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Biomedical subjects

Y Otsuka

Publications and source records attributed to Y Otsuka.

At least 217 records · Page 12Linked to original sources
PubMed1978

Effect of spironolactone on urinary excretion of immunoreactive prostaglandin E in essential hypertension and primary aldosteronism.

To determine the effect of aldosterone antagonist on renal prostaglandin E synthesis, the rate of urinary excretion of immunoreactive prostaglandin E was measured radioimmunologically before and during the oral administration of an aldosterone antagonist, spironolactone, in 5 patients with essential hypertension, 3 with primary aldosteronism and 2 with postoperative primary aldosteronism. Spironolactone was administered at an oral dose of 25 mg 4 times daily for about 1 week. In the control state, the rates of urinary prostaglandin E excretion ranged from 151 ng/day to 4,527 ng/day in essential hypertension. The rates were not augmented in primary aldosteronism but decreased after the removal of an aldosterone producing adenoma. No obvious relationship was observed between plasma aldosterone concentration and the rate of urinary prostaglandin E excretion. On the first day of spironolactone administration, the excretion rates of urinary prostaglandin E were markedly increased independently of basal plasma aldosterone level in all cases except one case of essential hypertension. Urinary prostaglandin E excretion was increased with the concominant increase of urinary Na/K ratio in essential hypertension and primary aldosteronism. After the second day, the augmented urinary prostaglandin E excretion was decreased and the changes of urinary prostaglandin E excretion varied from case to case. These results suggest that synthesis of renal prostaglandin E is not mainly regulated by aldosterone in essential hypertension and primary aldosteronism.

Adult↗
PubMed1977

Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

Urinary kallikrein excretion was measured before and after administration of spironolactone in 12 patients with essential hypertension (including 7 patients with low renin and 5 patients with normal renin) and 6 patients with primary aldosteronism. In low renin essential hypertension, two types of urinary kallikrein excretion were observed. In one type, urinary kallikrein decreased from 6.2+/-2.1 (S.E.) EU/day to 2.7+/-0.3 EU/day after the treatment. In another type, urinary kallikrein increased from 3.1+/-0.5 EU/day to 6.4+/-1.0 EU/day. In the former, plasma aldosteron showed high levels (12.3+/-2.1 ng/100 ml), while in the latter, it was normal (3.2+/-0.5 ng/100 ml). In normal renin essential hypertension, urinary kallikrein excretion did not alter after the treatment. In primary aldosteronism, urinary kallikrein showed moderate decrease after the spironolactone treatment from 8.5+/-1.6 EU/day to 4.2+/-1.6 EU/day. Spironolactone is said to compete directly with the effect of aldosterone at renal distal tubules. The present investigation suggests that urinary kalikrein excretion is related to the effective levels of aldosterone at renal distal tubules, and alteration of aldosterone levels mediates the release of kallikrein, and that there are different mechanisms in the renal handling of sodium and kallikrein in low renin essential hypertension, in normal renin essential hypertension, and in primary aldosteronism.

Adult↗
PubMed1977

Effects of 1-Sar-8-Ile-angiotensin II on urinary prostaglandin excretion in patients with essential hypertension.

To investigate the interaction between the renin angiotensin aldosterone system and the renal prostaglandin (PG), urinary excretion of PGE, urinary excretion of main urinary metabolite (MUM) of PGF2a, urinary excretion of aldosterone, and plasma renin activity were measured before and after infusion of 1-Sar-8-Ile-Angiotensin II, a specific competitive inhibitor of angiotensin II, in 18 patients with essential hypertension under normal and low sodium diets. The values of urinary sodium excretion in these patients before the infusion of the peptide were 160.8 +/- 13.3 and 27.0 +/- 2.7 mEq per day on normal and low sodium diet, respectively. On normal sodium diet, urinary excretion of PGE was found to correlate with the level of plasma renin activity before the infusion (r = 0.6977, p less than 0.01), and it was decreased slightly from 0.37 +/- 0.05 ng/min to 0.26 +/- 0.04 ng/min after the infusion of the antagonist. On low sodium diet, urinary excretion of PGE was not significantly changed by the infusion of the peptide and showed no correlation with the level of plasma renin activity before the infusion, while urinary excretion of PGE showed a significant correlation with the excretion of urinary aldosterone (r = 0.6719, p less than 0.02). Excretion of PGF2aMUM decreased after the infusion of this peptide on both sodium diets, but the changes were not statistically significant. The present data suggest that angiotensin II influences the synthesis or release of renal PG in patients with essential hypertension on normal sodium diet, but not when they are on low sodium diet.

Adolescent↗
PubMed1976

Metabolism of PG in man: effect of furosemide on the excretion of the main metabolite of PG F2alpha.

The excretion rates of main urinary metabolite of PG F2alpha were measured radioimmunologically in 4 healthy persons and in 13 essential hypertensives. The resting values were 9.3+/-0.73 in the former and 10.4+/-2.17 ng/min in the latter. There was no significant differences between them. The excretion of the metabolite decreased prominently after the administration of furosemide. The percent decrease was 57% in healthy persons and 70% in essential hypertension. The percent result supports that furosemide inhibit the catabolism of PG F2alpha.

Depression, Chemical↗
PubMed1976

Interaction of dopamine, methyldopa and reserpine in the sympatho-adrenal system in essential hypertension.

1. The interactions of dopamine, reserpine and methyldopa on blood pressure of normal subjects and of those with essential hypertension were examined. 2. When biosynthesis of noradrenaline from dopamine was blocked by reserpine, dopamine induced a prominent depressor effect in essential hypertension. 3. The long-term treatment with methyldopa induced a marked potentiateion of the pressor action of domapine in hypertension, although no significant pressor response was found in normal subjects. 4. It is suggested that methylnoradrenaline may accumulate in peripheral nerve endings of patients with essential hypertension in comparison with normal subjects, and this accumulated methylnoradrenaline potentiates the pressor response to dopamine in essential hypertension.

