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Biomedical subjects

T Saruta

Publications and source records attributed to T Saruta.

At least 577 records · Page 32Linked to original sources
PubMed1980

The diuretic effect of piretanide in man.

The effects of 4-phenoxy-3-(1-pyrrolidinyl)-5-sulfamoylbenzoic acid (piretanide), a new loop diuretic, were investigated in five male subjects under the conditions of water load and water restriction. The results of investigations of various parameters indicate that the mode of action of piretanide is similar to that of furosemide. In particular, THC2O and CH2O were markedly reduced after the administration of piretanide, indicating that piretanide acts principally on the ascending portion of the loop of Henle and the distal tubules.

Adult↗
PubMed1979

Central and peripheral effects of bradykinin and prostaglandin E2 on blood pressure in conscious rats.

Bradykinin or prostaglandin E2 (PGE2), when injected intravenously, decreased blood pressure of conscious rats in a dose-dependent manner, while intracerebroventricular injections of bradykinin or PGE2 caused a dose-dependent increase in blood pressure. SQ 14,225, an inhibitor of angiotensin converting enzyme, potentiated the central pressor or peripheral depressor effect of bradykinin. Indomethacin, an inhibitor of prostaglandin synthesis, almost completely inhibited the central pressor effect of bradykinin when injected intraventricularly. Indomenthacin, when injected intravenously, failed to inhibit the peripheral depressor effect of bradykinin, whereas it significantly attenuated the peripheral depressor effect of bradykinin when the angiotensin converting enzyme was inhibited with SQ 14,225. These results suggest that the central pressor effect of bradykinin is mainly mediated by the synthesis of prostaglandins in the central nervous system, while only a small fraction of peripheral depressor effect of bradykinin is, at least in conscious rats, mediated by the synthesis of prostaglandins in the systemic circulation.

Animals↗
PubMed1979

Effects of intracerebroventricular administration of prostaglandins I2, E2, F2 alpha and indomethacin on blood pressure in the rat.

The effects of intraventricularly administered prostaglandins I2 (PGI2), E2 (PGE2), F2alpha (PGF2 alpha) and indomethacin on systemic blood pressure were investigated in conscious rats. PGI2 (1.25--10 micrograms/kg) decreased blood pressure in a dose-related manner, whereas PGE2 (100--1000 mg/kg) dose-dependently increased blood pressure. Both PGF2 alpha (0.31--20 micrograms/kg) and indomethacin (0.625--40 micrograms/kg) had no effects on blood pressure. These results indicate that intraventricular injection of PGI2 or PGE2 can induce significant changes in blood pressure, while endogenous prostaglandins synthesized in the brain seem to play a minor role in direct regulation of systemic blood pressure in the rat.

Animals↗
PubMed1979

Effect of prostaglandin E2 on vascular reactivity to norepinephrine in isolated rat mesenteric artery, hind limb and splenic artery.

The effects of prostaglandin E2 (PGE2) and indomethacin on the vascular reactivity to norepinephrine were tested in three different isolated rat vascular beds (mesenteric artery, hind limb and splenic artery) perfused with the Krebs bicarbonate solution. In these vascular beds PGE2 (0.1-64 ng/ml) or indomethacin (09.1-96 microgram/ml) in the perfusate did not change the basal pressure. In the mesenteric vascular bed and the hind limb, PGE2 dose-dependently potentiated the vascular response to norephinephrine, whereas PGE2 dose-dependently inhibited the vascular response to norepinephrine in the splenic artery. In these three vascular beds indomethacin in the perfusate dose-dependently attenuated the vascular response to norepinephrine. In the mesenteric artery and the hind limb PGE2 restored the effect of indomethacin, but in the splenic artery PGE2 did not restore the inhibitory effect of indomethacin. These results indicate that the modulating effect of exogenously administrated PGE2 on the vascular action to norepinephrine varies in different vascular beds. It is also suggested that the contribution of endogenous PGE2 synthesized in the vascular wall to the vascular reactivity to norepinephrine is, as well as the effect of exogenous PGE2, different in different vascular beds.

Animals↗
PubMed1979

Active and inactive renin in pregnancy and in women on estrogen-containing oral contraceptives.

Total and active renin concentrations (TRC and ARC) were determined in pregnant women and in women on estrogen-containing oral contraceptives to study the variation of plasma renin forms in pregnancy. TRC was already elevated in the first trimester. After that TRC increased consistently reaching the maximum in the third trimester. The ratio of inactive renin concentrations (IRC) to TRC was between 20 and 30% throughout gestation. Therefore, it was supposed that the development of the placenta or the enlargement of the uterus do not affect the ratio of IRC to TRC too much. In women on oral contraceptives in whom plasma renin activity was increased due to elevation of renin substrate, the ratio of IRC to TRC was almost the same as that in normal controls. From these results, it was suggested that the development of the placenta and the enlargement of the uterus do not play an important role in the variation of plasma renin forms, although remarkable changes are observed in the renin substrate and total amounts of renin in pregnancy.

