Search PubMed⌕ Search

Biomedical subjects

S Shigetomi

Publications and source records attributed to S Shigetomi.

At least 55 records · Page 3Linked to original sources
PubMed1987

[Effects of dopamine and synthetic atrial natriuretic polypeptide on the release of norepinephrine and epinephrine from the adrenal medulla of rats].

We evaluated the effects of dopamine (DA) and synthetic atrial natriuretic polypeptide (ANP) on the release of catecholamines (CA) from the adrenal medulla. Adrenal glands of male Wistar rats were superfused with Ringer's solution saturated with 95%, O2, 5% CO2 by the use of a continuous flow incubation system, and norepinephrine (NE) and epinephrine (E) concentrations in the perfusate were continuously measured by high pressure liquid chromatography with fluorescent reaction. And the effects of DA and ANP on the CA release were evaluated. Next the effects of metoclopramide (MC), dopamine (D2) antagonist, and glucagon were added in the Ringer's solution, and the changes of NE and E in the perfusate were determined. Basal secretion of NE and E were 0.02-0.04 ng/mg.wet weight/min and 0.05-0.1 ng/mg.wet weight/min, respectively. DA remarkably decreased both NE and E release, and the suppressive effect was dependent on DA concentration in the perfusate. MC clearly raised NE and E release as well as glucagon. The increasing effect of MC was perfectly suppressed by 10(-4) M of DA. But the effect of glucagon was not blocked by the same dose of DA. Alpha rANP (10(-5)M) slightly decreased the releases of NE and E from adrenal medulla, and the magnitude of the effect of rANP was smaller than that of DA. MC significantly increased NE and E release even when the adrenal gland was superfused with Ringer's solution containing 10(-5)M of rANP. These data suggest that the release of CA from adrenal medulla may be regulated by DA, and that the receptors specifically binding to DA may exist in adrenal medulla as well as sympathetic presynaps. We concluded that DA (but not ANP) may play an important role in controlling (suppressing) the activity of sympathoadrenomedullary system.

Adrenal Medulla↗
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

[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↗
PubMed1984

[The effects of the angiotensin I-converting enzyme inhibitor, captopril, on serum lipoperoxides level and the renin-angiotensin-aldosterone and kallikrein-kinin systems in hypertensive patients].

In order to evaluate the effect of the angiotensin I-converting enzyme inhibitor, captopril, on lipid metabolism, we measured serum lipoperoxides concentration ( LPX ) as well as plasma levels of renin activity (PRA), aldosterone (PAC) and bradykinin ( PBK ) before and after captopril administration in 15 hypertensive patients. Captopril significantly lowered the LPX (p less than 0.05 by repeated measures ANOVA) from the control value of 3.25 +/- 1.16 (mean +/- S.D.) to 2.92 +/- 0.94, 2.83 +/- 1.10, and 2.89 +/- 1.31 nmol/ml 30, 60, and 120 min after the administration, respectively. A significant reduction of blood pressure (p less than 0.0001) and PAC (p less than 0.01) was observed following captopril administration, while PBK increased significantly (p less than 0.001) from a baseline level of 10.85 +/- 4.07 to 13.95 +/- 5.29, 16.25 +/- 6.85, and 15.71 +/- 7.65 pg/ml 30, 60, and 120 min after captopril administration, respectively. There was no significant correlation between changes in serum LPX and in mean blood pressure, PRA and PAC, though a significant inverse relationship was found between changes in serum LPX and in PBK 120 min after the administration (r = -0.576, p less than 0.05, n = 13). Although the mechanisms by which serum LPX is decreased by captopril are not clear, it is suggested from the results that captopril is a beneficial antihypertensive agent for preventing LPX -induced atherosclerosis in hypertensive patients.

Adult↗
PubMed1983

[Studies on the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension].

