methylxanthine for 10 min, then incubated with varying concentrations of ANF, SNP, and LTD4 for 3 min. cGMP content was determined by radioimmunoassay. cGMP production (fmol.glomerulus-1.3 min-1) was not increased by LTD4. cGMP accumulation was increased by ANF (1 microM) and SNP (100 microM) remarkably from 0.19 +/- 0.09 to 3.24 +/- 0.21 (n = 7, mean +/- SE), and from 0.19 +/- 0.09 to 3.67 +/- 0.47 (n = 4), respectively. The increase in cGMP production by ANF was significantly and dose-dependently inhibited by LTD4 (P less than 0.05). Maximum suppression was observed at the concentration of 100 nM (from 3.06 +/- 0.33 to 1.43 +/- 0.09; P less than 0.05). However, LTD4 caused no significant change in the level of cGMP production induced by SNP. Second, particulate or soluble guanylate cyclase from glomeruli were similarly investigated. ANF selectively activated particulate guanylate cyclase and the response was selectively inhibited by LTD4 from 9.07 +/- 1.79 fmol.micrograms-1.3 min-1 (n = 6) to 4.70 +/- 0.70 (n = 6, P less than 0.05). These results suggest the site where LTD4 has effect on cGMP production induced by ANF was the particulate guanylate cyclase system, but not the soluble guanylate cyclase system.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Effect of daily energy expenditure on the creatinine clearance and daily urinary protein excretion of patients with mesangial proliferative glomerulonephritis.

In the present study, the relationships among daily energy expenditure, renal function (creatinine clearance, Ccr), and daily urinary protein excretion were examined. In total, 104 adult patients (from 9 renal clinics in Japan) with primary chronic glomerulonephritis were fitted with a portable calorie counter for about two weeks to estimate their daily energy expenditure. On two separate days when the energy expenditure was expected to be contrastingly different, urine collection and blood sampling were performed, and the Ccr and daily urinary protein excretion were determined. Multiple regression analysis of Ccr clearly demonstrated a significant correlation between its acceleration and increase in the daily protein intake or protein excretion. In mesangial proliferative glomerulonephritis showing a constant level of protein intake, the enhancement of Ccr revealed a significant inverse relation to the increase in daily energy expenditure (%BMR). It was demonstrated statistically that a daily energy expenditure exceeding 150 %BMR slowed the Ccr down. This limit was almost the same as the level in healthy adults living in urban cities of Japan. The urinary protein excretion was significantly correlated with the daily protein intake. These results should be taken into consideration in prescribing for each individual patient an allowable degree of labor or any other activity and an adequate dietary regimen, and also in evaluating the efficacy of a drug for glomerulonephritis.

Adolescent↗
PubMed1988

Red-cell-volume distribution curves in diagnosis of glomerular and non-glomerular haematuria.

The distribution curves of urinary red-blood-cell (RBC) size were obtained from automated blood-cell analysis in 146 patients with definite causes of haematuria. In 65 of 67 patients (97%) with haematuria and glomerulonephritis demonstrated by renal biopsy, urinary RBC had an irregular and asymmetrical distribution with RBC size showing a much smaller volume than that of venous RBC. This "glomerular" distribution contrasted with the "non-glomerular" normal distribution when the peak for RBC was at a larger volume than that for peripheral RBC. In 46 of 47 patients with haematuria who had lower urinary tract lesions other than infection, a non-glomerular distribution was obtained; 30 of these cases also showed glomerular distribution, and were classified as "mixed". All 32 patients with urinary tract infection had either a glomerular or mixed distribution, suggesting that they excreted distorted and dysmorphic urinary RBC. After excluding infections, this simple, rapid, reproducible, and non-invasive technique provides reliable information in distinguishing glomerular bleeding from other causes of haematuria.

Diagnosis, Differential↗
PubMed1988

Primary role of hyperkalemia in the acidosis of hyporeninemic hypoaldosteronism.

