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Biomedical subjects

E Ogata

Publications and source records attributed to E Ogata.

At least 307 records · Page 17Linked to original sources
PubMed1984

Na+,K+-ATPase activity and responsiveness of vascular smooth muscle to norepinephrine, angiotensin II and calcium ionophore A23187 in guinea pig aortic strips.

The functional significance of the Na+,K+-ATPase activity in defining the sensitivity of vascular smooth muscle response to pressor stimuli was studied in guinea pig aortic strips. Subthreshold doses of ouabain (10(-8), 10(-7), 10(-6)M), potentiated the norepinephrine- and angiotensin II-induced contractile responses, dose-dependently. Furthermore, in the presence of subthreshold dose of ouabain (10(-6)M), tension developments were observed with subthreshold doses of norepinephrine and angiotensin II. The mechanism by which subthreshold dose of ouabain potentiated the norepinephrine-induced contractile response was revealed to involve the enhancement both of sensitivity and contractile activity. Ouabain (10(-6)M) potentiated the norepinephrine- and A23187-induced contractile responses, even in the presence of verapamil. These facts indicate that suppression of the vascular Na+,K+-ATPase activity could favor the development of hypertension through potentiating contractile responses to various stimuli and that the potentiation could be a reflection, at least partly, of the decrease in Ca2+-efflux.

Angiotensin II↗
PubMed1984

Propylthiouracil-induced diffuse interstitial pneumonitis.

Cough productive of sputum, exertional dyspnea, and hypoxemia developed in two patients with Graves' disease after six months (patient 1) or three weeks (patient 2) of treatment with propylthiouracil, 300 mg/day. Chest roentgenograms and transbronchial lung biopsy specimens revealed diffuse interstitial pneumonitis. Lymphocyte transformation by phytohemagglutinin was highly stimulated by propylthiouracil. Symptoms and signs improved after cessation of the drug therapy and administration of prednisolone acetate. These cases represent the first report of a complication of diffuse interstitial pneumonitis induced by propylthiouracil.

Aged↗
PubMed1983

Stimulatory effect of prostaglandin E2 on 1 alpha,25-dihydroxyvitamin D3 synthesis in rats.

The effect of prostaglandin E2 on accumulation in plasma of 1 alpha,25-dihydroxy[3H]vitamin D3 from 25-hydroxy[3H]vitamin D3 was studied in vivo using vitamin D-deficient thyroparathyroidectomized rats. Intra-arterial infusion of 10-50 micrograms of prostaglandin E2/h caused a significant stimulation of 1 alpha,25-dihydroxy[3H]vitamin D3 production. No significant changes in plasma Ca2+ and Pi concentrations or urinary cyclic AMP excretion were observed after prostaglandin E2 infusion. Theophylline did not enhance the effect of a submaximal dose of prostaglandin E2 on 1 alpha,25-dihydroxy[3H]vitamin D3 production. These data indicate that prostaglandin E2 stimulates plasma accumulation of 1 alpha,25-dihydroxy[3H]vitamin D3 independent of the adenylate cyclase/cyclic AMP system, and suggest that prostaglandin E2 has a modulatory role in the regulation of 25-hydroxyvitamin D3 1 alpha-hydroxylase in the kidney.

Animals↗
PubMed1983

The rate of cardiac structural protein synthesis in perfused heart.

Synthesis of cardiac structural protein was studied in perfused rabbit hearts using [3H]lysine and perfluorochemical blood substitute. Relative synthesis rate was estimated in adult rabbit heart when both ventricles worked against zero pressure. The decreasing order was troponin complex, actinin complex, myosin, tropomyosin, and actin and was almost the same as that found in an in vivo study. The synthesis rates of myosin B in left and right ventricles were almost equal in hearts without left and right ventricular pressure load. In young rabbit heart with a right ventricular pressure load, an increase in the synthesis rate of right ventricular myosin B was observed along with the concomitant increase in that of left ventricle. As those increases were blocked by neither propranolol nor verapamil, it was suggested that these increases were not mediated by Ca2+ influx or beta-adrenergic receptors.

Actins↗
PubMed1983

Inhibitory effect of [Asu1 . 7]-eel calcitonin on glucagon-induced glycogenolysis in perfused rat liver.

