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Biomedical subjects

T Haruyama

Publications and source records attributed to T Haruyama.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1981

A circadian variation in the excretion of urinary kinin, kallikrein and prostaglandin E in normal volunteers.

The present study shows that there is a circadian variation in the excretion of urinary kinin, kallikrein and prostaglandin E (PGE) as well as urine flow, urinary sodium excretion and urinary potassium excretion in recumbent healthy volunteers. The present data, that the acrophase of urinary kallikrein excretion was 1.5 hr later than that of plasma aldosterone concentration (PAC) and that a significant positive correlation was found in circadian variations between urinary kallikrein and PAC, suggest that the circadian variation of urinary kallikrein excretion may be regulated by aldosterone. The pattern of circadian variation of average urinary kinin excretion coincided with those of average urine flow, urinary sodium excretion and urinary PGE excretion, suggesting that renal kinin and PGE may be involved in the regulation of water-sodium excretion. The present data that the phase of circadian variation of urinary kinin was delayed from that of urinary kallikrein and that there was a mirror image between the circadian variation in urinary kinin and kallikrein suggest that there may be a feedback mechanism in renal kallikrein-kinin system.

Adult↗
PubMed1981

Blood pressure regulation in chronic hypotensive and hypertensive patients with chronic renal failure.

We studied the regulatory mechanism of blood pressure in uremic patients (UP) treated with long-term hemodialysis. The cardiac index (CI) was higher in UP than in normal control (NC). Total peripheral resistance (TPR) in hypertensive (U-Hyper) and normotensive (U-Normo) uremic patients was almost the same as that in NC but TPR in hypotensive uremic patients (U-Hypo) was lower than in NC. High CI in U-Hyper and low TPR in U-Hypo seem to be the causes of their blood pressure abnormalities. All patients had severe anemia. There was a significant positive correlation between hematocrit (Ht) and TPR in UP as well as in NC. The regression line of correlation between Ht (x axis) and TPR (y axis) in UP was shifted to the left from that of NC, suggesting TPR was higher even in U-Hypo than in NC. There was a significant negative correlation between Ht and CI in UP as well as in NC. The regression line of correlation between Ht (x axis) and CI (y axis) in UP was shifted to the left from that in NC, suggesting that CI was lower even in U-Hyper than that in NC. Therefore, higher TPR relative to Ht in U-Hyper and lower CI relative to Ht in U-Hypo may actually be principal causes of their blood pressure abnormalities. Circulating plasma volume and extracellular fluid volume were significantly higher in UP even after hemodialysis but there was no significant difference among subgroups of uremia. Plasma renin activity (PRA) was higher in UP than in NC. However, PRA in U-Hypo was significantly lower than that in U-Hyper or U-Normo. PRA in UP, even in U-Hypo, was inappropriately high relative to sodium/volume status. There was a significant positive correlation between TPR and PRA in UP. Therefore, higher TPR in UP relative to Ht than NC might be a result of elevated PRA. The level of blood pressure in UP seems to be regulated mainly by renin-angiotensin system. All patients were dialysed under the same condition. Heart rate and TPR increased after dialysis in U-Hyper and U-Hypo. However, no change occurred in these parameters throughout dialysis in U-Hypo. The responsiveness of renin secretion upon dialysis was lower in U-Hypo than in other two groups. Therefore, autonomic dysfunction may partly contribute to the development and maintenance of chronic hypotension in U-Hypo.

Adult↗
PubMed1981

The role of monocytes and prostaglandin E in the regulation of mitogen response.

The incubation of human monocyte rich fraction with PWM and SRBC revealed the production of significant amount of PGE in the supernate, suggesting the participation of PGE produced by monocytes in mitogen response. Con A-induced 3H-thymidine incorporation by lymphocytes was enhanced by addition of monocytes, and was further increased in the presence of indomethacine. These indicate that monocytes have helper effect in mitogen stimulation and are regulating the response through the production of PGE.

