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Biomedical subjects

S Fukuchi

Publications and source records attributed to S Fukuchi.

At least 127 records · Page 7Linked to original sources
PubMed1987

Efficacy of sucralfate in the prevention of recurrence of peptic ulcer--double blind multicenter study with cimetidine.

A double blind, multicenter, six-month maintenance study was performed to assess the efficacy and safety of sucralfate (S), cimetidine (C), and their combination (S + C) in the prevention of peptic ulcer recurrence in a six-month observation period. 127 patients with gastric ulcer (GU) (group S: 39, group S + C: 48, group C:40) and 103 patients with duodenal ulcer (DU) (group S: 35, group S + C: 36, group C:32) were available for statistical analysis. Six to 12 months after healing of GU, the cumulative recurrence prevention rates by Kaplan-Meier method were 89.7----80.3% in group S, 97.6----72.6% in group S + C, 84.5----44.6% in group C. In duodenal ulcer they were 75.9----41.9% in group S, 87.8----47.7% in group S + C, 80.8----40.5% in group C. These results indicate that maintenance therapies of S and S + C are effective and safe for the prevention of gastric ulcer recurrence.

Adult↗
PubMed1987

Treatment of pheochromocytoma with dilevalol.

Dilevalol, an alpha- and beta-blocking agent, has been evaluated in two patients with pheochromocytoma. Dilevalol could be a useful agent for the treatment of pheochromocytoma, especially for the adrenaline-dominant type.

Administration, Oral↗
PubMed1986

Biochemical evidence for existence of immunoreactive renin in human prolactinoma tissue.

High activity of renin was demonstrated in human prolactinoma tissue. This activity was almost completely inhibited by specific antibody raised against human renal renin, indicating that it was not due to the nonspecific action of proteases. The specific activity of renin was 5.04 ng of angiotensin I generated/mg of protein per h, comparable to that of the pituitary tissue prepared from postmortem human subjects. The biochemical properties of the prolactinoma renin were generally similar to those of well-known kidney enzyme, such as molecular mass (Mr = 46,000), optimum pH (6.0), and glycoprotein nature. However, the isoelectric points (pI) of the prolactinoma renin (pI = 4.90, 5.04, 5.24 and 5.41) differed somewhat from those of plasma and kidney renins reported hitherto. These results indicate that true renin can be produced in human prolactinoma tissue.

Chromatography, Affinity↗
PubMed1986

[Increased activity of sympatho-adrenomedullary system and decreased renal dopamine receptor content after short-term and long-term sodium loading in rats].

UNLABELLED: We investigated the effects of short-term and long-term sodium loading on the sympathoadrenomedullary system and renal dopamine receptor. Male Wistar rats (n = 30) were raised drinking 1% NaCl for four weeks. Urinary norepinephrine and epinephrine excretion (UNE and UE) were measured before and 1, 2, 4 weeks after sodium loading by the use of high pressure liquid chromatography with fluorescence spectrophotometer. Renal plasma membranes were prepared by the ultracentrifugation method, and maximal binding capacity (Bmax) and dissociation constant (Kd) of renal dopamine receptor were determined by Scatchard analysis using 3-H-spiperone. RESULTS: Sodium loading caused a slight but not significant decrease of free UNE after 1 and 2 weeks then clear increments of total (free + conjugated) UNE, free UE and total UE after 4 weeks. Bmax of renal dopamine receptor did not change after 1 and 2 weeks but significantly decreased after 4 weeks (before: 535.9 fmol/mg X protein, after 4 weeks: 327.2 fmol/mg X protein). Kd of renal dopamine receptor slightly elevated 1 week after sodium loading and then returned to the initial level. CONCLUSION: These data suggest that short-term sodium loading may suppress the sympathetic activity, but long-term sodium loading may increase the activity of the sympathoadrenomedullary system with the decrease of renal dopamine receptor concentration. Increased catecholamines and decreased renal dopamine after long-term sodium loading may contribute to sodium-dependent hypertension.

Adrenal Medulla↗
PubMed1986

Demonstration and characterization of angiotensin-converting enzyme in human pituitary tissue.

High activity of angiotensin-converting enzyme was demonstrated in human pituitary tissue. This activity required the presence of chloride ion and was almost completely inhibited by a specific converting enzyme inhibitor captopril (10 nM), indicating that the activity measured is indeed angiotensin-converting enzyme. The specific activity of the enzyme was 1.68 +/- 1.20 nmol hippuric acid generated mg of protein-1 min-1 (mean +/- SD, for 11 specimens). The biochemical features of the enzyme were closely related to the well-characterized human lung converting enzyme, such as molecular weight (290,000), optimum pH (8.0-8.5), the presence of glycoprotein residues, and dependence on chloride ion concentration. These results provide definitive evidence for the presence of angiotensin-converting enzyme in human pituitary tissue.

Chlorides↗
PubMed1986

[The effect of metoclopramide and dopamine on mineralocorticoid secretion--in vivo and in vitro studies].