These studies were undertaken to clarify the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension (EH), and the following examinations were performed: 1) Urinary free norepinephrine and epinephrine excretion (UNEf and UEf), urinary conjugated norepinephrine and epinephrine excretion (UNEconj and UEconj), plasma norepinephrine and epinephrine concentration (PNE and PE), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 52 patients with EH, who were divided into two groups (borderline EH: b-EH, and sustained EH: s-EH), and fifteen normals (N). 2) Cardiac index (CI), total peripheral resistance index (TPRI), appearance time, mean transit time and stroke index (SI) were determined by the dye-dilution method in eight patients with b-EH, ten patients with s-EH and ten N. 3) Clonidine was administered orally in a single dose of 150 micrograms to seven patients with s-EH and three patients with b-EH, and PNE, PE and growth hormone (GH) were measured before and after the administration. 4) Isoproterenol was infused intravenously in a dose of 0.02 microgram/kg/min for 30 min to 18 patients with s-EH and six N, then plasma cyclic AMP (c-AMP) and PRA were determined before, during and after the infusion. 5) Methacholine was injected intramuscularly in a dose of 10 mg to seven N, and PNE, PE and PRA were measured before and after the injection. There were no significant differences of PNE, PE, UNEf and UEf among the three groups (b-EH, s-EH and N), but UNEconj in both b-EH and s-EH was higher than in N (b-EH: p less than 0.1, s-EH: p less than 0.05). PRA in s-EH was slightly lower not only in N but also in b-EH. PAC in b-EH and s-EH was slightly lower than in N. The difference of PAC between b-EH and s-EH was not found. CI and SI were higher than in N (p less than 0.05), but TPRI was normal. In s-EH, TPRI was slightly elevated as compared with b-EH (p less than 0.1). In s-EH, clonidine caused a significant lowering of both blood pressure and PNE with a simultaneously marked increment of GH; on the other hand, in b-EH blood pressure and PNE did not change significantly in spite of the distinct rise of GH. After the isoproterenol infusion, PRA and c-AMP increased, and there was a significant correlation between the initial level of PRA and the maximal increment of PRA after the infusion in both s-EH and N.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1983

[Relation between dopamine secretion and saltsensitivity in essential hypertension].

The study was designed to explore the mechanism of dopamine secretion related to blood pressure in patients with essential hypertension. The 19 patients with essential hypertension were administered to first 153 mEq of sodium and 70 mEq of potassium diet, next 51 mEq of sodium and finally 340 mEq of sodium for every one week. The patients whose mean blood pressure elevated 10 mmHg or more on the high-sodium loading and depleted 10 mmHg or more on the low-sodium loading were classified as A-, and depleted 10 mmHg or more on the high-sodium loading and elevated 10 mmHg or more on the low-sodium loading as B- and the other patients as C-group. The hypertensive patients were also classified to low- (below 1.0 ng/ml/h), normal- (from 1.0 to 6.0 ng/ml/h) and high- (above 6.0 ng/ml/h) renin groups from the results of plasma renin activity (PRA) obtained after an intravenous injection of furosemide (1 mg/kg) followed by 2-hour ambulation. PRA, plasma aldosterone concentration (PAC), plasma epinephrine concentration (PE), plasma norepinephrine concentration (PNE), plasma dopamine concentration (PDC), circulating plasma volume, body weight, hematocrit and pulse rate were measured at 8 a.m. after sodium loading for 8-days. The patients with essential hypertension were classified into 6 of A- and 2 of B- and 11 of C-groups with the maneuver of sodium loading. The A-group contained 5 patients with low-renin. The circulating plasma volume was relatively large (44.7 +/- 4.8 ml/kg) and markedly increased on the high-sodium loading in 6 patients of A-group. The increment of body weight was higher in A-group than the other groups on the high-sodium loading. In the 2 patients of B-group, hematocrit and pulse rate increased on the low-sodium and decreased on the high-sodium loading, and the variability were larger than the other groups. In the A-group, PRA was significantly low (0.5 +/- 0.4 ng/ml/h) and increased on the low-sodium loading and decreased on the high-sodium loading, and the variability of PRA was lesser than the other groups. In the A-group, PAC was within normal range (5.4 +/- 2.8 ng/dl) and the variation of PAC paralleled with the change of PRA, but the variability of PAC was remarkably low. PE and PNE were unchanged in the A- and the C-groups, but the significant high values were observed in the B-group on the high-sodium loading.

