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Biomedical subjects

M Yasujima

Publications and source records attributed to M Yasujima.

At least 163 records · Page 9Linked to original sources
PubMed1982

Prostaglandin E synthesis in the kidney in renin subgroups of essential hypertension.

To assess the pathophysiological role of renal prostaglandin E (PGE) in renin subgroups of essential hypertension, urinary excretion of PGE before (24 hours urine) and after the administration of furosemide (1 mg/kg, iv) and 2 hours upright posture was estimated in 66 essential hypertensives, classified into high, normal and low renin subgroups. In each renin subgroup, the administration of furosemide and 2 hours upright posture induced marked increases in urinary excretion of PGE and sodium, and in plasma renin activity. However, there were no significant differences in basal values of urinary excretion of PGE among the 3 subgroups, nor in the values after the administration of furosemide and 2 hours upright posture. The present data do not support the hypothesis that the difference in renin level in essential hypertensives is dependent on the synthesis of renal PGE.

Adolescent↗
PubMed1982

Effect of dietary sodium intake on the metabolism of prostaglandins in the kidney in hypertensive patients.

To investigate the role of renal prostaglandins (PGs) in the renal handling of sodium, urinary excretion of PGE, PGF2 alpha and PGF2 alpha MUM (main urinary metabolite of PGF2 alpha) were measured after various manipulations of dietary sodium intake in 8 hypertensive patients. A low sodium intake increased urinary excretion of PGF2 alpha MUM (p less than 0.05), but failed to change urinary excretion of PGE and PGF2 alpha. In contrast, a high sodium intake increased urinary excretion of PGE (p less than 0.01) and decreased urinary excretion of PGF2 alpha MUM (p less than 0.02). A low sodium intake decreased the ratio of urinary PGE/PGF2 alpha MUM and high sodium increased it (both p less than 0.001). There was a significant positive correlation between urinary excretion of sodium and that of PGE (p less than 0.001). Additional oral administration of potassium chloride did not change urinary excretion of PGs. These results may suggest that dietary sodium intake may be one of the regulators of the metabolism of PGs in the kidney, supporting the hypothesis that renal PGE has a natriuretic action in humans.

Adult↗
PubMed1982

Influences of low sodium diets on vascular effects of bradykinin and on bradykinin receptors in the uterine smooth muscle in the rats.

A low sodium diet for 7 days in the rat induced an enhancement of the vascular effects of bradykinin, determined as the blood pressure response, by 56%. However, this enhancement reverted after 28 days of a low sodium diet. A sustained increase in the number of uterine smooth muscle bradykinin receptors during low sodium diets was observed, 1.3 times of the control on the 7th day and 1.7 times on the 28th day. No change in binding affinity was found in any of the studies. These results suggest that the vascular effects of bradykinin after low sodium diets may be regulated by homeostatic mechanisms via the change in the number of vascular smooth muscle bradykinin receptors at subcellular levels, and that the number of uterine smooth muscle bradykinin receptors may be affected by sodium status per se.

Animals↗
PubMed1982

Effect of acute water loading on urinary excretion of prostaglandin E in hypertensive patients.

To assess the relationship or urine flow to the urinary excretion of prostaglandin E (PGE), urinary excretion of PGE was measured before and after acute water loading (20 ml/kg orally) in patients with hypertension. Water loading promptly increased urinary excretion of PGE as well as urine flow rate and decreased urine osmolality (all p less than 0.001), but did not affect urinary excretions of sodium, potassium and creatinine, plasma renin activity and plasma aldosterone concentration. There was a significant positive correlation between urine flow rate and urinary PGE excretion rate (p less than 0.01). Urinary PGE concentration correlated negatively with urine flow rate when the flow was lower than 5 ml/min (p less than 0.01). Urinary PGE concentration correlated negatively with urine flow rate when the flow was lower than 5 ml/min (p less than 0.01), whereas it did not change when the urine flow rate was larger than 5 ml/min. These results may support the hypothesis that urinary excretion of PGE is determined mainly by urine flow rate in the situation of water diuresis.

