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Biomedical subjects

E Ogata

Publications and source records attributed to E Ogata.

At least 253 records · Page 14Linked to original sources
PubMed1987

Pertussis toxin inhibits somatostatin-induced K+ conductance in human pituitary tumor cells.

The effect of pertussis toxin on somatostatin-induced K+ current was examined in dissociated human pituitary tumor cells obtained from two acromegalic patients. Somatostatin-induced hyperpolarization or K+ current was observed in 20 of 23 cells in adenoma 1 and 10 of 11 cells in adenoma 2. After treatment with pertussis toxin for 24 h, these responses were completely suppressed (0/14 in adenoma 1, 0/10 in adenoma 2). Spontaneous action potentials, K+, Na+, and Ca2+ currents were well preserved after pertussis toxin treatment. When crude membrane fraction was incubated with [32P]NAD, a 41K protein was ADP-ribosylated by pertussis toxin. Hormone release was inhibited by somatostatin and this inhibition was blocked by pertussis toxin treatment.

Action Potentials↗
PubMed1987

Blood Ca2+ modulates responsiveness of renal 25(OH)D3-1 alpha-hydroxylase to PTH in rats.

To clarify whether extracellular Ca2+ modulates renal 25-hydroxyvitamin D3 [25(OH)D3]-1 alpha-hydroxylase, thyroparathyroidectomized rats were infused with 15 mM CaCl2, 20 mM EGTA, and/or 2.5 U/h parathyroid hormone (PTH), and blood Ca2+, serum 1,25-dihydroxyvitamin D [1,25(OH)2D], and renal 1 alpha-hydroxylase activity were determined. Rats with CaCl2, EGTA, or PTH infusion (group 1) exhibited low blood Ca2+, serum 1,25(OH)2D, and 1 alpha-hydroxylase activities. Infusion of CaCl2 alone (group 2) caused a significant increase in blood Ca2+ and a reduction in serum 1,25(OH)2D and 1 alpha-hydroxylase compared with group 1. Administration of PTH alone (group 3) markedly elevated blood Ca2+, serum 1,25(OH)2D, and 1 alpha-hydroxylase activity. When EGTA was infused along with PTH (group 4), blood Ca2+ was significantly reduced compared with group 3, and serum 1,25(OH)2D and renal 1 alpha-hydroxylase were further elevated. In contrast, when CaCl2 was infused with PTH (group 5), blood Ca2+ was higher than that in group 3, and serum 1,25(OH)2D and 1 alpha-hydroxylase activities were significantly reduced compared with group 3. No significant difference in serum inorganic phosphate or urinary cAMP excretion was observed by CaCl2 or EGTA infusion in both PTH-treated and nontreated rats. These results demonstrate that extracellular Ca2+ modulates the responsiveness of renal 1 alpha-hydroxylase to PTH as well as the base-line activity of the enzyme in the absence of PTH. These effects of extracellular Ca2+ on renal 1 alpha-hydroxylase may serve to offer an efficient way of regulating 1,25(OH)2D production and serum 1,25(OH)2D concentration by altering the responsiveness of 1 alpha-hydroxylase to PTH and possibly other stimulations depending on the demand for Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1987

The role of insulin in the stimulation of renal 1,25-dihydroxyvitamin D synthesis by parathyroid hormone in rats.