Adult↗
PubMed1979

Central hypertensive actions of angiotensin I, II and III in conscious rats.

The effects of intracerebroventricular administrations of three natural angiotensins, angiotensin I (ANG I 3.8 X 10-11-9.4 X10-10 mol/kg body weight), II (9.6 X 10-12-2.4 X 10-10 mol/kg body weight) and III (2.7 X 10-10 2.5 X 10-9 mol/kg body weight) on systemic blood pressure were investigated in conscious rats. Angiotensin II (ANG II), ANG I and angiotensin III (ANG III), increased blood pressure in a dose-related manner. The order of potency of angiotensins was ANG II greater than ANG I greater than ANG III. The intraventricular administration of a converting enzyme inhibitor (SQ 14225, 6.9 X10-8 mol/kg) abolished the central effect of ANG I, while an angiotensin II analogue ([Sar1-Ala8]ANG II, 1.1 X 10-8 mol/kg) administered intraventricularly inhibited the central pressor effects of these three angiotensins. These results suggest that ANG II is a main mediator of the renin-angiotensin system in the central nervous system.

Angiotensin I↗
PubMed1979

Responses of aldosterone-producing adenomas to ACTH and angiotensins.

To elucidate the control mechanism of aldosterone production in primary aldosteronism, in vivo and in vitro studies were done in 7 patients with aldosterone-producing adenomas. In the in vivo study, plasma aldosterone was stimulated more significantly by (Formula: see text), synthetic ACTH than by angiotensin II or furosemide. Diurnal variations of plasma aldosterone, which were studied in 4 patients, were similar to those seen in normal controls. In agreement with the results in the in vivo study, the in vitro study also revealed ACTH stimulated aldosterone and deoxycorticosterone (DOC) from the adenoma more markedly than angiotensin II or III. There was no adenoma which was more sensitivie to angiotenion II or III than to ACTH. From these results it is considered that changes in plasma aldosterone induced by the exogenous administration of angiotensin II or ACTH in patients with aldosterone-producing adenoma are mainly based on changes in aldosterone production in the adenoma. Furthermore, in patients with an aldosterone-producing adenoma in whom diurnal variations of plasma aldosterone similar to those in normal subjects are observed, responses of aldosterone to angiotensin II are supposed to be less than those to ACTH.

Adenoma↗
PubMed1979

Finger print deposits of the kidney in pure monoclonal IgG kappa cryoglobulinemia.

In a male patient with pure monoclonal IgG kappa cryoglobulin associated with the nephrotic syndrome, finger print deposits were observed in the subendothelial space and mesangial matrix of the kidney by electron microscopy. The structure was similar to a unique tubular crystal structure of IgGl kappa cryoglobulin which was reported by Bogaars et al. [1973] in the serum of a patient with multiple myeloma. It was therefore supposed that the finger print deposits in the kidney of this patient were the precipitation of the monoclonal IgG kappa cryoglobulin in serum.

Cryoglobulins↗
PubMed1978

Renin and the juxtaglomerular apparatus in diabetic nephropathy.

In order to study the role of the renin-angiotensin system in patients with diabetic nephropathy, renin release and the juxtaglomerular apparatus were studied in 17 diabetic patients with proteinuria and in 23 without proteinuria; 8 normal subjects were used for conctrls. Despite hypertension and marked arteriosclerosis, plasma renin activity (supine posture) was normal; however, the renin response to salt restriction and upright posture was less in the diabetic patients with proteinuria than in the controls. Renal renin content, determined at autopsy, was also normal. Examination of the juxtaglomerular apparatus in the diabetic patients with proteinuria revealed hyalinization of the afferent and efferent arterioles in most of the glomeruli and various degrees of destruction of the juxtaglomerular cells. The findings suggest that renin production is not increased in diabetic patients with proteinuria plus marked vascular damage, and that the renin-angiotensin system in patients with diabetic nephropathy apparently does not play an important role in the exacerbation of hypertension or the degree of vascular damage.

Adult↗
PubMed1978

Serum uric acid and the renin-angiotensin system in hypertension.

To study whether the renin-angiotensin system is related to hyperuricemia in hypertension, the serum concentration of uric acid was determined in 96 patients with various types of hypertension and various degrees of plasma renin activity (PRA). In malignant hypertension, both PRA and the serum uric acid level were higher than in essential hypertension; but in primary aldosteronism or desoxycorticosterone-excess hypertension, they were lower than in the essential type. In renovascular hypertension, PRA was higher than in essential hypertension, but the serum uric acid levels were similar. There were no differences in PRA and serum uric acid concentration between Cushing's syndrome and essential hypertension. The serum uric acid level in high-renin essential hypertension was higher than in either the normal-renin or the low-renin type. There was a significant correlation between serum uric acid concentration and PRA in the basal state, and between the change in PRA and the change in serum uric acid induced by administration of furosemide. Apparently the close correlation between the renin-angiotensin system and the concentration of serum uric acid is related to changes in extracellular fluid volume, although an intrarenal effect of angiotensin II cannot be excluded.

Adolescent↗