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Biomedical subjects

S Hata

Publications and source records attributed to S Hata.

At least 253 records · Page 14Linked to original sources
PubMed1977

[The renin-aldosterone system in essential hypertension--hypotensive action of beta adrenergic blocking agents and variation of the renin-aldosterone system (author's transl)].

The effect of beta adrenergic blocking agents on the renin release from the kidney and its possible role in the hypotensive effect of these agents were studied in patients with essential hypertension. Oxprenolol induced a significant decrease in systolic blood pressure and PRA, but the correlation between the decrease in blood pressure and the decrease in PRA was not found. When the effect of carteolol, another beta adrenergic blocking agent, was studied, a decrease in blood pressure was obtained, but there was a rise in PRA. These observations suggest that the hypotensive action of beta adrenergic blocking agents does not result from their effects on PRA.

Adrenergic beta-Antagonists↗
PubMed1976

Freeze-etching observations of herpes simplex virus.

Herpes simplex virus isolated from the cheek lesions of a patient was propagated on FL cells. Pellets of infected cells were cryoprotected with glycerol, and processed for freeze-etching. Viral nucleocapsids were observed in the nucleus of FL cells. The cores were observed in three forms. Capsomeres were clearly shown. Release of virus particles from the nucleus and the plasmalemma was more clearly observed. Myeloid figures and lipid droplets were also found. The significance of these findings is discussed.

Capsid↗
PubMed1976

Aldosterone response to hypoglycemia: evidence of ACTH mediation.

Insulin-induced hypoglycemia caused an increase in plasma aldosterone as well as in renin activity and cortisol. After the suppression of the renin-angiotensin system by the prior administration of propranolol, insulin-induced hypoglycemia still caused a significant increase in plasma aldosterone similar to the increase in plasma cortisol, though plasma renin activity was suppressed. Conversely, after the suppression of endogenous ACTH by the prior admininstration of dexamethasone, insulin-induced hypoglycemia failed to induce a rise in plasma aldosterone and plasma cortisol, through plasma renin activity increased. The increase of plasma aldosterone in response to exogenous ACTH was not different with or without the prior administration of dexamethasone. We conclude that ACTH is largely responsible for the increased aldosterone secretion after insulin-induced hypoglycemia.

Adrenocorticotropic Hormone↗
PubMed1976

The effects of dietary sodium on the diurnal activity of the renin-angiotensin-aldosterone system and the excretion of urinary electrolytes.

Diurnal variations of five normal men were tested over three 24 h consecutive periods. The first experiment began at 0900 h after the subjects had fasted for 12 h and a normal sodium diet of about 70-80 mEq was given at 0900 h, 1200h, and 1630 h (total of about 220 mEq of Na). Significant variations in the plasma renin activity (PRA), in the plasma aldosterone (PA), and in the urinary Na and K outputs were found. The second experiment began at 1200 h with the first feeding time at 2100 h after fasting about 24 h and the subjects were given a normal sodium diet as in the first experiment, but with the meals given at 2100 h, 2400 h, and 0430 h. The diurnal variations in PRA, plasma aldosterone, and urinary electrolytes disappeared. From this study, it appears that the diurnal variation in urinary electrolyte excretion is a factor of the diurnal variation in PRA and plasma aldosterone. The diurnal variation in PRA and plasma aldosterone are related to the timing of sodium ingestion.

Adult↗