To evaluate the role of insulin in 1,25-dihydroxyvitamin D [1,25(OH)2D] production in response to PTH, 25-hydroxyvitamin D-1 alpha-hydroxylase activity in kidney homogenates as well as serum 1,25(OH)2D concentration was measured both after dietary calcium (Ca) deprivation and after PTH infusion in control and streptozotocin-diabetic rats. Although serum Ca and phosphate (Pi) levels did not change significantly after dietary Ca deprivation for 1 week, urinary cAMP excretion increased significantly, indicating that dietary Ca deprivation caused secondary hyperparathyroidism without a significant change in serum Ca level. In control rats, renal 1 alpha-hydroxylase activity increased markedly from 0.11 +/- 0.05 to 1.70 +/- 0.46 ng/300 mg tissue/20 min in parallel with the change in serum 1,25(OH)2D level from 121 +/- 8 to 360 +/- 54 pg/ml in response to Ca deprivation. In contrast, serum 1,25(OH)2D level (82 +/- 3 pg/ml) and 1 alpha-hydroxylase activity (0.07 +/- 0.02 ng/300 mg tissue.20 min) were lower in the diabetic rats on a normal Ca diet than those in control rats, and the increase in both 1,25(OH)2D level and 1 alpha-hydroxylase activity in response to Ca deprivation was suppressed in diabetic rats (136 +/- 24 pg/ml and 0.38 +/- 0.12 ng/300 mg tissue.20 min, respectively, after Ca deprivation). Insulin treatment of the diabetic rats restored the baseline levels of serum 1,25(OH)2D (125 +/- 14 pg/ml) and renal 1 alpha-hydroxylase activity (0.21 +/- 0.02 ng/300 mg tissue.20 min) as well as those after Ca deprivation (340 +/- 52 pg/ml and 2.05 +/- 0.30 ng/300 mg tissue.20 min, respectively). Furthermore, when control and diabetic rats were thyroparathyroidectomized and infused with a maximal stimulatory dose of PTH, the increase in serum 1,25(OH)2D and renal 1 alpha-hydroxylase activity in response to PTH was markedly inhibited in diabetic rats. In addition, the baseline levels of serum 1,25(OH)2D and renal 1 alpha-hydroxylase activity in thyroparathyroidectomized diabetic rats were not different from those in control rats. These results are consistent with the conclusion that insulin plays an important role in the regulation of renal 1 alpha-hydroxylase activity and serum 1,25(OH)2D levels in response to PTH.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1987

Renal magnesium wasting in a patient with short bowel syndrome with magnesium deficiency: effect of 1 alpha-hydroxyvitamin D3 treatment.

We studied a patient with severe hypomagnesemia due to small bowel resection who had marked renal magnesium (Mg) loss in response to iv Mg infusion. She had an undetectable serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] level before treatment. Although Mg infusion increased her serum Mg levels and enhanced renal PTH action, as evidenced by an elevation in nephrogenous cAMP, the serum 1,25-(OH)2D level remained low. After the administration of 1 alpha-hydroxyvitamin D3, her serum 1,25-(OH)2D level increased, and fractional excretion of Mg decreased. With the elevation in serum 1,25-(OH)2D, serum Mg levels could be maintained without Mg infusion, although they were still subnormal. These results are consistent with the assumption that patients with the short bowel syndrome and Mg deficiency have reduced renal tubular Mg reabsorption which causes renal Mg loss, and that impaired tubular Mg reabsorption is due at least in part to deficient renal action of 1,25-(OH)2D. Because depressed serum 1,25-(OH)2D levels cannot be corrected rapidly by Mg infusion, administration of 1 alpha-hydroxyvitamin D3 or 1,25-(OH)2D3 appears to be the treatment of choice for Mg deficiency in patients with short bowel syndrome.

Adult↗
PubMed1987

Two cases of anorexia nervosa associated with Graves' disease.

In this report on two cases of anorexia nervosa associated with Graves' disease, metabolism and the relationship between the two illness are considered. Case 1 was a 25-year-old female. Anorexia was associated with a stressful life situation following marriage. One year after the onset of anorexia, her condition was diagnosed as Graves' disease. In spite of high levels of serum thyroid hormone, she did not show the clinical signs and symptoms of hyperthyroidism. The hypermetabolic state of Graves' disease seems to be suppressed by the hypometabolism of anorexia. Case 2 was a 17-year-old female whose body weight, due to anorexia, at one time had decreased from 55 kg to 35.2 kg. A rebound from anorexia to bulimia increased her body weight to 80 kg in spite of an association with the hypermetabolic state of Graves' disease. In light of the abovementioned cases, it seems that the clinical picture of Graves' disease is usually hidden by the clinical symptoms of anorexia nervosa.

Adolescent↗
PubMed1987

Mitral valve prolapse in patients with anorexia nervosa. Two-dimensional echocardiographic study.