Adult↗
PubMed1976

Malignant hypertension and microangiopathic hemolytic anemia.

The fourth case found in Japan manifesting the features of malignant hypertension and microangiopathic hemolytic anemia (MHA) was reported. In this case, bilateral nephrectomy brought down the blood pressure and relieved MHA. The patient has since been maintained alive and well on hemodialysis up to the time of this report.

Adolescent↗
PubMed1976

Postoperative course of blood pressure and plasma renin activity in patients with renovascular hypertension.

Thirty patients with renovascular hypertension were treated surgically, and they were divided into two groups according to the kinds of operations they received; nephrectomized group (group A) and revascularized group (group B). Postoperative blood pressure was followed periodically in each patient of two groups. In all patients with an excellent result (diastolic pressure of 90 mmHg or lower without antihypertensive therapy), blood pressure returned to normal within 30 postoperative days. Normal blood pressures were obtained within 3 weeks in eighty-four per cent of them. The normalization of blood pressure following operation was more rapid in group B than in A. The postoperative plasma renin activity (PRA) was determined serially in 10 patients. PRA became normal in 9 within 3 days and in one within 7 postoperative days. The restoration of PRA preceded the normalization of blood pressure. The normalization of PRA was quicker in group A than in B. It is likely that the renal antihypertensive mechanism, suppressed in the ischemic kidney and set again in motion by revascularization, mainly causes this difference in the postoperative changes in PRA and blood pressure between the two groups. It may be concluded that these findings are suggestive of an important role of impaired renal antihypertensive function in the maintenance of high blood pressure in chronic renovascular hypertension in man.

Adolescent↗
PubMed1975

A case report of Turner's syndrome with ring X chromosome.

A case of Turner's syndrome with short stature and 45, XO/46, XXr mosaicism in chromosome study was presented. With special emphasis on endocrinological study, the size of the breasts was normal in contrast to the poor development of the breasts in most of types of Turner's syndrome. She showed normal thyroid function, slightly low level of urinary 17-OHCS, decreased 17-KS, poor response in metopirone test and poor response of HGH to insulin.

17-Hydroxycorticosteroids↗
PubMed1975

Plasma renin activity in patients with renovascular hypertension.

Plasma renin activity (PRA) in peripheral and renal vein blood was determined in 25 patients with renovascular hypertension. Significant elevation of resting peripheral vein PRA was observed in only 9 (36%) of them. 11 (61%) out of 18 patients whose conditions were improved by surgery had shown normal levels of resting peripheral vein PRA preoperatively. Provocation test for renin secretion was done in 20 patients. 10 patients showed a hyper-response. 7 out of 15 patients who benefited from surgery had shown no response in PRA on the stimulation. Renal vein PRA was determined in 23 patients. In 16 significantly higher renal vein PRA was found on the affected side. However, measurement of renal vein PRA failed to predict the surgical results in one-third of the patients. Postoperative PRA and blood pressure were followed serially in 10 patients. PRA became normal within 3 days postoperatively in 9 patients. While the normalization of blood pressure following operation was more rapid in 3 revascularized patients than in 7 nephrectomized, the normalization of PRA was quicker in the latter patients than in the former. These data indicate that measurement of PRA in peripheral and renal vein is not an infallible mean to determine the functional significance of renal arterial lesions.

Adolescent↗
PubMed1975

Renal effects of prostaglandin E1 in hypertensive patients.

The effects of prostaglandin E1 on fluid and sodium excretion, creatinine clearance and renin release were examined in 26 hypertensive patients including 9 cases of essential hypertension, 10 of renovascular hypertension and 7 of primary aldosteronism. When prostaglandin was infused intravenously in a total dose of 120 mug in 60 min, urine volume was increased in 70% of cases, and sodium excretion in 61%, but little changes were observed in creatinine clearance. The most prominent diuresis and natriuresis were obtained in primary aldosteronism (mean increase was 319% in urinary volume, and 222% in sodium output). The average increases in urinary volume were 61% in patients with essential hypertension and 97% in renovascular hypertension. And urinary output of sodium was increased by 63% in the former and 56% in the latter. The remarkable renal effects of prostaglandin E1 in primary aldosteronism were completely abolished after the administration of spironolactone. Significant elevation of plasma renin activity resulted from prostaglandin E1 infusion in essential hypertension, while no constant effect was obtained in renovascular hypertension and primary aldosteronism. The present experiments indicate that prostaglandin E1 has different effects on the kidney according to the types of hypertension and the effects correlate closely with patient's status of extracellular fluid volume or sodium balance.

Adolescent↗
PubMed1975

Urinary kallikrein excretion and sodium metabolism in hypertensive patients.

Urinary kallikrein excretion was measured in 21 healthy subjects and 44 patients with various types of hypertension. The kallikrein activity was determined by the method of esterolytic assay. The excretion rates in normal subjects were 112.9 +/- 11.1 (S.E.) EU/day. The kallikrein excretion was decreased in patients with essential hypertension, the mean estimated values were 75.2 +/- 10.0 EU/day. In this disease, however, an enhancement of urinary kallikrein was observed after sodium depletion. An obvious increase in kallikrein excretion was found in the primary aldosteronism. In primary aldosteronism and renovascular hypertension, one of the secondary aldosteronisms, there was a good correlation between the urinary kallikrein output and the urinary sodium excretion. The present data indicate that the renal kallikrein-kinin system, one of the renal antihypertensive factors, is suppressed in essential hypertension and is under the influence of mineralocorticoid levels.

Adolescent↗