PubMed Health⌕ Search

Biomedical subjects

T Shiigai

Publications and source records attributed to T Shiigai.

At least 91 records · Page 5Linked to original sources
PubMed1986

Intracellular electrical potentials in the rabbit collecting ducts perfused in vitro.

Cortical collecting ducts (CCD) and inner stripe of outer medullary collecting ducts (OMCD) of the rabbit were perfused in vitro and the electrical potential was measured with 0.5 M KCl-filled conventional microelectrodes. In CCD, the transepithelial potential (Vte) was -1.9 +/- 0.5 (S.E.) mV and the intracellular potential (Vb) was -74.5 +/- 1.3 mV, while in OMCD, Vte was +2.0 +/- 0.4 mV and Vb was -24.6 +/- 1.0 mV. Acute reduction of peritubular HCO3- concentration from 25 to 5 mM (from pH 7.4 to 6.9) decreased Vb slowly but markedly from -26.3 +/- 1.8 to -18.9 +/- 1.6 mV (p less than 0.001) in OMCD, while it depolarized Vb slightly in CCD (from -75.6 +/- 1.9 to -74.3 +/- 2.1 mV, P less than 0.05). Acute peritubular pH reduction with HCO3- -free HEPES-buffered solution also depolarized Vb of OMCD from -24.7 +/- 2.1 to -15.9 +/- 1.6 mV (p less than 0.001). Although the mechanism(s) of Vb depolarization in OMCD is unclear at the moment, this depolarization suggests that OMCD is responsive to peritubular pH alterations. The results of this study provide the evidence that the collecting duct is heterogeneous in Vb values and its response to the peritubular pH change.

Animals↗
PubMed1986

Localization and properties of NAD-dependent 15 hydroxyprostaglandin dehydrogenase activity in spontaneously hypertensive rat kidney.

To evaluate the pathophysiological significance of renal NAD-dependent 15 hydroxyprostaglandin dehydrogenase (PGDH) in young spontaneously hypertensive rats (SHR), the intranephron distribution of PGDH was compared with age-matched Wistar Kyoto rats (WKY). With supernatants of kidney homogenates, PGDH activities in 3 week-old SHR were significantly lower than those in WKY, and no difference in PGDH activities was found between male and female in both WKY and SHR. By using microdissected nephron segments of 3 week-old WKY and SHR, PGDH activities in both groups were found to be exclusively distributed in the proximal tubules, within which the activity of the straight portion (PST) was several fold higher than that of the convoluted one (PCT). In 3 week-old SHR, a significant decrease of PGDH activity was observed only in PST, possibly indicating a decrease of enzyme content in PST because of similar Km values in both groups. These results may suggest that intraproximal PG concentration could be regulated by the change of PGDH in PST of young SHR.

Animals↗
PubMed1985

Effect of chronic metabolic acidosis on ammonia production from L-glutamine in microdissected rat nephron segments.

To evaluate the role of each nephron segment in renal ammoniagenesis, distribution of renal ammoniagenic activity along the nephron in control and acidotic rats was examined. We used our original aerobic incubation system and ammonia produced from glutamine in 7 defined segments of microdissected nephron was measured using the enzymatic cycling method. When ammonia production in the control was compared in each nephron segment, the highest specific activity of ammoniagenesis per mm tubular length and that per microgram protein were observed in the proximal straight tubule (PST) and the thick ascending limb of Henle's loop, respectively. Chronic metabolic acidosis increased ammonia production per mm tubular length markedly in the proximal convoluted tubule (PCT) (+171%), moderately in the medullary collecting tubule (+123%) and PST (+77%), and slightly in the distal convoluted tubule (+52%), revealing that the highest activity of ammoniagenesis was located in PCT and PST in acidosis. These data indicate that proximal tubules have major roles in renal ammoniagenesis both in the control and in acidosis. From the early observation of glutaminase I isoenzyme distribution along the nephron, our data suggest that not only phosphate-dependent glutaminase but also phosphate-independent glutaminase may have important roles in renal ammoniagenesis.

Acidosis↗
PubMed1985

Renal handling of urate in the syndrome of inappropriate secretion of antidiuretic hormone.

Three patients with the syndrome of inappropriate secretion of antidiuretic hormone had elevated uric acid clearances. Their uric acid clearances decreased markedly after the administration of pyrazinamide. Probenecid was given to two of them and it produced large increases in uric acid clearance. These data suggest that enhanced secretion in the renal tubules was responsible for the increased clearance of uric acid. This article provides evidence that hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone is due to increased tubular urate secretion.

Aged↗
PubMed1984

Relation of family history of hypertension to platelet aggregation, ratio of total cholesterol to HDL cholesterol and urinary kallikrein excretion.

Some of the relatively easily measurable and possibly hypertension-associated parameters were evaluated in thirty normotensive young subjects divided into the PHT (either parent hypertensive) group and the PNT (both parents normotensive) group. In subjects of the PHT group, the platelet aggregating sensitivity to the arachidonic acid and the ratio of total cholesterol to HDL cholesterol were significantly (p less than 0.05) increased while urinary kallikrein excretion was decreased without simultaneously significant elevation of blood pressure. The enhanced platelet aggregating sensitivity to the arachidonic acid and the increased ratio of total cholesterol to HDL cholesterol suggest that subjects with a positive family history of hypertension might have a greater tendency to atherosclerosis and could contribute to the development of essential hypertension. Decreased urinary kallikrein excretion suggests that the vasodepressive activity of the kallikrein-kinin system might be inhibited in subjects with a positive family history of hypertension.

