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Biomedical subjects

T Saruta

Publications and source records attributed to T Saruta.

635 records · Page 36Linked to original sources

Pressor and hormonal responses to intravenous injection of metoclopramide in normotensive and hypertensive patients.

To assess the dopaminergic regulation of blood pressure and the renin-angiotensin-aldosterone system in fourteen essential hypertension (EHT) and six normotensives (NT), intravenous injections of 10 mg of the dopamine antagonist, metoclopramide (MCP), were given. Essential hypertension patients were divided into two subgroups according to the basal values of plasma renin activity (PRA). Plasma prolactin (PRL), aldosterone (ALDO), norepinephrine (NE) and epinephrine (E) in seven high-renin EHT revealed significantly higher basal values than normal- and low-renin EHT. Intravenous injections of MCP caused significant increases in PRL and ALDO but not in NE, E and PRA in all subjects. However, in high-renin EHT the responses of PRL and ALDO were significantly marked compared to other subjects. In spite of these hormonal changes after MCP, blood pressure was unaltered. The present data suggest that "tonic inhibition" of PRL and ALDO by the dopaminergic system is partially regulated by the renin-angiotensin system regardless of the levels of blood pressure.

Adult↗

Takayasu's arteritis with heart failure due to atherosclerosis.

An autopsy case of an elderly man with Takayasu's arteritis and atherosclerosis is presented. Ischemic signs and symptoms including anginal attack were aggravated with activity of arteritis despite administration of prednisolone throughout the entire course. The autopsy revealed severe atherosclerosis over the aorta and its branches, and arteritis in the fibrotic stage in localized area. Vessels of vital organs including heart and kidneys, did not show Takayasu's arteritis but were atherosclerotic. This case highlights the numerous problems encountered in the treatment of elderly patients with vasculitis such as Takayasu's arteritis.

Aged↗

Differential expression of an orphan receptor COUP-TFI and corepressors in adrenal tumors.

Recently, it has been shown that CYP17 gene transcription is activated by SF-1 (Steroidogenic Factor-1) binding to a cyclic AMP-responsive sequence within the promoter region of the gene, whereas it is inhibited by COUP-TF (Chicken Ovalbumin Upstream Promoter-Transcription Factor) binding to the sequence. We have shown that transcriptional repression by COUP-TFI is mediated by corepressors, N-CoR (nuclear receptor corepressor) and SMRT (silencing mediator for retinoid and thyroid hormone-receptor). Therefore, we compared the expression of COUP-TFI, N-CoR and SMRT in non-hyperfunctioning adrenocortical adenomas and normal adrenal glands. We found significantly higher expression of COUP-TFI mRNA in non-hyperfunctioning adenomas (n=5, 227+/-18%) than in normal adrenals (n=5, 96+/-4%). Interestingly, the pattern of N-CoR and SMRT expression was different compared with COUP-TFI expression. These data suggest that COUP-TFI, N-CoR, and SMRT may play a differential role in steroid biosynthesis of non-hyperfunctioning adenomas.

Adenoma↗

The possible role of apoptosis-suppressing genes, bcl-2 and mcl-1/EAT in human adrenal tumors.

The expression levels of bcl-2, mcl-1/EAT, and bax were examined by Northern blot analysis and semi-quantitative RT-PCR method in 25 adrenal tumors, including seven adrenal pheochromocytomas (PHE), seven aldosterone-producing adenomas (APA), four adrenal cortisol-producing adenomas (CS), one deoxycorticosterone-producing adenoma (DOC) and six non-hyperfunctioning adrenal cortical adenomas (NF). Northern blot analysis revealed both bcl-2 and mcl-1/EAT mRNAs in all of the adrenal tumors. The expression levels differed greatly among the tumor samples. Mcl-1/EAT mRNA levels were enhanced in APA and CS compared with those in NF. In contrast, bcl-2 levels in NF were higher than in other tumors. Our results suggest that deregulation of such apoptosis-suppressing genes may contribute to the multistep tumorigenesis of human adrenal tumors and that mcl-1/EAT, one of the bcl-2 family genes, has a different role from that of bcl-2 in such pathways.

Adrenal Gland Neoplasms↗

Dexamethasone hypertension in rats: role of prostaglandins and pressor sensitivity to norepinephrine.

Glucocorticoid hypertension was induced by oral administration of dexamethasone (DX) in male Wistar rats. The mechanism of hypertension was studied by observing the changes in plasma renin activity, urinary excretion of prostaglandin E2 (PGE2), and the pressor response to norepinephrine. Following administration of DX (0.1 mg/day), the blood pressure began to rise within 3 days and reached a plateau on the 5th day (from 108 +/- 2 to 162 +/- 7 mm Hg, mean +/- SE). On the other hand, urine volume and urinary excretion of sodium were increased. In spite of the marked natriuresis and diuresis, the administration of DX resulted in a marked decrease in the urinary excretion of PGE2. This decrease in PGE2 excretion appeared before the blood pressure rose and continued throughout the experiment. Plasma renin activity did not change. The pressor response to norepinephrine was enhanced on the 2nd day of DX treatment, at which time the blood pressure was not yet elevated, and it was further augumented on the 6th day. In the DX-treated rats, the pressor response to norepinephrine was not enhanced by administration of indomethacin, whereas the pressor response was significantly potentiated by indomethacin in control rats. These results suggest that DX-induced hypertension in rats is associated with inhibition of prostaglandin synthesis leading to increased sensitivity in the vascular response to norepinephrine.

Animals↗