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Biomedical subjects

T Saruta

Publications and source records attributed to T Saruta.

At least 505 records · Page 28Linked to original sources
PubMed1984

Aldosterone and other mineralocorticoids in Bartter's syndrome.

Plasma levels of aldosterone and other mineralocorticoids were determined in six patients with Bartter's syndrome. In spite of a remarkable elevation of plasma renin activity, the plasma aldosterone and 18-hydroxycorticosterone levels varied in each patient. These levels were slightly increased in three of the six patients, almost normal in two patients, and slightly reduced in one patient. The plasma deoxycorticosterone and corticosterone levels were within the normal range in all patients. The responses of plasma aldosterone to infusion of angiotensin II were reduced in all patients. Plasma aldosterone and 18-hydroxycorticosterone significantly increased with supplement of potassium, and the responses of plasma aldosterone to infusion of angiotensin II were also improved after supplement of potassium. Our results suggest that plasma aldosterone in Bartter's syndrome is dependent on potassium balance, even though plasma renin activity is remarkably increased, and that hyperaldosteronism is not an inevitable finding in Bartter's syndrome.

18-Hydroxycorticosterone↗
PubMed1984

[The immunohistological study of developing human spinal cord--the localization of vimentine, GFAP in radial glial cell].

The morphological changes of radial glial cells in developing human spinal cord have been studied immunohistologically. The specimens extracted from developing human spinal cords, gestational age of 15 weeks, 30 weeks and 35 weeks, were prepared with cryostat for the investigation of anti vimentin mouse monoclonal antibody and of GFAP rabbit serum. We have stained the specimens for vimentin in accordance with ABC method, for GFAP in accordance with PAP method. On gestational age of 15 weeks, the fibers radially oriented from the central canal to pial surface were positive for vimentin and GFAP. Partially, early differentiated astrocytic cells were found. On gestational age of 30 weeks, radially oriented fibers were positive for vimentin and GFAP. They took more tortuous course, branching than those of 15 weeks. More differentiated astrocytic cells were found. On gestational age of 35 weeks, the staining for vimentin was very weak on radially oriented fibers and these fibers were more tortuous, branching than those of 30 weeks. More differentiated astrocytic cells than those of 30 weeks were found in rich amount. From results above, we concluded: 1) Radial glial cells in developing human spinal cord were positive for vimentin and GFAP. 2) The show weaker staining for vimentin in process of gestational age. 3) They differentiate to astrocyte. 4) They appear in earlier stage than suggested by previous reports.

Astrocytes↗
PubMed1983

Urinary prostaglandin E2 and kallikrein excretion in glucocorticoid hypertension in rats.

1. Oral administration of dexamethasone (about 2.5 X 10(-7) mol/day) caused hypertension in rats. The blood pressure rose from 108 +/- 6 (mean +/- SD) to 156 +/- 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. In this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein-kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

Aldosterone↗
PubMed1983

Effect of metoclopramide on the secretion of aldosterone and other adrenocortical steroids.

The aim of this study was to determine the effect of metoclopramide, a dopamine antagonist, on the secretion of aldosterone and other adrenocortical steroids in normal subjects. An i.v. bolus injection of 10 mg of metoclopramide significantly increased the plasma PRL, plasma aldosterone and 18-hydroxycorticosterone, but the plasma renin activity, plasma deoxycorticosterone, corticosterone and cortisol remained unchanged. The changes in plasma aldosterone induced by metoclopramide were significantly correlated with the basal levels of plasma aldosterone and renin activity. These results suggest that the response of plasma aldosterone to metoclopramide in normal subjects is influenced by the basal activity of renin-angiotensin-aldosterone system and the late step of aldosterone synthesis is stimulated by metoclopramide.

18-Hydroxycorticosterone↗
PubMed1983

Mechanism of the central effects of dopamine and metoclopramide on aldosterone regulation in the rat.

To investigate the mechanism of the central action of dopamine and its antagonist, metoclopramide, on the regulation of aldosterone, studies were performed in 54 conscious rats with and without bilateral nephrectomy. In normal and sham-operated rats, intracerebroventricular injection of dopamine resulted in a significant suppression of plasma renin activity and plasma aldosterone at 30 min, and intracerebroventricular injection of metoclopramide resulted in a significant elevation of plasma renin activity and plasma aldosterone at 30 min without altering the plasma corticosterone and potassium levels. In bilaterally nephrectomized rats, the plasma renin activity was significantly reduced and it did not respond to dopamine or metoclopramide. In these rats, intracerebroventricular injection of metoclopramide exerted no effect on the plasma aldosterone, but intracerebroventricular injection of dopamine increased the plasma aldosterone slightly. However, this increase was not statistically significant. These findings suggest that the dopaminergic system in the brain is involved in the regulation of aldosterone secretion, mainly with changes in the peripheral renin-angiotensin axis in rats.