Adult↗
PubMed1984

Long-term furosemide treatment in idiopathic edema.

Of 12 patients with idiopathic edema, ten patients had received total doses of furosemide of up to about 950 g. A good negative correlation was observed between the creatinine clearance and the duration of daily oral furosemide intake of more than 40 mg, and a highly significant correlation was found between the logarithm of the creatinine clearance and the duration of daily furosemide ingestion. Cessation of furosemide and institution of a sodium-restricted diet was followed by improvement in the creatinine clearance. Three patients had acute renal failure with myoglobinuria. All patients examined showed tubular and/or interstitial changes. This study shows that in idiopathic edema, long-term furosemide treatment gradually impairs renal function, with reversal to a considerable degree after cessation of the drug, and that it causes organic changes in the kidney.

Adolescent↗
PubMed1983

Increased urinary kallikrein-like activity in the syndrome of inappropriate secretion of antidiuretic hormone.

The role of the kallikrein system in the natriuresis of SIADH was studied in 3 patients. Following free water intake, serum Na decreased. Urinary Na excretion, urinary aldosterone excretion and urinary kallikrein-like activity (UKaV) increased. Significant relationships were observed between UKaV and urinary aldosterone excretion during the study. Further, there were significant relationships between serum Na and UKaV, and between uric acid clearance and UKaV. In 1 patient, who was observed for a longer period, a significant relationship was observed between Na clearance and UKaV. We conclude that UKaV is increased during hyponatremia in SIADH by volume expansion. This increase in UKaV may play a role in the natriuresis in SIADH.

Aged↗
PubMed1983

Sulbenicillin-induced kaliuresis in man.

The mechanism of kaliuresis induced by massive antibiotic administration was studied using alpha-sulfobenzyl penicillin (SBPC). In experimental group (n = 8), urinary electrolytes excretion were compared between following the infusion of 10 g SBPC in 200 ml water at a constant rate and following the infusion of 48 mmol of NaCl (equal to that contained in 10 g SBPC) in 200 ml water. For the control group, 96 mmol NaCl in 400 ml water was infused (n = 5). In the experimental group, urinary Na (UNaV) and urinary K excretion (UKV) increased relative to the control period. In the control group, UKV was not increased although UNaV was increased (p less than 0.05). UKV following SBPC infusion was correlated with UNaV (p less than 0.05) and urinary SBPC excretion (p less than 0.05). The ratio of urinary anion gap to urinary cation [1-(urinary Cl concentration/(urinary Na concentration + urinary K concentration))] was significantly increased following SBPC infusion (p less than 0.005) but not in the control group. This increase in anion gap is possibly due to urinary SBPC, which will be ionized over 90% as nonreabsorbable anion in maximally acidic urine. We conclude that the kaliuresis induced by massive SBPC administration in man is probably caused by the nonreabsorbable anion effect of SBPC itself.

Acid-Base Equilibrium↗
PubMed1982

A case of familial renal hypouricemia associated with increased secretion of para-aminohippurate and idiopathic edema.

A 42-year-old housewife had hypouricemia (serum uric acid ranging from 0.5 to 1.5 mg/dl; 30-89 mumol/l), increased uric acid clearance (47.6-83.0 ml/min), increased maximum tubular secretory capacity for para-aminohippurate, and idiopathic edema. Urate excretion was only minimally suppressed by pyrazinamide, and paradoxically decreased by probenecid. Uric acid clearance did not show any appreciable change after long-term administration of ticrynafen. In response to an increment of extracellular volume by hypertonic saline infusion or long-term 9 alpha-fluorohydrocortisone administration, urate clearance did not show any substantial increase. These data may suggest that not only presecretory but possibly also postsecretory reabsorption of urate is impaired in this patient. No other renal tubular abnormalities were detected. Family study revealed that her renal hypouricemia is hereditary. She was unable to increase urinary excretion of sodium during hypertonic saline infusion and failed to change the response to the sodium-retaining action of 9 alpha-fluorohydrocortisone, presumably accounting for her edema.

Adult↗
PubMed1982

Renin-angiotensin-aldosterone system in mild diabetic nephropathy.

The mechanism of lowered renin-aldosterone system was investigated in 17 patients with diabetic nephropathy (serum Cr less than 3 mg/100 ml) with concomitant control of the blood sugar level. The response of plasma renin activity (PRA) to upright stimulation was lower in the low renin group (group I) than in the normal to high renin group (group II) and in the control group. The PRA response to theophylline was delayed in group I. The percentage of the luminal area of the arteriole in the biopsy specimens was larger in group I and the control group than in group II. Plasma aldosterone concentration (PAC) was not increased by angiotensin II in group I. Low PRA in diabetic nephropathy with slightly to moderately impaired renal function may not be due to hyaline destruction of the arteriolar walls, but to other factors such as sympathetic nervous dysfunction. The adrenal responses of PAC to angiotensin II may also be impaired.

Adolescent↗