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Biomedical subjects

E Ogata

Publications and source records attributed to E Ogata.

At least 325 records · Page 18Linked to original sources
PubMed1982

A case of pituitary adenoma with possible simultaneous secretion of thyrotropin and follicle-stimulating hormone.

A TSH- and FSH-screening pituitary adenoma was demonstrated in a 23-yr-old man who presented with bitemporal hemianopsia, but without clinical or laboratory evidences of hyper- or hypothyroidism or hypogonadism. Basal TSH (29-45 microunits/ml) and FSH (44-63 mIU/ml) were moderately elevated. GH and ACTH secretion were impaired, and basal PRL and testosterone were normal. TRH and LRH elicited a significant increase in TSH and FSH, respectively. The plasma glycoprotein alpha-subunit concentration was normal, and its response to simultaneous administration of TRH and LRH was low. Plasma TSH was not suppressed completely by exogenous T3. After operation and radiotherapy, elevated TSH and FSH as well as failure of T3 to suppress TSH were corrected. No significant changes in thyroid hormone concentration in the blood were detected in spite of the reduction of TSH. TSH and FSH concentrations in the tumor extract were lower than those in normal pituitaries. Histologically, the tumor was very vascular and consisted mostly of a single type of cell. The tumor cells were positively stained for FSH beta-subunit by immunohistochemical study, but for none of other pituitary hormones or subunits examined. Electron microscopic examination revealed relatively abundant single type secretory granules of high electron density. It is possible that the tumor simultaneously secreted TSH and FSH, the former possibly being immunologically active, but biologically inactive.

Adenoma↗
PubMed1982

Involvement of calcium in calcitonin induced stimulation of glycolysis in rat kidney in situ.

The effects of intravenous salmon calcitonin on tissue carbohydrate and redox metabolism were studied in rat kidney in situ and were compared to the effects of EGTA infusion. Calcitonin (0.8 MRC U, in bous) caused, after 10-20 min, a reductive shift of the cytosolic NAD redox pair, and an oxidative shift of the mitochondrial NAD redox pair. It also caused a stimulation of glycolysis with the cross-over between phosphoenolpyruvate and pyruvate. These results were reproduced by treatments of hypocalcemia with EGTA or with thyroparathyroidectomy. Most of the effects were opposite in direction to the reported effects of CaCl2 and parathyroid hormone. The above results suggest that in kidney calcitonin causes a stimulation of pyruvate kinase, and/or inhibition of phosphoenolpyruvate carboxykinase, and that the effects are related to changes in the intracellular calcium.

Animals↗
PubMed1982

Reversal by a dopamine antagonist of saline-induced attenuation of aldosterone response to angiotensin II infusion in man.

In an attempt to elucidate the dopaminergic involvement in the regulation of the effect of angiotensin II on the adrenals, plasma aldosterone response to angiotensin II infusion (5 ng/kg/min, for 60 minutes) was studied in five normal volunteers in various experimental conditions. Prior infusion of dopamine (3 micrograms/kg/min) or saline (1000 ml/hour) caused an attenuation of the aldosterone response to angiotensin II. Concurrent infusion of a dopaminergic antagonist, metoclopramide (10 micrograms/kg/min), abolished the inhibitory effect of dopamine and saline. These results suggest that the dopaminergic mechanism is involved in the adaptive aldosterone response of the adrenal to acute saline loading in man.

Adult↗
PubMed1982

Effects of testosterone and estradiol on serum somatomedin A and growth rate of rats.

The mode of involvement of sex steroids in the growth spurt during adolescence was studied in Wistar rats with a special reference to the level of serum somatomedin A (SMA) determined by radioreceptor assay. Intramuscular administration of testosterone propionate (T; 1 mg/day, alternately for 10 days) to female or gonadectomized male rats provoked a small but significant increase in their body weight or body length without affecting the serum SMA level. In contrast, in hypophysectomized (hypox) male rats T caused a considerable increase in body weight and the serum SMA level only when administered concurrently with bovine growth hormone (bGH; 0.2 U/day, ip). T did not affect the sulfation activity in vitro. These results suggest that androgen participates in the growth spurt during adolescence by enhancing the SMA effect and/or potentiating the SMA production by GH. Estradiol benzoate (E2; 100 micrograms/day, alternately for 10 days) caused a decrease in the serum SMA level and the growth rate in normal male rats. However, E2 produced an increase in the SMA level when administered to hypox male rats, although the growth was retarded and sulfation potency of the serum was sharply reduced. These results indicate that E2 may suppress the growth by lowering SMA generation in normal rats and cause a production of biologically inactive SMA in hypox male rats.

Animals↗
PubMed1982

Effects of bovine parathyroid extract and [Asu1,7]-eel calcitonin on 35S incorporation into chick embryonic cartilage.