A 65-year-old woman with mild renal insufficiency had persistent hyperkalemia and hyperchloremic acidosis. Her plasma aldosterone level was relatively low for her hyperkalemia, and her urine pH was low. Fludrocortisone acetate administration corrected both hyperkalemia and acidosis by increasing urinary excretion of potassium and net acid, implicating deficient mineralocorticoid activity in the distal renal tubule in this patient. During this medication urinary ammonium excretion increased, but urine pH remained low, so that urinary titratable acid excretion did not decrease. On the other hand, correction of hyperkalemia by administration of a potassium-calcium exchange resin alone also resolved the acidosis by increasing urinary ammonium excretion. This increment exceeded the decrement of urinary titratable acid excretion, which was caused by raised urine pH secondary to increased urinary ammonium excretion, and resulted in increase of net acid excretion. Thus, in this patient, hyperkalemia appears to be a decisive causative factor in the acidosis, with deficient mineralocorticoid effect only contributing in part to the reduction of net acid excretion and the acidosis.

Acidosis, Renal Tubular↗
PubMed1988

KCl co-transport across the basolateral membrane of rabbit renal proximal straight tubules.

Mammalian renal proximal tubules reabsorb large amounts of chloride. Mechanisms of the transcellular chloride transport are poorly understood. To determine whether KCl co-transport exists in the basolateral membrane of mammalian renal proximal tubule, isolated rabbit proximal straight tubules (S2 segment) were perfused in vitro, and intracellular activities of potassium and chloride (aKi, aCli) were measured by double-barreled ion-selective microelectrodes. aCli did not change when basolateral membrane voltage was altered by application of a direct current through perfusion pipette. aCli changes in response to bath chloride elimination were not affected by current application as well, indicating that the basolateral chloride transport is electroneutral. An increase in potassium concentration of the bath fluid from 5 to 20 mM reversibly increased aCli by 10 mM. This response of aCli to a change in the bath potassium concentration was also observed when luminal chloride was removed, or ambient sodium was totally removed. aKi significantly decreased by 5 mM when chloride was removed from the bath. These data demonstrate the existence of an electroneutral Na+-independent KCl co-transport in the basolateral membrane of the rabbit proximal tubule. Calculated electrochemical driving force was favorable for the movement of KCl from the cell to the peritubular fluid.

Absorption↗
PubMed1987

Generation of pH gradient across the rabbit collecting duct segments perfused in vitro.

Ability of pH gradient generation was examined in three segments of rabbit collecting duct, cortical collecting duct (CCD), outer medullary collecting duct (OMCD) and inner medullary collecting duct (IMCD). These segments were perfused in vitro, and the steady-state luminal pH in stop-flow condition (pHs) and the electrochemical potential difference of H+ (EH) were determined using double-barreled liquid membrane pH microelectrode punctured into the lumen. In CCD, pHs was 7.71 +/- 0.08 in normal rabbits, 7.72 +/- 0.08 in DOCA-treated rabbits and 7.27 +/- 0.05 in starved rabbits, while peritubular fluid was kept at pH 7.5 EH (positive value means H+ accumulation in the lumen above electrochemical equilibrium) was -15.3 +/- 5.2, -31.3 +/- 3.7 and 10.3 +/- 3.1 mV, respectively. Peritubular acidification (peritubular pH 6.8) by reducing HCO3-concentration decreased pHs, but increased its negativity of EH in all groups. In OMCD pHs was 6.57 +/- 0.08 in normal, 6.58 +/- 0.11 in DOCA-treated and 6.47 +/- 0.12 in starved animals. EH was 54.5 +/- 4.6, 57.7 +/- 6.8 and 64.2 +/- 6.9 mV, respectively. Peritubular acidification lowered pHs further, 5.51 +/- 0.07, 5.67 +/- 0.16 and 5.41 +/- 0.19, respectively. EH was enhanced in all groups. In IMCD pHs was 7.36 +/- 0.04 with EH being 6.8 +/- 2.9 mV, and peritubular acidification did not generate pH gradient. These data suggest that the generation of a steep acid pH gradient is mainly due to OMCD. Luminal alkalinization predominated in CCD except in starved rabbits. IMCD did not generate appreciable pH gradient.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1987

Mechanism of bicarbonate exit across basolateral membrane of rabbit proximal straight tubule.