To examine the prevalence of mitral valve prolapse (MVP) and to define the mechanisms of its development in patients with anorexia nervosa, we studied the cardiac function of 23 patients with anorexia nervosa by two-dimensional (2-D) echocardiography. MVP was present in 19 of 23 patients (82.6%), 10 having double MVP in both the anterior and posterior mitral leaflets and 9 having a single MVP in the anterior leaflet. There was no difference in echocardiographic parameters between the MVP(+) and MVP(-) groups. The heart rate was lower in the double MVP group (46.3 +/- 8.1; mean +/- SD) than in the non MVP group (64.0 +/- 6.3; p less than 0.01) and the single MVP group (55.9 +/- 10.9; p less than 0.05). The presence of bradycardia in these patients suggests an increase in vagal tone. The present study suggests that the incidence of MVP in anorexia nervosa is among the highest compared with its incidence in association with any other disorders, and an increase in vagal tone may be responsible for the development of MVP in patients with anorexia nervosa.

Adolescent↗
PubMed1987

Ca2+ ionophore A23187-induced rise in cytoplasmic free calcium and iodide discharge in porcine thyroid cells: measurement of cytoplasmic free calcium by aequorin.

The cytoplasmic concentration of free calcium was measured using aequorin, a calcium-sensitive photoprotein. The Ca2+ ionophore A23187 induced a rise in cytoplasmic free calcium and iodide discharge in cultured porcine thyroid cells. The minimum dose of A23187 effecting an increase in cytoplasmic free calcium induced iodide discharge. The A23187-induced rise in cytoplasmic free calcium was followed by iodide discharge. The results indicate that A23187-induced iodide discharge is mediated by a rise in the cytoplasmic concentration of free calcium.

Aequorin↗
PubMed1987

Potentiation of the phosphaturic effect of calcitonin by indomethacin in thyroparathyroidectomized rats.

The influence of indomethacin on phosphaturic effect of calcitonin (CT) was examined in conscious, restrained thyroparathyroidectomized (TPTX) rats. Constant infusion of 0.5 units/h CT caused a transient phosphaturic response which peaked within 2 h after the start of the CT infusion. Indomethacin enhanced and prolonged the CT-induced phosphaturia without affecting serum phosphate levels or creatinine clearance. Because the urinary excretion of prostaglandin E2 (PGE2) was markedly suppressed by indomethacin, the potentiation of the phosphaturic effect of CT by indomethacin appears to be due to an inhibition of renal PG synthesis. These observations as well as our previous findings that exogenously administered PGE2 inhibits the phosphaturic effect of CT and stimulation of 1 alpha-hydroxylase in TPTX rats [Yamada et al. Endocrinology 116: 693-697, 1985] are consistent with the hypothesis that PG interacts with CT to modulate the effects of CT in the proximal renal tubules.

Animals↗
PubMed1987

[Hydronephrosis in pregnancy and its etiology].

Using ultrasonography, the cause and incidence of hydronephrosis were investigated in humans and rabbits and the following results were obtained. The degree of hydronephrosis was classified into grade I (calyceal diameter; up to 5 mm) to grade V (calyceal diameter; 21 mm or more). In normal non-pregnant women, the calyceal diameter was within grade I. The hydronephrosis was found in 45.5-87.0% of pregnant women in the right kidney and in 29.1-51.0% in the left. Throughout pregnancy, the incidence was significantly higher in the right than in the left. On the 6th puerperal day, the incidence of hydronephrosis was lowered, but the diameter did not return to the non-pregnant level. Comparison of women who practised swimming during pregnancy and those who did not reveal the incidence of hydronephrosis was lower in the swimming group than in the non-swimming. In rabbits, calyceal dilatation increased as gestation advanced and hydronephrosis was found in progesterone-treated ovariectomized rabbits. It was concluded that the hydronephrosis in the 1st trimester was due to increased steroid hormones, but also that, in the 2nd trimester, the combined effect of hormones and mechanical obstruction was responsible for its occurrence.

Adult↗
PubMed1987

Association of primary hyperparathyroidism with myotonic dystrophy in two patients.