35S incorporation into embryonic chick pelvic cartilage was measured using the method of somatomedin bioassay and the effects thereupon of the bovine parathyroid extract (PTE) and the synthetic [Asu1,7]-eel calcitonin (CT) were examined. Bovine PTE potentiated 35S incorporation stimulated by normal human serum. [Asu1,7]-eel CT did not affect the sulfation activity in the presence of normal human serum. However, it showed a slight stimulation of 35S incorporation in the absence of normal human serum. No definite interaction on 35S incorporation between PTE and CT was observed. It is speculated from these results that PTH may be involved in the stimulation of the cartilage growth in concert with somatomedins in vivo.

Animals↗
PubMed1982

Factitious Bartter's syndrome induced by surreptitious intake of furosemide.

Studies on the electrolyte metabolism and the renin-angiotensin-aldosterone system were made in a 47-year-old female patient with factitious Bartter's syndrome induced by surreptitious use of furosemide. The diagnosis was confirmed later by detection of the diuretic in the urine. In metabolic studies patient exhibited abnormalities similar to those reported in Bartter's syndrome; viz, hypokalemic alkalosis, blunted response to exogenous angiotensin II, which reverted to normal by volume expansion with an albumin solution, and diminished fractional free water clearance per fractional distal sodium delivery. The above data, along with the known pharmacological effects of furosemide, suggest that the abnormality in Na+ or Cl- reabsorption in the ascending limb of Henle's loop is a primary cause of Bartter's syndrome.

Absorption↗
PubMed1982

Inhibition by calcium channel blockers of the glycogenolytic effect of glucagon in perfused rat liver.

Verapamil and diltiazem, calcium channel blockers, inhibited significantly the glucagon-induced glucose output and 45Ca efflux from perfused rat liver at concentrations higher than 50 microM when the perfusate contained calcium. Although the blockers partially interfered with glucagon-induced elevation of cyclic AMP in the tissue, they also inhibited the effects of cyclic AMP. The blockers did not show the inhibitory effects in the absence of perfusate calcium. However, the inhibition of calcium influx into hepatocytes by omission of extracellular calcium or addition of EGTA did not interfere with these effects of glucagon and cyclic AMP. In the presence of extracellular calcium, the blockers did not inhibit cyanide-induced glucose output, indicating that the activity of glycogen phosphorylase and later processes leading to glucose output were not affected by the blockers. These data suggest that, in the presence of calcium, the blockers inhibit the effect of glucagon also at a step (or steps) subsequent to cyclic AMP production and before the activation of phosphorylase b, probably by inhibiting glucagon-induced mobilization of calcium from intracellular calcium pools rather than inhibiting calcium influx into hepatocytes.

Animals↗
PubMed1982

Metabolism of cardiac structural proteins in normal and hypertrophied rabbit heart.

In an attempt to elucidate the characteristics of the metabolic response of the hypertrophying heart, the rates of amino acid incorporation into cardiac structural proteins were studied in female rabbit hearts in vivo by use of a pulse-label isotope (3H-lysine) method. Hypertrophy of the left ventricle was produced by applying mild aortic constriction. Structural proteins were separated from the heart excised 24 h after the pulse, and the rate of 3H incorporation was calculated as cpm. 3H/mg lysine of the protein. In the control (without aortic constriction), left ventricular structural proteins exhibited the following relative incorporation rate (the rate in actin being taken as 1.0): native tropomyosin, 2.79 +/- 0.38 (mean +/- SE, n = 5); 10S-actinin and alpha-actinin complex, 2.52 +/- 0.29; heavy chain of myosin, 2.09 +/- 0.25; light chain of myosin, 1.82 +/- 0.28; soluble protein, 1.79 +/- 0.30; and actin, 1.0. In the rabbits with aortic stenosis the rates of amino acid incorporation showed a striking increase up to 7 days after surgery, and declined to the control level by 1 month. Among the protein fractions, native tropomyosin and the light chain of myosin showed a much higher rate of isotopic incorporation during the earlier phase of the response. These results seem to indicate the presence of a unique pattern of metabolic response in cardiac muscle confronted with a workload.

Amino Acids↗
PubMed1982

Application of newly synthesized 1-34 human parathyroid hormone for diagnostic tests.

1-34 human parathyroid hormone (1-34 hPTH) was synthesized by a liquid-phase method and prepared for clinical use (specific activity, 3281 U/mg). With this preparation, the toxicity was studied in 22 normal volunteers and the metabolic effects in 15 individuals. Intradermal administration of 4 ng of 1-34 hPTH caused neither abnormal local skin reactions nor toxicity in terms of subjective and objective parameters. When administered intravenously at doses of from 2 to 20 microgram as a bolus, the preparation caused no acute or subacute toxicity judging from the results of various clinical and laboratory studies, except for transient mild hypotension and headache in a minority of subjects. For diagnostic use, 20 microgram of 1-34 hPTH administered intravenously was found to produce effects almost equivalent to those of 200 USPU U of Parathormone (PTE, Eli Lilly). Thus, the criteria for differentiation of hypoparathyroidism from pseudo-hypoparathyroidism devised with 2000 USP U of PTE as a test substance was found to be applicable when 20 microgram of 1-34 hPTH was utilized.

