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Biomedical subjects

J Tajima

Publications and source records attributed to J Tajima.

32 records · Page 2Linked to original sources
PubMed1983

Reduced urinary excretion of prostaglandin E in essential hypertension.

To ascertain whether renal prostaglandin (PG) E synthesis is decreased in patients with essential hypertension (EH), urinary PGE excretion (UPGEV) was measured in 47 normal females and 62 female patients with EH. In order to avoid contaminations of urine by seminal fluids, only female subjects were studied. UPGEV was also measured in female patients with renovascular hypertension (RVH) as well as primary aldosteronism (PA) or idiopathic hyperaldosteronism (IHA). As a whole, UPGEV was lower in patients with EH (226.9 +/- 13.7 ng/day) than that in normal females (317.3 +/- 22.1 ng/day, p less than 0.001). Younger patients (15 to 39 years) had significantly lower UPGEV than normal females of corresponding ages. However, there was no significant difference in UPGEV between older patients (over 40 years) with EH and normal females of the same age range. There were no significant differences in UPGEV among patients with low renin EH, normal renin EH, RVH, PA and IHA. We reconfirmed the decrease in UPGEV in patients with EH as compared with normal controls by studying female subjects. Further, it is suggested that renal PGE synthesis is not influenced by the renin-angiotensin system in these hypertensive states.

Adult↗
PubMed1983

Active and inactive renin after captopril (SQ 14225) administration in hypertensive patients.

The changes in active and inactive renin after oral administration of captopril (SQ 14225) were studied in 29 hypertensive patients. Inactive renin was calculated as plasma renin activity (PRA) after cold storage (total renin) minus PRA before cold storage (active renin). The patients were divided into 2 groups, responders and non-responders, according to the response of active renin to captopril. In 9 responders, the active renin increased markedly, while the inactive renin decreased. On the other hand, in 20 non-responders, both renin activities increased only slightly. Total renin increased markedly in responders; it increased in much smaller degree but significantly in non-responders. These data suggest that captopril promotes the conversion of inactive renin to active one and augments the renin release as a whole.

Adolescent↗
PubMed1983

Acute effects of MK421, a new angiotensin converting enzyme inhibitor, in man.

Acute effects of MK421 were examined in 11 male normal volunteers. Oral administration of 5 mg of MK421 did not induce any changes in blood pressure or pulse rate. Plasma renin activity increased significantly from 7.3 +/- 2.9 ng/ml to 22.2 +/- 7.1 (p less than 0.05), whereas plasma aldosterone concentration did not change. Blood kinin, or urinary excretion of kallikrein and of prostaglandin E did not change. However, urinary excretion of sodium increased significantly from 44.0 +/- 6.8 mEq/4 hr to 56.5 +/- 6.5 (p less than 0.02) following the administration of MK421. The present results show that an increased renin release induced by MK421 is independent of change in blood pressure, and also suggest that MK421 may have a direct action on the renal tubules.

Adult↗
PubMed1983

Renal kallikrein and PGE in the exaggerated fractional Na excretion in patients with chronic renal failure.

The present study was performed to investigate the roles of renal kallikrein and prostaglandin (PG) E in the mechanism of the exaggerated fractional Na excretion in hypertensive patients with advanced renal disease by means of the determination of urinary excretion of kallikrein and PGE, and fractional Na excretion in 20 healthy volunteers and 41 patients with chronic glomerulonephritis (14 normotensive patients; 9 borderline hypertensive patients; 18 sustained hypertensive patients). Urinary excretion of kallikrein and PGE was significantly decreased in patients with sustained hypertension as compared with healthy volunteers, while not decreased in those with normotensive or borderline hypertensive patients. Four times higher values for the fractional Na excretion and four or five times higher values for the urinary excretion of PGE corrected for creatinine clearance, were found in patients with borderline or sustained hypertension. There was a significant positive correlation (r = 0.6777) between the two. These results suggest 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. The urinary excretion rate of kallikrein corrected by creatinine clearance was three times greater in patients with borderline hypertension, but no significantly increase in those with sustained hypertension compared with that in healthy volunteers. There was no significant correlation between the fractional Na excretion and urinary kallikrein excretion corrected for creatinine clearance.

Adult↗
PubMed1982

Captopril attenuates pressor responses to norepinephrine and vasopressin through depletion of endogenous angiotensin II.

The influence of captopril on pressor responses to exogenously administered vasopressor substances was investigated in normal subjects. Norepinephrine (0.05, 0.1 and 0.2 micrograms/kg . min -1; n = 5), angiotensin II (5, 10 and 20 ng/kg . min -1; n = 5) and vasopressin (2 mU/kg . min -1; n = 5) were infused each for 10 minutes; each infusion was repeated twice. Captopril (50 mg orally) significantly attenuated the pressor response to norepinephrine (0.1 [p less than 0.05], 0.2 [p less than 0.01] micrograms/kg . min -1; n = 7) and to vasopressin (p less than 0.01, n = 5), but not to angiotensin II; these responses were reproducible. Attenuation of the pressor responses to norepinephrine did not occur when a subpressor dose of angiotensin II (ng/kg . min-1) was infused in addition to captopril (n = 5). Infusion of a subpressor dose of bradykinin (0.1 ng/kg . min-1) had no influence on the pressor responses to norepinephrine (n = 5). In the five subjects treated with indomethacin (225 mg/54 hours) captopril still attenuated the pressor responses to norepinephrine. These results suggest that the attenuation by captopril of the pressor responses to norepinephrine and vasopressin might have been due to reduction of endogenous angiotensin II.