In two patients primary hyperparathyroidism developed in association with myotonic dystrophy (MyD). Both patients had solitary adenoma, and the adenomas were surgically removed. After the operation, subjective improvement of muscle weakness was found in one patient. Because parathyroid hormone secretion is regulated by extracellular calcium concentration and because abnormalities in transmembrane calcium transport are thought to play a role in the pathogenesis of MyD, the concurrence of these rather rare disorders in two patients raises the possibility that abnormalities in transmembrane calcium transport may underlie the development of primary hyperparathyroidism in patients with MyD. Although further studies are needed to clarify the possible link between these two disorders, the present study emphasizes the importance of evaluation of parathyroid function in patients with MyD.

Calcium↗
PubMed1986

Comparison of the changes in cytoplasmic free calcium concentration induced by phenylephrine, vasopressin and angiotensin II in hepatocytes.

Effects of phenylephrine, vasopressin and angiotensin II on cytoplasmic free calcium concentration, [Ca2+]c, were examined by monitoring aequorin bioluminescence in isolated hepatocytes preloaded with aequorin. In the presence of 0.5 mM calcium in the medium, the pattern of changes in aequorin bioluminescence induced by phenylephrine was different from that induced by vasopressin or angiotensin II. When extracellular calcium concentration was reduced to 1 microM, however, these three agents induced identical changes in aequorin bioluminescence. These results suggest that the mode of action of phenylephrine on cytoplasmic free calcium concentration differs from that of either vasopressin or angiotensin II and that the difference in ability to increase calcium influx may account for the distinct patterns induced by these agents.

Aequorin↗
PubMed1986

Evidence for direct effect of tolbutamide on hepatic glycogenolysis induced by Ca2+-dependent hormones.

The effects of tolbutamide and glibenclamide on hepatic glycogenolysis in perfused rat liver were investigated. Tolbutamide per se did not influence glucose output from the liver, but at therapeutic concentrations (about 350 microM) it significantly inhibited the glycogenolysis induced by phenylephrine, vasopressin and angiotensin II, while glibenclamide did not. Neither tolbutamide nor glibenclamide inhibited the glycogenolysis induced by glucagon. Tolbutamide potentiated the inhibitory effect of submaximal concentrations of insulin on glycogenolysis induced by phenylephrine. This effect of tolbutamide was elicitable even in the absence of calcium in the perfusate, and was additive to that of trifluoperazine. However, tolbutamide did not potentiate the inhibitory effect of insulin on glucagon-induced glycogenolysis. Tolbutamide inhibited the glycogenolysis induced by A23187, a calcium ionophore. These results indicate that, in addition to its known effect on insulin secretion, tolbutamide has a direct effect on the liver to inhibit glycogenolysis induced by Ca2+-dependent hormones (catecholamines, vasopressin and angiotensin II) and A23187. Thus, it is likely that tolbutamide inhibits the effect of Ca2+ mobilized by Ca2+-dependent hormones to stimulate glycogenolysis.

Angiotensin II↗
PubMed1986

Action of TMB-8 (8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate) on cytoplasmic free calcium in adrenal glomerulosa cell.

To clarify the action of 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) on cellular calcium handling, changes in cytoplasmic free calcium concentration ([Ca2+]c) were studied in adrenal glomerulosa cell with a calcium-sensitive photoprotein, aequorin. Results of our previous study demonstrate that 100 microM TMB-8 almost completely blocks aldosterone response to angiotensin II (Biochem. J. 232 (1985) 87-92). At 50 or 100 microM, TMB-8 decreased basal [Ca2+]c significantly; however, these doses of TMB-8 had little effect on an angiotensin-induced increase in [Ca2+]c. When angiotensin-induced calcium release from an intracellular pool(s) was assessed by measuring changes in [Ca2+]c in the presence of 1 microM extracellular Ca2+, 100 microM TMB-8 had little inhibitory effect on angiotensin-induced calcium release. A higher dose of TMB-8 (250 microM) slightly inhibited calcium release. Additionally, TMB-8 did not affect exogenous arachidonic acid-induced calcium release. In contrast, 50 microM TMB-8 markedly inhibited 8 mM potassium-induced increase in [Ca2+]c. These results indicate that a major action of TMB-8 on cellular calcium is an inhibition of calcium influx but not of calcium release. We suggest that TMB-8 should not be used as an 'inhibitor of calcium release'.