Animals↗
PubMed1981

Evidence for acute inhibitory effects in vivo of 1 alpha-hydroxycholecalciferol on parathyroid hormone secretion in rats.

In an attempt to elucidate the influence of 1 alpha-hydroxycholecalciferol (1 alpha OHD3) on parathyroid hormone (PTH) secretion, sequential measurements were made of 1) serum calcium and urinary excretion of cAMP in conscious perfused rats, and 2) serum calcium in nephrectomized rats; also, the effects of a single iv injection of 1 alpha OHD3 on these parameters were examined. In conscious perfused rats, 6.25 micrograms/kg (15 nmol/kg) 1 alpha OHD3 reduced the urinary excretion of cAMP (approximately 40% of the initial value; P less than 0.05), which reached a level compatible with that of parathyroidectomized rats at 4 h; this fall was sustained for 24 h. Serum concentrations of calcium (total and ionized) did not change at 6 h, and increased at 24 h. In parathyroidectomized rats which were continuously infused with bovine PTH (0.75 U/h), the vitamin D preparation had no significant effect on the urinary excretion of cAMP. Nephrectomy, followed by an injection of the vehicle (0.05 ml 99.5% ethanol), induced a transient hypercalcemia (13.12 +/- 0.39 mg/dl at 6 h). This hypercalcemic response was prevented by prior parathyroidectomy. Injections of 1.25 and 6.25 micrograms/kg 1 alpha OHD3 caused a significant suppression of the hypercalcemia (P less than 0.05 and P less than 0.1, respectively) in the presence of parathyroid glands, whereas a dose-related hypercalcemic effect was observed in their absence. These results suggest that in rats, 1 alpha OHD3, either directly or most probably after conversion into 1 alpha, 25-dihydroxycholecalciferol, 1) acutely inhibits PTH secretion without causing a significant rise in serum calcium, and 2) suppresses PTH secretion in secondary hyperparathyroidism induced by nephrectomy.

Animals↗
PubMed1981

Refractoriness to phosphaturic action of parathyroid hormone occurring independent of phosphate depletion in hyperparathyroid rats.

In an attempt to clarify the underlying mechanism(s) in the disappearance of phosphaturic response to bolus parathyroid hormone (PTH) in hyperparathyroid patients, the effects of bolus bovine PTH (10 USP U) were studied in conscious thyroparathyroidectomized (T . PTX) male Wistar rats that had been infused with a dose of PTH (2.5 U/hr, for 16 hours) so as to reproduce hyperparathyroidism. These animals responded with an increase in urinary cyclic AMP, but without an increase in renal clearance of phosphate. The loss of phosphaturic response was not prevented by pretreatment with actinomycin D at a dosage close to full toxicity (0.1 mg/kg BW, ip, for 3 days). Actinomycin D at this dosage did not affect the normal stimulatory effects of bolus PTH on urinary cyclic AMP and renal clearance of phosphate in T . PTX rats. The continuous infusion of PTH produced nearly maximal phosphaturia throughout in the face of a significant depletion of phosphate. In addition, pretreatment with actinomycin D did not cause a further increase in urinary phosphate excretion during the infusion. These results, along with the report of Shah et al. (1979) indicating that the development of antiphosphaturic adaptation to acute phosphate depletion was prevented by comparable amounts of actinomycin D, indicate that the disappearance of phosphaturic response to bolus PTH by prior PTH infusion simply signifies the continuation of maximal phosphaturic response to the preceding PTH infusion. It is also suggested that the continuous action of PTH prevents, at least phenomenologically, the development of the gene-activation-mediated refractoriness to PTH or antiphosphaturia induced by acute phosphate depletion.

Animals↗
PubMed1981

Inhibitory effects of 1 alpha, 25-dihydroxycholecalciferol on parathyroid hormone secretion in rats.

In an attempt to study the influence of vitamin D metabolites on PTH secretion, serum calcium and urinary excretion of cAMP were sequentially measured in conscious perfused rats, and the effects of a single iv injection of the metabolites on these parameters were examined. Four hours after the administration of 0.25 microgram/kg (0.6 nmol/kg, probably a physiological dose) of 1 alpha, 25-dihydroxycholecalciferol [1 alpha, 25 (OH)2D3], the urinary excretion of cAMP decreased to a level compatible with that of parathyroidectomized rats (approximately 60% of the initial value; P less than 0.05) and this level was sustained for nearly 24 h. Serum concentrations of calcium (total and ionized) did not change. In parathyroidectomized rats which were continuously infused with bovine PTH (1 U/h), the vitamin D metabolite had no significant effect on the urinary excretion of cAMP. 24 R, 25-dihydroxcholecalciferol (12.5 microgram/kg) had no significant effect either on the urinary excretion of cAMP or on serum calcium. These results suggest that in rats, a physiological dose of 1 alpha, 25(OH)2D3 inhibits PTH secretion without causing a significant rise iu serum calcium, reflecting a feed-back mechanism between active vitamin D metabolite, 1 alpha, 25(OH)2D3 and the parathyroid glands.

24,25-Dihydroxyvitamin D 3↗