Adult↗
PubMed1982

[The localization of aldosterone-producing adenoma on computed tomography--a comparative study with adrenal scintigraphy and plasma aldosterone concentration in the adrenal or renal vein].

The evaluation of computed tomography (CT) for detecting aldosterone-producing adenoma in primary aldosteronism was performed by comparison with adrenal scintiscan; determination of aldosterone in adrenal or renal veins, retroperitoneal pneumography and adrenal venography was reliable for diagnosis of adrenal tumors in pheochromocytoma or Cushing's syndrome, but not so effective for small adenoma of primary aldosteronism. An abdominal CT scan was performed on six patients with primary aldosteronism, one with idiopathic hyperaldosteronism and one with glucocorticoid responsive hyperaldosteronism; in an attempt to evaluate the utility of this noninvasive procedure. Diagnosis of hyperaldosteronism was made by demonstrating the elevated plasma aldosterone concentration and aldosterone secretion rate, normal excretion rate of urinary 17-OHCS and 17-KS, and low plasma renin activity. The CT scan correctly predicted unilateral adrenal adenoma in all the patients with primary aldosteronism of which the findings were identical to those demonstrated by surgery. The diameter of these tumors ranged from 10 X 7 X 6 to 19 X 17 X 14 mm. Also the CT scan in idiopathic hyperaldosteronism and glucocorticoid responsive hyperaldosteronism showed bilateral adrenal hyperplasia and bilateral normal adrenal glands, respectively. The pathological findings in these two cases disclosed the adrenal hyperplasia of zona glomerulosa and adrenal hyperplasia of zona subglomerulosa accompanied by a normal thickness of the adrenal gland, respectively. The precision of the CT scan, adrenal scintigraphy and determination of plasma aldosterone in the adrenal or renal veins were almost equal to the diagnosis of the localization of adrenal adenoma. It is concluded that the CT scan is a noninvasive and most useful method for the localization of aldosterone-producing adenoma and helpful in distinguishing adrenal adenoma from adrenal hyperplasia.

Adenoma↗
PubMed1982

[The effect of trilostane, a new inhibitor of adrenal steroid biosynthesis, on blood pressure, plasma aldosterone and other steroid hormones, serum potassium and plasma renin activity in primary aldosteronism (author's transl)].

Six patients with primary aldosteronism (PA), one with idiopathic hyperaldosteronism (IHA), one with glucocorticoid responsible hyperaldosteronism (GRHA) and eight with essential hypertension (EH) were treated with trilostane (MWD-1822) (4 alpha, 5-epoxy-17 beta-hydroxy-3-oxo-5 alpha-androstane-2 alpha-carbonitrile), an inhibitor of adrenal steroid biosynthesis, for 9-47 days with a daily dose of 30-960 mg. Blood pressure decreased slightly and gradually from 30 min. to 360 min, plasma aldosterone (PAC) and cortisol concentration (F) decreased, and plasma dehydroepiandrosterone concentration (DHEA) increased 120 min. after the administration of a single dose of 120 mg of trilostane. In the patients with PA, IHA and GRHA on long term therapy with trilostane, blood pressure decreased, PAC and F were depleted, serum improved within normal limits and DHEA increased, but plasma progesterone concentration (Prog.) changed variously and plasma renin activity (PRA) remained suppressed. In the patients with EH, systolic pressure decreased in 5 out of 8 (under - 20 mmHg), and diastolic pressure decreased in 3 out of 8 (under - 10 mmHg), DHEA increased in all, but the changes in serum potassium, PAC, F, Prog. and PRA were various. There was no remarkable reaction after the administration of trilostane. It is concluded that trilostane is an effective inhibitor of 3-hydroxysteroid dehydrogenase in vivo and that it is useful in the treatment of primary aldosteronism and other hypertension due to hyperproduction of aldosterone.

Adult↗