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Biomedical subjects

T Saruta

Publications and source records attributed to T Saruta.

At least 613 records · Page 34Linked to original sources
PubMed1975

Oestrogen hypertension in rats.

1. A large dose of oestrogen elevated the blood pressure in male Westar rats. 2. Plasma renin substrate and renin activity increased significantly but plasma renin concentration was unchanged. 3. The increase in blood pressure induced by oestrogen was significantly reduced by salt loading, plasma renin concentration was suppressed and the increase in plasma renin activity was reduced. 4. The increase in plasma renin activity induced by the increase of plasma renin substrate concentration may play a role in oestrogen-induced elevation of blood pressure.

Animals↗
PubMed1975

The effects of cyclic AMP, theophylline, angiotensin II and electrolytes upon renin release from rat kidney slices.

The effects of cyclic AMP, theophylline, angiotensin II and electrolytes upon renin release were examined by incubation of rat kidney slices. Angiotensin inhibited renin release with increasing concentrations. On the other hand, cyclic AMP and theophylline stimulated it. Calcium also seemed to play an important role in the control of renin release from kidney slices. However, the direct effects of sodium and potassium upon renin release were not conspicuous.

Angiotensin II↗
PubMed1972

Adrenocortical steroidogenesis: studies on the mechanism of action of angiotensin and electrolytes.

The effects of adrenocorticotropin (ACTH), angiotensins I and II, increased potassium, and decreased sodium concentrations upon steroid synthesis were examined by incubation of beef adrenal tissue slices. Angiotensin II shared with ACTH the need for calcium and an inhibition of its effect in the presence of puromycin but differed in not stimulating cyclic adenosine monophosphate (AMP). Angiotensin I was effective in steroidogenesis. The stimulation of aldosterone synthesis by increased potassium concentration was accompanied by an increased level of cyclic AMP and was inhibited in the presence of puromycin. Decreased sodium concentration stimulated aldosterone synthesis but, alone of these stimuli, simultaneously decreased corticosterone levels. It therefore appears that ACTH and potassium stimulate steroidogenesis at an early step in the biosynthetic pathway through the activation of cyclic AMP, whereas the effect of angiotensins I and II involve another mechanism and decreased sodium concentration affects a later step in steroidogenesis.

Adrenal Cortex Hormones↗
PubMed1972

Adrenocortical steroidogenesis: the effects of prostaglandins.

Prostaglandins E(1) and E(2) significantly stimulated the synthesis of aldosterone, corticosterone, and to a lesser degree, cortisol in the outer slices of beef adrenal tissue. PGA, PGF(1a), and PGF(2a) were ineffective.PGE(1) was found to stimulate steroidogenesis in a manner similar to that of adrenocorticotropin (ACTH) in (a) needing calcium, (b) being inhibited by puromycin but not actinomycin D, (c) increasing the levels of cyclic AMP, and (d) not having an additive effect to exogenous cyclic AMP. PGE(1) did not produce an additive effect with either submaximal or maximal amounts of ACTH but did have an additive effect with angiotensin. These results are in keeping with the hypothesis that PGE(1) shares a receptor site on the plasma membrane with ACTH.

Adrenal Cortex Hormones↗