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Biomedical subjects

S Morimoto

Publications and source records attributed to S Morimoto.

At least 829 records · Page 46Linked to original sources
PubMed1979

Effects of some anti-rheumatic agents on copper-catalyzed thermal aggregation of gamma globulin.

Gerber has shown that specific anti-rheumatics, D-penicillamine and aurothiomalate, inhibit copper(II)-catalyzed thermal aggregation of human gamma globulin. Various anti-rheumatics were tested for the activity. Steroidal and non-steroidal anti-inflammatory agents were almost ineffective, while a new non-steroidal anti-inflammatory agent, TAI-284 (6-chloro-5-cyclohexyl-1-indancarboxylic acid), was found to be one half as active as aurothiomalate. The structure-activity relationship of TAI-284 derivatives and the mode of action of TAI-284 were investigated.

Anti-Inflammatory Agents↗
PubMed1979

A calcitonin-like action of prostaglandin E1.

The pharmacological effects of PGE1 (6 and 9 days, 2-1,250 micrograms/kg per day subcutaneously) upon the growth and the bone resorption of mammals were studied using the proximal tibia and upper incisor of immature rats along with lead acetate as a time marker, and upon the serum calcium and inorganic phosphorus levels. The following results were obtained. 1. PGE1 hardly affected the body weight or the weight of organs of the rats but apparently inhibited the longitudinal growth of proximal tibia in a dose related manner. 2. PGE1 clearly inhibited not only the longitudinal growth (incisor growth) but also the appositional growth (dentin formation) of incisal dentin. 3. The grade of the inhibitory effect on the growth was in the order of bone growth greater than dentin formation greater than incisor growth. 4. The occurrence of osteoporosis due to a low calcium diet was inhibited by the simultaneous administration of PGE1, the mechanism being considered to be mainly due to the inhibitory effect on the bone resorption. 5. PGE1 lowered the level of serum calcium and the lowering effect was not observed in the thyro-parathyroidectomized rat. From the facts that the above effects were exactly the same as those of calcitonin (1), the possibility that the subcutaneous injection of PGE1 may induce a calcitonin-like action, a part of which may dependent on the calcitonin secretion is suggested.

Animals↗
PubMed1979

Changes of urinary cyclic AMP excretion and plasma parathyroid hormone levels before and after parathyroidectomy in patients with primary hyperparathyroidism.

Urinary cyclic AMP excretion and plasma parathyroid hormone(PTH) levels were examined in three patients with primary hyperparathyroidism before and after parathyroidectomy. Plasma PTH and urinary cyclic AMP in the individual patients decreased in parallel following parathyroidectomy. During surgery there was a statistically significant correlation between PTH levels and cyclic AMP excretion in individual patients. These findings support the claim that the rate of urinary cyclic AMP excretion reflects endogenous PTH activity in patients with primary hyperparathyroidism.

Adult↗
PubMed1979

The resting membrane potential of frog sartorius muscle.

1. The absolute resting membrane potential of the frog sartorius muscle was determined in Ringer solution at 20 degrees C. 2. Membrane potentials were measured with 0.03, 0.1, 0.3, 1.0 and 3.0 M-KCl electrodes; potentials, including the micro-electrode-tip potentials, were -62.4, -75.7, -83.0, -87.7 and -90.7 mV respectively. 3. Membrane potentials were corrected for the liquid junction potentials between the Ringer and KCl solutions, and the myoplasm and the KCl solutions of the micro-electrodes, using the Henderson's liquid junction equation. 4. The cation (U) and anion (V) conductances of the myoplasm were adjusted to give a constant membrane potential after correction for liquid junction potentials. The final values for U and V were 5.6 and 1.3 mmho/cm respectively, resulting in a membrane potential of -93.0 mV. 5. The correction for the liquid junction potential was -2.6 mV when a 3 M-KCl micro-electrode was used.

Animals↗
PubMed1979

Effect of sodium restriction on plasma renin activity and renin granules in rat kidney.

The present study was carried out to procure detailed information on the relationship between chronic sodium restriction and renin content of kidneys at a subcellular level in the rat. Renin granules (RG) were separated by a discontinuous sucrose-density gradient (from 1.2 to 1.7 M) centrifugation. In control rats, RG were mainly recovered in the fractions corresponding to 1.5 M sucrose, whereas most of the mitochondria, lysosomes, and microsomes equilibrated in upper fractions. The RG fraction contained approximately 60% of total granular renin activity. Low sodium intake for 4 wk resulted in a 12.4-fold increase in plasma renin activity and led to a 2.6-fold increase in renin activity of the RG fraction. But in sodium-restricted rats there was no alteration in the distribution pattern of renin activity on sucrose-density gradients, indicating that there was no change in the density of RG. These results provide evidence for increased renin activity in storage granules following chronic sodium restriction.