Adult↗
PubMed1981

Exaggerated fractional sodium excretion in hypertension with advanced renal disease: the role of renal prostaglandin and kallikrein.

1. The role of renal prostaglandin E (PGE) and kallikrein in the mechanism of the exaggerated fractional sodium excretion in hypertensive patients with advanced renal disease was investigated. 2. Urinary excretion of PGE and kallikrein was significantly decreased in patients with sustained hypertension. 3. Four times higher values for fractional sodium excretion and four or five times higher values for the urinary excretion of PGE corrected for creatinine clearance were found in patients with sustained hypertension. There was a significant positive correlation (r = 0.677) between the two, suggesting that PGE in the renal tubular compartment may be involved in the mechanism of the exaggerated fractional Na excretion in patients with advanced renal disease. 4. The urinary excretion rate of kallikrein corrected for creatinine clearance was three times greater in patients with borderline hypertension, but not significantly increased in those with sustained hypertension, compared with that in healthy volunteers.

Adult↗
PubMed1980

Effect of propranolol on the urinary excretion of prostaglandin E and plasma renin activity in hypertensive patients.

To investigate the role of the renin-angiotensin (R-A) system in the release of renal prostaglandin E (PGE), urinary excretion of PGE, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured before and after the manipulation of the R-A system in hypertensive patients. After 7 days of the control sodium diet, the R-A system was stimulated by a combination of low sodium diet and oral administration of furosemide for 7 days. From the 4th day of sodium restriction, 40 mg/day of propranolol was administered per os for 2 days, and the dose was doubled for the following 2 days. PRA and PAC were significantly increased after the sodium restriction, but no change in urinary excretion of PGE was observed. Additional administration of propranolol for the following 4 days suppressed PRA significantly and PAC moderately, but it also failed to change urinary excretion of PGE. These results may suggest that renal medullary PGE synthesis, as reflected in urinary excretion of PGE, is not strongly dependent on the R-A system in these hypertensive patients.

Adolescent↗
PubMed1980

Bartter's syndrome with normal urinary excretion of prostaglandin E: therapeutic effects of propranolol, spironolactone, indomethacin and potassium chloride.

Urinary excretion of prostaglandin E (PGE) in 8 patients with Bartter's syndrome measured by the radioimmunoassay method was not augmented over the normal values. In one of them, urinary excretion of sodium, potassium, chloride and PGE, serum sodium, potassium and chloride, plasma renin activity and plasma aldosterone concentration were studied before and after the administration of propranolol, spironolactone, indomethacin and potassium chloride. Neither propranolol nor spironolactone affected any of these parameters. Indomethacin promptly reduced urinary excretion of sodium, potassium, chloride and PGE, and markedly suppressed the renin-aldosterone system. Serum potassium was elevated, but remained still in hypokalemic range. Potassium chloride was most effective in raising the serum potassium level during the first 4 weeks of administration. These results suggest that overproduction of renal PGs is not the primary cause of Bartter's syndrome, and that the renal potassium wastage is one of the etiological factors in this syndrome. It has also been suggested that hyperreninemia in this syndrome was associated in some way with renal PGs, not PGE but other series of PGs.

Adult↗
PubMed1980

Management of severe hypertension with nifedipine in combination with clonidine or propranolol.

The hypotensive effect of nifedipine was studied in 9 patients with severe hypertension. After oral administration of 20 mg nifedipine mean arterial pressure (MAP) fell, reaching lowest values about 1 h p.a. The antihypertensive effect lasted 7 h. Treatment with nifedipine alone (80 mg/day) lowered MAP significantly on the first day, but it tended to rise again therealter. Addition of clonidine (450 micrograms/day) or propranolol (120 mg/day) enhanced the hypotensive effect. Furosemide (120 mg/day) was ineffective when added to the above described regimen. Without nifedipine the combine drugs failed to keep MAP down. The decrease of MAP observed when giving this combination of drugs was associated with a significant fall in total peripheral resistance and plasma renin activity, but did not alter cardiac output and blood volume. We concluded that nifedipine together with clonidine or propranolol is very effective in the management of severe hypertension.