There is considerable information suggesting that dopamine is a physiological regulator of aldosterone secretion. Metoclopramide, a specific dopamine antagonist, elicits a rapid rise in plasma aldosterone independent of the known aldosterone-regulating factors. However, the mechanism and the site of action of metoclopramide, whether adrenal or extra-adrenal, in stimulation of aldosterone production remain to be defined. The present studies were designed to investigate the mechanism of dopaminergic control of corticosteroid secretion and to determine at which step in the aldosterone biosynthetic pathway metoclopramide and dopamine exert their effect. Plasma concentrations of progesterone, 11-deoxycorticosterone (DOC), and cortisol were not altered by a bolus intravenous administration of 10 mg metoclopramide in 8 healthy male volunteers. Metoclopramide increased plasma aldosterone from 6.9 +/- 2.8 (Mean +/- 2SD) ng/100 ml to a maximum level of 18.2 +/- 4.7 ng/100 ml, 18-hydroxycorticosterone (18-OHB) from 12.6 +/- 6.5 ng/100 ml to a maximum of 41.3 +/- 7.3 ng/100 ml and corticosterone from 0.36 +/- 0.09 microgram/100 ml to a maximum of 0.85 +/- 0.22 microgram/100 ml. The aldosterone, 18-OHB and corticosterone responses displayed a parallel time course, with a significant response of each occurring within 5 minutes after metoclopramide administration. These data suggest that metoclopramide may modulate the activities of 18-hydroxylase and 11 beta-hydroxylase. Studies in vitro revealed that metoclopramide (10(-8)-10(-4) M had little effect on basal production of aldosterone, 18-OHB and corticosterone from human adrenal slices. Dopamine (10(-4) M) did not alter the basal secretion of aldosterone, 18-OHB and corticosterone, but suppressed the secretion of these 3 mineralocorticoids by ACTH, which were diminished by addition of 10(-4) M metoclopramide. There was a concentration-dependent inhibitory effect of dopamine on conversion of corticosterone to 18-OHB and DOC to corticosterone in vitro using bovine adrenal mitochondrial fractions. IC50 of dopamine inhibiting 18-hydroxylation and 11 beta-hydroxylation were 7.5 X 10(-7) M and 9.5 X 10(-4) M, respectively. It appears that physiological concentration of dopamine can modulate the activity of 18-hydroxylase enzyme. In summary, it can be concluded that the in vivo and in vitro studies are compatible with a view that dopamine has a physiological role in the regulation of aldosterone by modulating the activity of 18-hydroxylase enzyme.

18-Hydroxycorticosterone↗
PubMed1986

[Role of renal dopamine receptor in the pathogenesis of hypertension after sodium loading].

UNLABELLED: The purpose of this study is to clarify the role of renal dopamine receptor in the pathogenesis of salt-dependent hypertension. Male Wistar rats were raised under three different conditions, control, 1% NaCl loading (NaCl) and 1% NaCl plus metoclopramide with a dose of 1.5 mg/kg daily (MC), for 2 weeks. Then, renal plasma membranes were prepared by ultracentrifugation method, and maximal binding capacity (Bmax) and dissociation constant (Kd) were determined by Scatchard analysis using 3H-spiperone. And plasma aldosterone and prolactin concentration in these three groups were measured by radioimmunoassay. RESULTS: Systolic blood pressure measured tail-cuff method significantly elevated in MC group, but not control and NaCl group. Bmax of renal dopamine receptor was 535.9 +/- 85.0 fmol/mg protein, 594.9 +/- 159.3 fmol/mg protein, 529.1 +/- 166.1 fmol/mg protein, in control, NaCl and MC group, respectively. Kd of renal dopamine receptor in NaCl group was significantly lower than control (p less than 0.05). Renal dopamine contents of NaCl and MC group were lower than control. There was a negative correlation between renal dopamine content and Bmax of renal dopamine receptor in NaCl group (r = -0.95, p less than 0.02). In MC group, plasma aldosterone concentration was slightly higher than control and NaCl group, but there was no differences in plasma prolactin concentration among these three groups.

Aldosterone↗
PubMed1986

Two adult familial cases of selective hypoaldosteronism due to insufficiency of conversion of corticosterone to aldosterone.

A 57-year-old woman (case 1) and her daughter aged 29 (case 2) with hyperkalemia exhibited subnormal plasma aldosterone (ALD) in the face of elevated plasma renin activity. Their physical findings were normal. Their arterial blood gas analysis showed that metabolic acidosis and renal function of these cases were slightly impaired. Urinary 17-OHCS and 17-KS excretions in these cases were normal. Baseline levels of corticosterone (B) and 18-hydroxycorticosterone (18-OH-B) were clearly elevated. Plasma deoxycorticosterone (DOC), B and 18-OH-B as well as cortisol remarkable increased after ACTH injection, but the increase in plasma ALD was very small. Angiotensin II infusion in case 1 resulted in a clear rise in plasma 18-OH-B but in slight depletion of B, and no increase in ALD. 9-alpha-fludrocortisone acetate treatment was performed in case 1. Serum potassium was normalized and blood pressure elevated from 82/52 to 120/78 mmHg. Arterial blood gas analysis was corrected. We concluded that these two cases with subnormal plasma ALD and hyperreninemia may exist as a congenital and familial abnormality of the final step of aldosterone boisynthesis due to the impairment of the conversion of B to ALD.

Adrenocorticotropic Hormone↗