Acid Phosphatase↗
PubMed1979

Reduced response of plasma aldosterone to acute ACTH stimulation during long-term treatment with spironolactone in essential hypertension.

The response of plasma aldosterone (PA) to ACTH administration (250 micrograms alpha 1-24 ACTH i.m.) before and during treatment with spironolactone (Sp, 75--100 mg/day) for at least 8 months was studied in 11 patients with essential hypertension. These responses were compared with those before and during prolonged treatment with hydrochlorothiazide (Th, 50--75 mg/day), with or without potassium supplement, in 14 hypertensives. PA and plasma cortisol (PC) were determined by radioimmunoassay in which Sp showed minimal cross-reactivity. Both Sp and Th treatments caused similar increases in plasma renin activity accompanied by nearly identical decreases in blood pressure and body weight. PA was also increased by both treatments, but to a significantly greater extent in the Sp-treated group. Serum potassium concentration was increased only by Sp treatment. The response of PA, but not of PC, to acute ACTH stimulation was blunted in the Sp-treated group. That is, the maximal increment of PA above the baseline level was significantly lower during Sp treatment than either before Sp treatment of during Th treatment. These results demonstrate that long-term treatment with Sp can inhibit aldosterone production by acute ACTH stimulation in patients with essential hypertension.

Adrenocorticotropic Hormone↗
PubMed1979

Selective hypoaldosteronism with hyperreninemia in a diabetic patient.

A 62-yr-old diabetic woman exhibited low plasma and urinary aldosterone levels in the face of markedly elevated PRA during the course of nonketoacidotic hyperglycemic precoma with dehydration, hyponatremia, and hyperkalemia, for which she was hospitalized. Studies performed after her recovery from precoma revealed hyperreninemic hypoaldosteronism with normal adrenoglucocorticoid function. While the patient was supine, PRA on a 256-meq sodium intake was at or above the upper limit of the normal range for a 200-meq sodium intake; furthermore, after sodium depletion with furosemide and 4 h of ambulation, PRA markedly increased. No increases in plasma inactive renin were found. Plasma renin substrate concentration was normal. Plasma levels and urinary excretion of aldosterone were low and increased slightly during sodium restriction with insulin treatment, accompanied by hyperkalemia and sodium loss, despite markedly elevated PRA. Repository ACTH administration induced sodium retention and potassium loss with a normal increase in urinary 17-hydroxycorticosteroids. Plasma levels of deoxycorticosterone, corticosterone, and 18-hydroxycorticosterone were normal, while plasma aldosterone was low. Levels of these mineralocorticoids remained unchanged during angiotensin II infusion on both 256-meq and 100-meq sodium intakes. Rapid ACTH administration produced normal increases in plasma deoxycorticosterone and corticosterone but caused a subnormal increase in plasma aldosterone. These results suggest adrenal insensitivity to angiotensin II, possibly a defect in adrenal angiotensin II receptors, as the cause of hypoldosteronism with hyperreninemia in this patient.

Aldosterone↗
PubMed1979

Effects of dimorpholamine on frog sciatic nerve-sartorius preparation.

The present study describes the potentiating effect of dimorpholamine on twitch contraction of skeletal muscle and its mechanism on a cellular basis. Low concentrations (about 2 x 10(-5) g/ml) of dimorpholamine potentiate the twitch contraction of frog sartorius muscle. In relatively high concentrations of 10(-4)--10(-3) g/ml, however, the potentiation was followed by depression. Endplate potential was not affected by the drug. Dimorpholamine depolarized slightly the muscle membrane. The contracture tension vs. membrane potential relationship was hardly affected by the drug in the presence of 2 x 10(-7) M tetrodotoxin. Action potentials recorded from muscle fibers treated with ethylene glycol showed marked and progressive increases in duration during exposure to the drug, and were finally blocked. It was concluded that twitch potentiation caused by dimorpholamine is due to the prolongation of the action potential. A likely molecular mechanism of this drug is discussed in terms of the kinetic model proposed by Adrian et al. (J. Physiol. 208, 607--644, 1970) for the excitable membrane of frog sartorius muscle.

Action Potentials↗