In an attempt to elucidate the mechanism by which calcitonin modulates glucose metabolism, the effect of elcatonin ([Asu1 . 7]-eel calcitonin), a potent synthetic eel calcitonin analogue, on hepatic glycogenolysis was investigated by use of perfused liver from fed rats. Elcatonin, as infused into the portal vein at concentrations between 10 mU/ml and 200 mU/ml did not affect glucose output into the hepatic venous effluent. At concentrations higher than 100 mU/ml, it inhibited the glycogenolysis stimulated by submaximal concentrations of glucagon which was perfused concurrently. This aspect of elcatonin effect was reproduced by synthetic salmon calcitonin. Though elcatonin showed a marked inhibition of the glycogenolytic activity induced by glucagon at or less than 5.7 X 10(-11) M, the inhibitory effect became undetectable when higher concentrations of glucagon were employed. Elcatonin did not inhibit the glycogenolysis induced by dibutyryl cyclic AMP at near (0.5 microM) or less than half-maximally effective (0.2 microM) concentrations. In addition, it did not inhibit the glycogenolytic activity half-maximally stimulated by alpha-adrenergic agonist (phenylephrine, 0.4 microM) or vasopressin (0.2 mU/ml). Elcatonin inhibited the cyclic AMP production of the tissue induced by glucagon infusion. These data indicate that elcatonin modulates hepatic glycogenolysis by preventing the glucagon effect at a step before cyclic AMP production and with an apparently competitive kinetics. In view of the concept that Ca++ is involved in the glycogenolytic effect of alpha-adrenergic agonist and vasopressin, the fact that elcatonin did not influence the action of these agents suggests that Ca++ fluxes are not involved in the elcatonin effect on liver.

Animals↗
PubMed1983

Outcome of patients with Graves' disease after long-term medical treatment guided by triiodothyronine (T3) suppression test.

The value of the T3 suppressed 20-min uptake test for the prediction of post-treatment outcome was studied in 193 unselected patients with Graves' disease treated with thionamide drugs and T3. One hundred and twenty-nine of 193 patients were studied previously and followed thereafter (Group A). Sixty-four were newly treated patients: thirty-three (Group B) were treated at the same hospital as Group A; thirty-one (Group C) were treated at another hospital. In total 126 patients out of 193 satisfied our criteria for suppression (total suppression rate, 65%). The suppression rate for new patients (55% in Group B, 52% in Group C) was similar to that for Group A in 1977 (49%) after comparable duration of treatment. The suppression rate for Group A increased with prolongation of the treatment period (49% in 1977 and 71% in 1981). As to the time course of suppression, it was observed that about two-thirds of the suppressed patients satisfied the criteria for suppression within 3 years of starting treatment. The number of suppressed patients per year decreased thereafter as the treatment periods increased. However, the yearly suppression rate did not decrease with time. The time course of suppression in each patient could not be predicted from the results of initial thyroid function tests. The overall remission rate among the 120 suppressed patients followed for 1-13 (mean, 4) years was 96%, which was almost equal to the value obtained in Group A in 1977 (95%) with the average follow-up period of 2 years. Among the 46 patients in Group A followed for 5-13 (mean, 7) years, no increase in relapse was observed with prolonged follow-up periods. Examination on the relationship between the duration of treatment and the post-treatment outcome revealed that, as a whole, the duration of treatment for the patients with relapse were rather short as compared with those for the patients in remission. These results confirm the usefulness of our T3 suppression test for predicting sustained remission of Graves' disease after treatment, and clearly indicate that long-term medical therapy could increase the number of remissions in patients with Graves' disease.

Adolescent↗
PubMed1982

[Diagnostic criteria for pseudohypoparathyroidism and related diseases].

In order to make a statistical survey of Japanese patients with pseudohypoparathyroidism and related diseases, we defined the diagnostic criteria for seven disease states described below. The criteria were mainly based on practical data readily available at standard hospitals. In the text, the seven diseases are described separately in the order of a) definition or conception, b) pathophysiology, c) proposed diagnostic criteria, d) comments on the diagnostic criteria. The diseases are (1) Pseudohypoparathyroidism Type I, (2) Pseudohypoparathyroidism Type II, (3) Pseudohypo-hyperparathyroidism, (4) Pseudopseudohypoparathyroidism, (5) Pseudoidiopathic hypoparathyroidism, (6) Vitamin D dependency type I and (7) Hypophosphatemic vitamin D resistant rickets. Based on these diagnostic criteria, a nation-wide investigation on patients with these diseases was performed (The detailed report will appear in a separate paper). The results indicated that these criteria are of considerable value in establishing diagnoses from questionnaires answered by practicing physicians.