Adult↗
PubMed1979

Change in plasma renin activity by cold storage of plasma in normal subjects and patients with essential hypertension and primary aldosteronism.

The time courses of change in renin activity after cold storage of human plasma at -5 degrees C and pH 7.4 were examined in 5 normal subjects, 6 patients with essential hypertension and one female patient with primary aldosteronism before and after extirpation of the adrenal tumor. In the 5 normal subjects and 6 essential hypertensives, the gradual increase in plasma renin activity was observed until 10 days of cold storage. The same result was obtained in the case of primary aldosteronism. However, there was no increase in renin activity despite of cold storage for 10 days in plasma which was sampled from this patient 45 days after operation. These data indicate that a period of 4 days for cryoactivation of human plasma renin as has been reported by Sealey et al. is not sufficient to accomplish activation of renin by cold storage.

Adolescent↗
PubMed1979

Effect of triamterene on urinary excretion of immunoreactive prostaglandin E in essential hypertension.

The effect of triamterene on urinary excretion of prostaglandin E was studied, and the results were compared with those obtained with spironolactone. Urinary excretion of immunoreactive prostaglandin E was measured radioimmunologically. Triamterene was administered in a dose of 100 mg/day for 8 days to 7 patients with essential hypertension. Following the administration of triamterene, urinary prostaglandin E tended to increase. However, the increment was not significant. The lack of significant increase in urinary prostaglandin E excretion during the administration of triamterene contrasted with our previous finding with spironolactone, in which a significant increase in prostaglandin E excretion was observed on the first day of spironolactone administration. Urinary Na excretion and urinary Na/K ratio were significantly increased and urine volume also tended to increase following the administration of triamterene. Plasma renin activity and plasma aldosterone concentration were increased in all cases. However, there was no significant correlation between these parameters and urinary prostaglandin E. These results suggest that the effect of triamterene on renal prostaglandin E synthesis is different from that of spironolactone and that the change in urinary prostaglandin E after the administration of triamterene is not the reflection of the change in the renin-angiotensin-aldosterone system.

Adolescent↗
PubMed1979

Renal kallikrein-kinin system and prostaglandin in hypertension: their relation to renin-angiotensin-aldosterone system.

The present study was done to investigate the interrelationships between renal kallikrein-kinin, renal prostaglandin E and renin-angiotensin-aldosterone systems in normal subjects and in essential hypertension by means of measuring urinary excretion of kallikrein and prostaglandin E, plasma renin activity and plasma aldosterone concentration before and after stimulation or inhibition of the renin-angiotensin-aldosterone system and inhibition of renal prostaglandin E generation. Urinary kallikrein excretion was increased after the stimulation of the renin-angiotensin-aldosterone system by low Na diet or the administration of furosemide and upright posture, while it decreased after the inhibition of the action of aldosterone by spironolactone. These data show that the change in urinary kallikrein excretion was related to that in the renin-angiotensin-aldosterone system following various stimuli, suggesting that renal kallikrein-kinin system may regulate blood pressure by opposing the action of the renin-angiotensin-aldosterone system. Urinary PGE excretion was decreased after sodium depletion and increased after the administration of furosemide in spite of the augmentation of the renin-angiotensin-aldosterone system. The change in urinary PGE excretion was closely related to that in urinary Na output after various stimuli, and a significant positive correlation was found between basal levels of urinary PGE and those of urinary Na, suggesting that renal prostaglandin E may be involved in the regulation of blood pressure by affecting renal sodium handling. The present data show that basal level of urinary excretion of PGE and kallikrein was lower in essential hypertension than in normal subjects and that the release of renal kallikrein and PGE after the furosemide administration was also suppressed in patients with essential hypertension compared with that in normal subjects, suggesting that there exists, in this disease, an impaired defense mechanism against the renin-angiotensin-aldosterone system resulting in sodium retention.

Adolescent↗