Adrenal Glands↗
PubMed1986

Pertussis toxin blocks angiotensin II-induced calcium influx but not inositol trisphosphate production in adrenal glomerulosa cell.

Involvement of GTP-binding proteins in angiotensin II-induced mobilization of calcium has been examined in adrenal glomerulosa cells by using pertussis toxin. Pretreatment of glomerulosa cells with pertussis toxin abolishes angiotensin II-induced calcium influx without blocking inositol trisphosphate production. These results suggest a role of the pertussis toxin-sensitive GTP-binding protein in transducing angiotensin II-receptor occupancy into opening of calcium channel.

Adenosine Diphosphate Ribose↗
PubMed1986

Direct demonstration of adrenocorticotropin-induced changes in cytoplasmic free calcium with aequorin in adrenal glomerulosa cell.

Effects of adrenocorticotropin (ACTH) on cytoplasmic free calcium concentration, [Ca2+]c, have been measured in adrenal glomerulosa cells using a calcium-sensitive photoprotein, aequorin. ACTH causes a rapid and transient increase in [Ca2+]c. Dose response study demonstrates that 1 pM ACTH induces an elevation of [Ca2+]c and that effect of ACTH appears to be saturated at 100 pM. ACTH action is greatly inhibited but not abolished by removal of extracellular calcium and is completely blocked in medium containing no added calcium and 1 mM EGTA. Under similar conditions, angiotensin II induces a remarkable rise in [Ca2+]c. ACTH action is not affected by pretreatment with dantrolene, which considerably decreases angiotensin II action on [Ca2+]c. One micromolar forskolin, which mimics 1 nM ACTH-mediated elevation of intracellular cAMP, does not increase [Ca2+]c nor modulates changes in [Ca2+] induced by a low dose of ACTH. One hundred micromolar forskolin or 1 mM 8-bromo-cAMP, however, increases [Ca2+]c even in calcium-free medium containing 1 mM EGTA. When glomerulosa cells are co-loaded with aequorin and quin2, angiotensin II-induced change in aequorin signal is greatly reduced, and ACTH-induced change is abolished. Quin2 loading results in accumulation of calcium in the cell under both unstimulated and stimulated conditions. These results indicate that ACTH increases [Ca2+]c by cAMP-independent mechanism, that ACTH action on [Ca2+]c is exclusively dependent on extracellular calcium, and that quin2 is unable to detect the rapid change in [Ca2+]c because of its calcium chelating activity.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1986

Phorbol ester inhibits angiotensin-induced activation of phospholipase C in adrenal glomerulosa cells. Its implication in the sustained action of angiotensin.

The present study was undertaken to determine whether an agonist-induced activation of C-kinase leads to an inhibition of phospholipase C in adrenal glomerulosa cells. When cells are treated with 100 nM-TPA (12-O-tetradecanoylphorbol 13-acetate), subsequent angiotensin ('angiotensin II')-induced aldosterone secretion is greatly inhibited. Treatment with TPA completely inhibits the angiotensin-induced increase in both inositol trisphosphate and the cytosolic Ca2+ concentration. The dose-response curve for TPA-induced inhibition reveals that quite a high concentration of TPA is necessary to block angiotensin action compared with that needed to stimulate aldosterone secretion. 1-Oleoyl-2-acetylglycerol has a weak inhibitory effect, whereas neither 4 alpha-phorbol 12,13-didecanoate or 4 beta-phorbol inhibits angiotensin action. When the time course of changes in inositol trisphosphate and diacylglycerol is measured, angiotensin action is sustained for up to 30 min. In addition, 100 nM-TPA added after 20 min of angiotensin addition attenuates production of both inositol trisphosphate and diacylglycerol. These results suggest that high dose of TPA inhibits angiotensin-induced activation of phospholipase C by acting, at least partly, on C-kinase, but that an inhibitory effect of TPA may be a pharmacological effect with little physiological significance in this system.

Adrenal Cortex↗