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Biomedical subjects

M Yasujima

Publications and source records attributed to M Yasujima.

At least 181 records · Page 10Linked to original sources
PubMed1978

Implication of renal prostaglandin E in urinary sodium excretion.

To investigate the role of renal prostaglandin in the regulation of sodium metabolism, ruinary prostaglandin E excretion, an indicator of renal prostaglandin synthesis, urinary sodium excretion, plasma renin activity and urinary aldosterone excretion were measured in 84 normal subjects and 55 patients with essential hypertension on ad lib intake of sodium. The excretion rates of urinary prostaglandin E were 736.8 +/- 32.2 ng/day in normal subjects and 394.3 +/- 28.7 ng/day in essential hypertensives. The excretion rate was significantly decreased in essential hypertensives (P less than 0.001). A significant positive correlation was found between urinary sodium excretion and urinary prostaglandin E excretion in normal subjects (r = 0.39, P less than 0.001), and in essential hypertensives (r = 0.62, P less than 0.001). There was no correlation between the renin-angiotensin-aldosterone system and urinary prostaglandin E excretion in normal subjects as well as in essential hypertensives. The present data show that renal prostaglandin might be involved in the renal handling of sodium, and prove the possibility that the decrease of renal prostaglandin synthesis is one of the etiological factors in essential hypertension.

Adolescent↗
PubMed1978

Effect of furosemide on urinary kallikrein excretion in patients with essential hypertension.

The effect of furosemide on urinary kallikrein excretion was studied in 10 patients with essential hypertension and 9 normal volunteer subjects. After intravenous administration of furosemide and 2 hours of upright posture, urine volume (UV), urinary sodium (UNaV) and potassium (UKV) excretion, plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary kallikrein markedly increased. However, the augmentation of urinary kallikrein in patients with essential hypertension (1.50 +/- 0.19 EU/2 hr) was less remarkable than that in normal subjects (2.33 +/- 0.24 EU/2 hr), although the same degrees of response were observed in PRA and PAC. The increments of UV, UNaV and UKV in patients with essential hypertension were also significantly lower than in normal subjects. Significant positive relations were found between urinary kallikrein and UV or UNaV in both hypertensive and normotensive groups, but there was no such correlation before fursemide administration. It is likely that diuresis and natriuresis induced by furosemide are somehow associated with an increase in urinary kallikrein excretion. Blunted response of urinary kallikrein in essential hypertension may suggest an abnormality in the renal kallikrein-kinin system in this disease.

Adult↗
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 furosemide on urinary excretion of prostaglandin E in normal volunteers and patients with essential hypertension.

Urinary excretion of prostaglandin E was measured radioimmunologically in 19 healthy persons (15 men and 4 women) and in 16 patients (10 men and 6 women) with essential hypertension before and after the administration of furosemide. The excretion rates were increased from 26.2 +/- 3.0 to 64.5 +/- 11.3 ng/hr in the former and from 11.9 +/- 2.7 to 26.9 +/- 8.5 ng/hr in the latter. There was a significant difference between them, healthy subjects showing a greater increase than patients with essential hypertension. There was an obvious sexual difference in urinary excretion of prostaglandin. In men, greater increase in the excretion rates was found than in the women. Greater increases were also obtained in healthy men than in hypertensive men and in healthy women than in hypertensive women. The present results suggest that furosemide enhances urinary excretion of prostaglandin E by mechanisms which entails either an increase in prostaglandin synthesis or a decrease in renal metabolism.

Adolescent↗
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

Clinical evaluation of angiotensin II antagonist in advanced hypertension.

Eighteen patients with advanced or malignant hypertension due to essential hypertension, systemic lupus erythematosus or chronic glomerulonephritis were infused intravenously with 1-Sar-8-Ile-Angiotensin II, a competitive antagonist of aniotensin II. The spectrum of responses was broad from a mild elevation to a marked fall in blood pressure. The changes in mean blood pressure caused by this peptide showed a significant correlation with the level of peripheral plasma renin activity immediately before the infusion (r=0.5652, p less than 0.02). This peptide infusion reduced blood pressre in 12 patients (responders), but not in 6 (non-respnders). There were no differences with age, sex and severity of hypertension except for the level of peripheral plasma renin activity between the two groups. Our retrospective study showed that in 12 responders propranolol reduced blood pressure to near the normal level, while in 6 non-responders furosemide induced similar depressor response. It is concluded that the vasodepressor effect of this peptide correlates with the levels of peripheral plasma renin activity and that the responses to this drug can be used as a guide for the selection of effective antihypertensive drugs.

Adolescent↗
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↗