Calcium↗
PubMed1982

Involvement of endogenous digitalis-like substance in genesis of deoxycorticosterone-salt hypertension.

In an attempt to evaluate the role of endogenous digitalis-like substance in the genesis of deoxycorticosterone (DOCA) -salt hypertension, the effects of intravenous anti-digoxin antibody on the blood pressure response were observed in male Wistar rats that underwent heminephrectomy followed by treatment with DOCA and saline. Administration of anti-digoxin antibody caused a marked decrease in the blood pressure which continued for about an hour. Such a change in the blood pressure was not observed in pertinent control animals. Thus, it seems that endogenous digitalis-like substance plays an important role in the genesis of DOCA-salt hypertension.

Animals↗
PubMed1982

Sources of calcium mobilized by alpha-adrenergic stimulation in perfused rat liver.

The glycogenolytic effect of catecholamine has been proposed to be mediated by calcium ions mobilized mainly from mitochondria. In this study, the contribution of mitochondria as a source of the mobilized calcium was evaluated by use of perfused rat livers. Phenylephrine-induced efflux of 45Ca from 45Ca preloaded liver was abrupt and transient, and almost ceased within 5 min. The perfusion with 5 microM phenylephrine for 5 min caused a significant decline in the content of 45Ca retained in the liver homogenate; control, 0.97 +/- 0.11 nmol of 45Ca/mg protein (mean +/- SEM) and phenylephrine, 0.41 +/- 0.08 nmol of 45Ca/mg protein (P less than 0.01), when calculated from the specific radioactivity of calcium in the perfusate used for loading perfusion. The contents of 45Ca in mitochondria isolated subsequently from the homogenate were 0.43 +/- 0.07 nmol/mg protein in controls and 0.22 +/- 0.03 nmol/mg protein (p less than 0.05) when phenylephrine was administered. Taking into consideration that mitochondrial protein is a fraction of homogenate protein, it is obvious that the decline in mitochondrial 45Ca represents only a small portion of the total reduction of radioactivity in the homogenate. In a series of experiments in which various perfusion periods were employed for 45Ca loading and for washing-out, it was found that phenylephrine induced 45Ca efflux also from a pool with a calcium turnover rate slower than that if mitochondria. These results suggest that alpha-adrenergic stimulation enhances release of calcium not only from mitochondria but also from other compartments with a slower turnover rate. The probability of plasma membrane is proposed as the other source of calcium released in response to alpha-adrenergic stimulation.

Animals↗
PubMed1982

Paradoxical response to parathyroid hormone of renal handling of phosphate in hyperparathyroid rats.

The effect of PTH given as a bolus on renal handling of phosphate in rats was studied by a perfusion balance study method. In vitamin D-fed rats, iv PTH as a bolus (10 USP units) elicited a phosphaturic response and an increase in urinary cAMP, whether or not the rats were thyroparathyroidectomized. When given to thyroparathyroidectomized rats receiving continuous infusion of PTH (2.5 USP units/h) for 16 h, PTH led to a paradoxical decline of phosphate clearance in spite of an increase in urinary cAMP. Vitamin D-deficient intact rats also showed this paradoxical response. Vitamin D-deficient thyroparathyroidectomized rats showed an ordinary phosphaturic response. When PTH had been supplied continuously (2.5 USP units/h) to these rats, the PTH bolus again produced the paradoxical response. Phosphate supplementation did not restore the phosphaturic response. (Bu)2cAMP infusion reproduced the paradoxical effect in vitamin D-fed, thyroparathyroidectomized rats receiving continuous infusion of PTH. These data indicate that a long-lasting excess of circulating PTH alters the nature of the response of the kidney to an iv bolus of PTH, so that PTH leads to a paradoxical decline of phosphate clearance, and that the mechanism responsible for the paradox may lie in a step (or steps) subsequent to cAMP production.

Animals↗
PubMed1982

Isolated adrenocorticotropin deficiency associated with polyglandular failure.

A female patient presented with isolated ACTH deficiency and diabetes mellitus. During the course of a year's replacement with hydrocortisone, goiter developed, which, on biopsy, was diagnosed as typical Hashimoto's thyroiditis. Four years later, she experienced tetany, and the diagnosis of idiopathic hypoparathyroidism was made. Immunological studies revealed the presence of antithyroid antibodies in the serum and cell-mediated immunity to the thyroid and parathyroid. These data strongly suggest that the autoimmune process is involved in the genesis of some, though not all, forms of isolated ACTH deficiency.

Adrenocorticotropic Hormone↗