Humans↗
PubMed1981

Analysis of 30 patients with malignant hypertension treated with hemodialysis.

For the past 7 years we have treated 30 patients with malignant hypertension with hemodialysis. The diagnosis of the disease was made according to the criteria recommended by the Ministry of Public Welfare, Japan, as described below. These patients were divided into three groups according to the therapies. Group A (15 patients) were medicated with large doses of beta-blockers for the control of hypertension. Characteristic features of this group were abnormally high reninemia, hyponatremia, and severe hypertension which were not controlled by large doses of beta-blockers in combination with dialysis. Their body weights were quite subnormal. Twelve patients out of 15 had essential hypertension (EH) as an underlying disease, and the remaining 3 had chronic glomerulonephritis (CN). Ten patients out of 15 died of hypertensive heart failure or hypertensive cerebrovascular accidents. Group B (6 patients) were treated by beta-blockers intermittently. They showed good results responding well to the treatment; high reninemia was brought down to normal level by the administration of beta-blockers and dialysis. Their underlying diseases were EH (3 patients) and CN (3 patients). Group C (9 patients) did not receive beta-blockers, because hypertension was easily controlled by dialysis alone. In the Group C patients, normoreninemia, normonatremia, and a favorable clinical course were characteristic. Their underlying disease was CN in all. From these results, it is concluded that the factors influencing the prognosis of te disease may be the existence of EH as an underlying disease, high reninemia, and hyponatremia which are not correctable either by administration of beta-blockers or by hemodialysis.

Adrenergic beta-Antagonists↗
PubMed1981

Development of malignant hypertension in patients with uremia under hemodialysis: a case report and discussions on its etiology.

A woman, now 28 years old, was diagnosed 6 years ago as chronic glomerulonephritis by renal biopsy. From August 15, 1975 she complained of nausea, loss of appetite and weight (about 7 kg within 2 weeks). Severe hypertension (200/130 mmHg), hyponatremia (123 mEq/liter), anemia, elevated plasma renin activity (PRA), advanced azotemia, and eye ground changes of KW-II were found. Dialysis treatment was started on September 2, 1975. From November 1975 massive amounts of sodium (5,000 mEq or more monthly) and water (26 liters or more monthly) were removed by the dialysis. These intensive dialyses resulted in an elevated PRA with recurrence of severe hypertension. At the end of March 1976 she became almost blind with retinopathy of KW-IV. Potent hypotensive drugs including beta-blockers were administered, but no improvements were obtained. On March 31, 1976 nephrectomy was performed to save her life. Marked hyalinization of glomeruli and heavy thickening of intima in interlobular arteries were found in the removed kidneys. Renal artery stenosis was not recognized either macroscopically or histologically. In this patient, the amount of sodium removed by the dialysis was dependent on her diastolic blood pressure and sodium concentration of the dialysis. It may be concluded that too enthusiastic dialysis may develop malignant hypertension due to excessive renin release.

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

Role of prostaglandin in the antihypertensive mechanism of captopril in low renin hypertension.

1. The role of endogenous prostaglandins in the antihypertensive mechanism of the angiotensin converting enzyme inhibitor, captopril, was investigated. 2. An unequivocal reduction in blood pressure and significant increase in plasma renin activity and urinary prostaglandin E excretion were found after the captopril administration. 3. The changes in blood pressure, plasma renin activity and urinary prostaglandin E excretion induced by captopril were reversed after the inhibition of endogenous prostaglandin synthesis by indomethacin. However, the responses in low renin hypertension were different from those in normal renin hypertension. 4. In low renin hypertensive patients who responded to captopril, the hypotensive effect was abolished after th addition of indomethacin, whereas no marked change in blood pressure was induced by indomethacin in normal renin hypertensive patients. In contrast, plasma renin activity was markedly increased after captopril administration in normal renin hypertension, and no significant change was found in low renin hypertension. 5. Potentiation of the prostaglandin system seems to be a principal factor in the antihypertensive mechanism of captopril in low renin hypertension, and inhibition of the renin-angiotensin system is important in normal renin hypertensives. 6. The increase in renin release after the administration of captopril was inhibited by indomethacin, suggesting that an endogenous prostaglandin system may contribute to the short feedback mechanism of renin release.