Adult↗
PubMed1982

Evaluation of the chronotropic property of captopril in hypertensive patients.

Captopril was administered (50 mg orally) to 88 untreated hypertensive patients (70 with essential hypertension, eight with renal arterial disease, 10 with renal parenchymal disease) and to 25 hypertensive patients treated with sympatholytic or beta-blocking agent (20 with essential hypertension, five with renal arterial disease). In the former group, captopril caused a decrease in heart rate (HR) in 18 patients and an increase in only two. As a whole, captopril caused significant decreases in blood pressure without increase in HR. Significant negative correlation was observed between change in HR and plasma renin activity obtained before captopril administration (n = 79, r = -0.425, p less than 0.0001). Hypotensive and chronotropic effects of captopril were almost identical in untreated and treated patients. Hypotensive effects caused by captopril and nifedipine (20 mg orally) were almost identical. Nifedipine caused reflex tachycardia, while captopril caused slight bradycardia. Absence of compensatory tachycardia appears to be related to reduction of endogenous angiotensin II by captopril.U

Adrenergic beta-Antagonists↗
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

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

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↗
PubMed1980

Hoarseness as an initial manifestation of sarcoidosis.

A patient had hoarseness, the cause diagnosed as left recurrent laryngeal nerve palsy derived from enlarged sarcoid mediastinal lymph nodes. His symptoms were alleviated by steroid therapy, which was accompanied by the improvement of mediastinal lymph node swelling noted on chest x-ray film. Hoarseness may be listed as one of the symptoms of sarcoidosis.

Adolescent↗
PubMedDate not supplied

Attenuation of pressor responses to norepinephrine and pitressin and potentiation of pressor response to angiotensin II by captopril in human subjects.

The present study was conducted to investigate the influence of captopril on cardiochemodynamic responses in 38 normal volunteers (20- to 35-year-old men) to exogenously administered vasopressor substances. Norepinephrine (NE), 0.05, 0.1, and 0.2 micrograms/kg min-1; angiotensin II (AII), 5, 10, and 20 ng/kg min-1; and pitressin (2 mU/kg min-1) were infused for 10 minutes. Each infusion was reported twice, and the responses were reproducible. Captopril (50 mg by mouth) significantly attenuated the pressor responses to NE and pitressin, but the decrease in heart rate in response to NE and pitressin was almost the same before and after captopril treatment, suggesting that captopril potentiates reflex slowing of the heart. Captopril significantly potentiated the pressor response to AII. Attenuation of pressor response and potentiation of reflex slowing of the heart, in response to NE and pitressin, disappeared when a subdepressor dose of AII (1 ng/kg min-1) was infused in addition to captopril. Infusion of a subdepressor dose of bradykinin (BK), 0.1 microgram/kg min-1, had no influence on the pressor response to NE. In the subjects treated with indomethacin (225 mg/54 hrs), captopril still attenuated the pressor response to NE. These results suggest that captopril attenuates the pressor responses to NE and pitressin primarily by depletion of endogenous AII; decreased AII may desensitize the contraction of arterial smooth muscle and may potentiate the compensatory reflex mechanism.

Adult↗
PubMedDate not supplied

Antihypertensive effect of MK-421 in rats. Role of the renal kallikrein-kinin system.

To study the hypotensive mechanism of the new oral converting-enzyme inhibitor, MK-421, we evaluated the antihypertensive effect of MK-421 in rats with hypertension induced by chronic administration of norepinephrine (NE) or vasopressin and measured urinary kallikrein and kinin excretions as indices of the renal kallikrein-kinin system. When 6 mg/kg/day of MK-421 was administered simultaneously with 1.8 mg/kg/day of NE, the systolic blood pressure of conscious rats rose on Day 1 to only 122.6 +/- 3.4 mm Hg compared with the rise to 146.3 +/- 1.6 mm Hg when NE alone was infused (p less than 0.001). Similarly, when the same dose of MK-421 was administered simultaneously with 7.2 U/kg/day of vasopressin, the systolic blood pressure of conscious rats rose on Day 1 to only 117.4 +/- 3.8 mm Hg compared with the rise to 141.6 +/- 3.4 mm Hg when vasopressin alone was infused (p less than 0.01). The antihypertensive effect of MK-421 was sustained for 6 days in rats infused with NE or vasopressin. Infusion of NE alone resulted in a small but significant increase in urinary kallikrein excretion and no change in urinary kinin excretion. The combined administration of NE with MK-421 induced additional increases in urinary kallikrein and kinin excretions. Vasopressin alone resulted in marked decreases in urinary kallikrein and kinin excretions. The combined administration of vasopressin with MK-421 induced no additional changes in urinary kallikrein and kinin excretion. These results indicate that the hypotensive effect of MK-421 may depend on a reduced sensitivity of the peripheral arteries to vasoconstrictor substances.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