To clarify the mechanism(s) of HCO3- (or related base) transport across the basolateral membrane, rabbit proximal straight tubules were perfused in vitro, and intracellular pH (pHi) and Na+ activity (aiNa) were measured by double-barreled ion-selective microelectrodes. Lowering bath HCO3- from 25 to 5 mM at constant PCO2 depolarized basolateral membrane potential (Vbl), and reduced pHi. Most of these changes were inhibited by adding 1 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) to the bath. Total replacement of bath Na+ with choline also depolarized Vbl and reduced pHi, and these changes were also inhibited by SITS. Reduction in aiNa was observed when bath HCO3- was lowered. Taken together, these findings suggest that HCO3- exists the basolateral membrane with Na+ and negative charge. Calculation of the electrochemical driving forces suggests that the stoichiometry of HCO3-/Na+ must be larger than two for maintaining HCO3- efflux. Total replacement of bath Cl- with isethionate depolarized Vbl gradually and increased pHi slightly, implying the existence of a Cl(-)-related HCO3- exit mechanism. The rate of decrease in pHi induced by lowering bath HCO3- was slightly reduced (20%) by the absence of bath Cl-. Therefore, the importance of Cl(-)-related HCO3- transport is small relative to total basolateral HCO3- exit. Accordingly, these data suggest that most of HCO3- exits the basolateral membrane through the rheogenic Na+/HCO3- cotransport mechanism with a stoichiometry of HCO3-/Na+ of more than two.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1987

Effect of vasopressin on Na+-K+-ATPase activity in rat cortical collecting duct.

Vasopressin (V) causes a sustained increase in Na reabsorption and K secretion in isolated cortical collecting ducts (CCD) from rats. Because increased Na reabsorption may be associated with increased Na+-K+-ATPase activity, we investigated effects of V, given either in vivo or in vitro, on Na+-K+-ATPase activity in isolated nephron segments of rats. Na+-K+-ATPase activities were measured by coupling the hydrolysis of ATP to the production of a fluorescent nucleotide. In addition to CCD, other microdissected structures were medullary thick ascending limbs of Henle's loop, cortical thick ascending limbs of Henle's loop, and outer medullary collecting duct. To determine the time course of the response, Na+-K+-ATPase activities were measured in CCD 1 h, 3 h, 1 day, 3 days, and 7 days after intramuscular administrations of V. There was a significant increase in Na+-K+-ATPase activity in CCD after in vivo V administration for 7 days but not in any other segment. The activities increased after 3 days of administration of V. For in vitro experiments, CCD were incubated with 10(-6) M V for 1-3 h. Na+-K+-ATPase activities did not change after 1- or 3-h exposure of V in CCD in vitro. We conclude that prolonged V administration in vivo increases Na+-K+-ATPase activity in CCD. Because, in vitro exposure to V does not increase Na+-K+-ATPase activity, we conclude that rapid V-dependent increases in Na and K transport previously demonstrated in isolated perfused tubules are not dependent on a change in maximal Na+-K+-ATPase activity.

Animals↗
PubMed1987

Hypouricemia due to increased tubular urate secretion.

A 45-year-old woman had hypouricemia (serum uric acid, 1.0-2.3 mg/dl) with increased uric acid clearance (29.8 +/- 9.3 ml/min/1.73 m2). Uric acid clearance to creatinine clearance ratio (Cua/Ccr) was suppressed markedly by pyrazinamide to 2.3% and surprisingly enhanced by probenecid to 227.8%. No other renal tubular or metabolic abnormalities were detected. This previously unreported high postprobenecid Cua/Ccr suggests that markedly increased urate secretion by the renal tubule is responsible for hypouricemia in this patient.

Creatinine↗
PubMed1987

Lack of effect of alpha-human atrial natriuretic polypeptide on volume reabsorption and p-aminohippuric acid secretion in the rabbit proximal straight tubule.