Adrenocorticotropic Hormone↗
PubMed1983

In vivo and in vitro effects of metoclopramide on aldosterone secretion in rats.

This study was designed to investigate the effects of metoclopramide, a dopamine antagonist, on in vivo and in vitro aldosterone production in the rat. In addition, we examined the effect of various levels of sodium intake on the response of plasma aldosterone to metoclopramide. Metoclopramide (2-50 mg/kg) was given by ip injection to conscious rats. Metoclopramide induced a dose-related increase in plasma aldosterone, whereas it only increased plasma renin activity at high doses (20 and 50 mg/kg). The response of plasma aldosterone to 10 mg/kg of metoclopramide in the low-sodium group was greater than that in the high-sodium group. Metoclopramide had no effect on aldosterone production in isolated zona glomerulosa cells in vitro.

Adrenal Glands↗
PubMed1983

Effects of intracerebroventricular administration of prostaglandin D2 and angiotensin II on blood pressure in conscious rats.

To evaluate the role of brain prostaglandins in the regulation of blood pressure, we examined the effects of intracerebroventricular injections of prostaglandin D2, angiotensin II and indomethacin on blood pressure in conscious rats. Intraventricular administration of prostaglandin D2, the major prostaglandin synthesized in the rat brain, did not elicit a significant change in blood pressure. On the other hand, intraventricular injection of angiotensin II resulted in an increase in blood pressure in a dose-related manner. However, this central pressor effect of angiotensin II was not affected by intraventricular pretreatment with indomethacin. Indomethacin per se did not induce any change in blood pressure. These results suggest that prostaglandin D2 in the brain does not play an important role in the regulation of blood pressure in conscious rats. It is also suggested that the central pressor effect of angiotensin II is not mediated by prostaglandin biosynthesis in the central nervous system.

Angiotensin II↗
PubMed1983

Effects of angiotensin I converting enzyme inhibitors on the renal excretory function, hemodynamics and renin release in isolated perfused rat kidney.

Direct renal effects of angiotensin I converting enzyme inhibitors (CEIs), captopril, SA446 and MK421, were examined in isolated rat kidneys perfused with a renin-substrate-free medium. Among three CEIs, only captopril induced a significant natriuresis, whereas SA446 and MK421 did not. UKV, renal vascular resistance and creatinine clearance were not affected by any of these CEIs. Renin release from perfused rat kidneys were not influenced by CEIs under the present experimental conditions. These results suggest that among three different types of CEIs, only captopril possesses natriuretic action in the isolated perfused rat kidney and that this action may be independent of its inhibitory action on angiotensin converting enzyme. It is also suggested that these three CEIs themselves do not have a direct effect on the renal vascular bed.

3-Mercaptopropionic Acid↗
PubMed1983

Effect of the intracerebroventricular injection of dopamine on blood pressure in the spontaneously hypertensive rat.

To examine the role of the central dopaminergic system in blood pressure regulation, dopamine was injected into the cerebral lateral ventricles of conscious, unrestrained spontaneously hypertensive rats (SHR), deoxycorticosterone (DOC)-salt hypertensive rats and Wistar-Kyoto normotensive rats (WKY). Intracerebroventricular (i.c.v.) injection of dopamine produced a significant dose-dependent decrease in blood pressure in the SHR as well as in the WKY and DOC-salt hypertensive rats. However, the SHR were significantly more sensitive than were the other 2 groups of rats. In the SHR, this central depressor effect of dopamine was significantly attenuated by pretreatment with i.c.v. metoclopramide, but not by phentolamine, suggesting that central dopamine receptors rather than alpha-adrenoceptors are involved in the mediation of the actions of dopamine in the brain. These results suggest that the central dopaminergic system plays a more important role in the regulation of blood pressure in the SHR than in the WKY and DOC-salt hypertensive rats.

Animals↗
PubMed1983

Prolactin, renin and catecholamines in essential hypertension.

In 40 male patients with essential hypertension less than the age of 36 years, the plasma prolactin (PRL), plasma renin activity (PRA) and plasma catecholamines (noradrenaline (NA) and adrenaline (A)) were determined simultaneously. Those levels were significantly increased compared to the levels in 14 age-matched healthy male control subjects. Furthermore, there were significant correlations between the PRL and plasma NA or PRA (p less than 0.05 in each case), and between the PRA and plasma NA (p less than 0.05). However, no significant relationships were observed between systolic or diastolic blood pressure and PRL, plasma NA or PRA. These findings indicate that the central dopaminergic activity is reduced in a number of young adults with essential hypertension, and that in the patients with the reduced central dopaminergic activity, the peripheral sympathetic activity is stimulated and PRA is also increased probably due to the increased peripheral sympathetic activity, and the possibility exists that such changes are related to the development of hypertension.

Adult↗