Adult↗
PubMed1980

Implication of endogenous prostaglandin system in the antihypertensive effect of captopril, SQ 14225, in low renin hypertension.

The role of endogenous prostaglandins in the antihypertensive mechanism of orally active angiotensin I-converting enzyme inhibitor in low renin hypertension was investigated. In the SQ 14225-responders with low renin hypertension, blood pressure was elevated to control level and antihypertensive effect of SQ 14225 was attenuated after the inhibition of endogenous prostaglandin synthesis with indomethacin, while no significant change in blood pressure was found in the SQ 14225-responders with normal renin hypertension. Urinary prostaglandin E excretion was not significantly increased after the SQ 14225 administration but significantly decreased after the administration of indomethacin. There was no significant difference in urinary prostaglandin E excretion between normal renin hypertension and low renin hypertension. These results suggest that SQ 14225 may potentiate extrarenal vasodilating prostaglandin system, probably vascular prostaglandin system, contributing to the antihypertensive mechanism in SQ 14225-responders with low renin hypertension. The augmented renin release following SQ 14225 administration was inhibited by indomethacin, suggesting that endogenous prostaglandin system may contribute to the negative short feedback mechanism of renin release.

Adult↗
PubMed1980

Exaggerated response of renin secretion to captopril (SQ 14225) in renovascular hypertension.

Captopril (SQ 14225), an orally active converting enzyme inhibitor, was administered in a dose of 50 mg to 12 normotensive subjects (Group I), 26 essential hypertensive patients (Group II), and 8 renovascular hypertensive patients (Group III). In Group III, 5 of the 8 patients had control plasma renal activity (PRA) similar to those in Groups I and II patients, but the PRA response to the administration of captopril was greater in 7 of the 8 patients than those in Groups I and II. These 7 patients had either bilateral or unilateral main renal artery stenosis. Captopril caused no increase in PRA in the remaining 1 who had unilateral renal artery stenosis with contralateral renin aplasia. It is concluded that this provocation test is useful as a screening procedure for the diagnosis of renovascular hypertension.

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

The effect of vitamin D2 on hypocalcemia in patients under chronic hemodialysis.

The effects of vitamin D2 (VD2) on hypocalcemia were studied in 54 hypocalcemic patients (29 males and 25 females) on chronic hemodialysis. Calcium lactate (3 g/day) or VD2 (10,000 IU/day, 50,000 IU/day and 80,000 IU/day) were administered for 4 months in order to correct the hypocalcemia. Serum calcium, phosphate and alkaline phosphatase levels were measured and the effects of VD2 on these parameters of calcium metabolism were followed. 1) Calcium lactate or 10,000 IU/day of VD2 were not effective for the correction of hypocalcemia, while 50,000-80,000 IU/day of VD2 were effective. The effects of VD2 on serum calcium concentrations were dose-dependent, and the normalization of serum calcium concentrations was achieved more rapidly with higher doses of VD2. However, in the group treated with 80,000 IU/day of VD2, many patients developed hypercalcemia, but in the group treated with 50,000 IU/day of VD2, only a few patients did it. From these results, suitable dose (initial and maintenance doses) of VD2 in dialysed patients would be 50,000 IU/day. 2) When the responder group (normal serum calcium levels after 4 months of treatment with 50,000 IU/day of VD2) and the non-responder group serum calcium levels lower than 4.2 mEq/liter on the same condition) were compared, the durations of dialysis were significantly shorter in the former than those in the latter. This fact may suggest that the effects of VD2 administration on hypocalcemia in dialysed patients are partly dependent on the residual renal function concerning the conversion of 25-OH-D3 into 1,25 (OH)2D3.

Adolescent↗