To assess a possible direct tubular action of alpha-human atrial natriuretic peptide (alpha-hANP), we studied the effects of alpha-hANP on volume reabsorption (JV), transepithelial voltage (VT), and p-aminohippuric acid (PAH) secretion in the rabbit proximal straight tubules (PST) by in vitro microperfusion technique. In superficial PST (SFPST), addition of alpha-hANP at various concentrations (10(-7), 10(-9), 10(-11) M) to the bath solution did not alter JV significantly. Bath alpha-hANP (10(-7) M) did not change VT in SFPST, either. In juxtamedullary PST (JMPST), addition of alpha-hANP (10(-7) M) to the bath solution changed neither VT nor JV significantly. The alpha-hANP (10(-7) M) in the luminal fluid caused no changes in either VT or JV in SFPST. Furthermore, alpha-hANP (10(-7) M) in the bath did not change the rate of PAH secretion in SFPST. Thus, we could not obtain any evidence for direct tubular action of alpha-hANP in rabbit PST. Accordingly, alpha-hANP may increase solute excretion without directly affecting solutes transport in PST of the rabbit kidney.

Aminohippuric Acids↗
PubMed1987

Hypouricemia due to subtotal defect in the urate transport.

Hypouricemia due to renal tubular defects is rarely reported. We report here our observations of two such patients who cannot be classified into any of the previously reported categories of renal hypouricemia. They showed no suppression of urate clearance to creatinine clearance ratio (Cua/Ccr) following the administration of pyrazinamide, and no increase of Cua/Ccr after probenecid. It is tempting to speculate upon the subtotal defect in the urate transport as a condition explaining the above results.

Adult↗
PubMed1987

Diabetic renal hypouricemia.

In diabetes, the serum uric acid level is low due to increased urate clearance; however, its mechanism remains unknown. We examined seven maturity-onset diabetic patients with rarely reported hypouricemia due to renal tubular abnormality to better understand the renal handling of urate by the diabetic kidney. The results of studies indicate that the increase in urate clearance was entirely accounted for by increased pyrazinamide-suppressible urate clearance. The maximal uricosuric response to probenecid administration was exaggerated. The effects of drugs on urate clearance were similar to those we have previously reported in the syndrome of inappropriate secretion of antidiuretic hormone. In four patients, the family survey did not reveal anyone with hypouricemia. These observations suggest that hypouricemia due to hyperuricosuria, which responds markedly to pyrazinamide and probenecid, is actually an indicator of renal tubular abnormality in diabetics.

Adult↗
PubMed1986

Glutamine transport in the rabbit proximal straight tubule: effect of acute acid pH.

Proximal straight tubules (PST) has been shown to be an important nephron segment of renal ammonia production. To clarify the nature of glutamine (substrate of ammonia production) transport in PST, both luminal resorption and peritubular uptake of glutamine were measured in isolated rabbit PST. Luminal glutamine resorption (Jgln) was measured at various perfusate glutamine concentration (0.05 to 20 mM) at 38 degrees C and 12 degrees C. Jgln measured at 12 degrees C were proportional to mean luminal glutamine concentrations. This flux was thought to be a passive glutamine flux. The flux, which was obtained by subtracting passive glutamine flux from Jgln obtained at 38 degrees C, was thought to be active luminal resorption. This flux exhibited saturation kinetics (Vmax 20.9 pmol min-1 X mm-1, km 5.2 mM). When bath pH (HCO3) was lowered from 7.4 to 6.8, Jgln showed no change or a small decrease (12%) at perfusate glutamine concentrations of 0.05 or 5 mM, respectively. When perfusate pH (HCO3) was lowered from 7.4 to 6.8 Jgln showed a small decrease (10%) at 5 mM perfusate glutamine concentration. Peritubular glutamine uptake was determined in isolated nonperfused PST incubated for 5 to 50 min in [14C]-glutamine containing solution. When incubated in pH 7.4 HCO3 buffer solution, cell to medium 14C concentration ratio was higher than unity (3.83 +/- 0.34, P less than 0.001) at 5 min, and reached a maximum (11.37 +/- 1.13) at 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