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Biomedical subjects

M Seino

Publications and source records attributed to M Seino.

At least 145 records · Page 8Linked to original sources
PubMed1984

Chronic effects of norepinephrine and vasopressin on urinary prostaglandin E and kallikrein excretions in conscious rats.

To assess in vivo functional interactions of vasopressor substances, norepinephrine and vasopressin, with renal prostaglandins and kallikrein-kinin system which are responsible for the vasodepressor mechanism in the kidney, we evaluated chronic effects of norepinephrine (1.8 mg/kg/day ip) and vasopressin (7.2 U/kg/day ip) on urinary prostaglandin E excretion and urinary kallikrein excretion in conscious rats. Both norepinephrine and vasopressin induced a sustained increase in systolic blood pressure. Norepinephrine induced slight but significant increases in urinary prostaglandin E excretion and urinary kallikrein excretion which were sustained for up to 6 days. Vasopressin induced a marked increase in urinary prostaglandin E excretion which was sustained for up to 6 days, whereas it induced a sustained decrease in urinary kallikrein excretion. Circulating angiotensin II levels was not changed by norepinephrine, but was decreased by vasopressin. These results indicate that renal prostaglandin E may not correlate with renal kallikrein-kinin and renin-angiotensin system in the responses to norepinephrine and vasopressin, and that vasopressin may be a more potent stimulator of the synthesis or release of renal prostaglandin E.

Angiotensin II↗
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

Risks of occurrence of psychoses in relation to the types of epilepsies and epileptic seizures.

The possible existence of the risks of occurrence of psychoses was examined in relation to the types of epilepsies and epileptic seizures. This study consisted of two investigations: 1) A study of 879 epileptic patients was conducted in which the incidence of psychoses in the different types of epilepsies was surveyed; the result was that the incidence in temporal lobe epilepsy was the highest, being relatively higher than that of other (non-temporal lobe) partial epilepsies but not significantly different from that of generalized epilepsies. 2) A comparative study was carried out on 96 patients with temporal lobe epilepsy in which 48 were psychotic and another 48 were non-psychotic which served as a control group. The differences of seizure symptomatology between the two groups were compared. The results were that the psychotic group was found to exhibit at a significantly higher rate generalized tonic-clonic convulsion and compound seizure manifestations in comparison with the non-psychotic group. The results appear to support the fact that generalizing mechanisms of temporal lobe epileptic manifestations are closely related to a physiopathogenic factor influencing psychoses.

Adolescent↗
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

Effects of nifedipine on the renal vascular responses and blood pressure responses to norepinephrine and angiotensin II in the anesthetized rabbit.

Effects of a Ca-antagonist, nifedipine, on renal vascular responses and systemic pressor responses to angiotensin II and norepinephrine were studied in anesthetized rabbits. The changes of renal blood flow were estimated by an electromagnetic flowmeter. After the intravenous administration of nifedipine (50 micrograms/kg), mean blood pressure decreased from 116 +/- 3.1 mmHg to 102 +/- 3.4 mmHg (p less than 0.001). Renal vascular responses to angiotensin II were attenuated significantly after the administration of nifedipine, but not changed to norepinephrine. Pressor responses to angiotensin II at a low dose were significantly diminished after the administration of nifedipine (p less than 0.05), whereas it had no effect at higher doses. Nifedipine tended to suppress the increase in arterial pressure induced by norepinephrine, but the changes were not statistically significant. These results suggest that calcium influx in the vascular smooth muscle cells is not likely to be a common pathway in the vasoconstrictor reaction to angiotensin II and norepinephrine in anesthetized rabbit.

Angiotensin II↗
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

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

Therapeutic concentration of antiepileptic drugs and the severity of epileptogenesis.

In sodium valproate monotherapy for generalized seizures and carbamazepine for partial seizures, it was found in a within-patient follow-up study that the effect-developing concentrations which were sufficient to suppress the clinical seizures were significantly higher than the effect-sustaining concentrations by which longstanding suppression was maintained. There was a delayed onset of therapeutic effect which worked to suppress the clinical and electrographic seizure manifestations, and the length of the delay depended on the nature of the epilepsy. In animal experiments, the possibility that the severity of epilepsy may become milder as a consequence of successful pharmacotherapy was reconfirmed in amygdaloid-kindled cats on chronic medication in place of kindling animals on acute prophylactic medication. Only when the established generalized seizures were completely suppressed, was the generalized seizure triggering threshold evidently elevated. Since epilepsy is a long-standing condition lasting for years to decades, short-spanned cross-sectional observations are often misleading. Whatever relationship might exist between the blood levels of antiepileptic drugs and the paroxysmal discharges in the EEG, the severity of epileptogenesis as well as the longitudinal time course must always be taken into consideration in the drug treatment of epilepsy.

Anticonvulsants↗
PubMed1982

Pharmacokinetic studies of AD-810, a new antiepileptic compound. Phase I trials.

Pharmacokinetics of 3-sulfamoylmethyl-1,2-benzisoxazole (AD-810), a new possible antiepileptic compound, were evaluated in Phase I trials in nine healthy male volunteers. The subjects, divided into three groups, were given single oral dose of 200 mg (Group A), and oral doses of 200 mg/d (B) and 400 mg/d (C) for two d, respectively. AD-810 was well tolerated by all subjects. No neurologic side effects were observed. Evaluation of the laboratory screening profiles (hematological and biochemical examination) showed no clinically significant abnormalities. Mean peak plasma concentrations of AD-810 at 5.3-6.0 h after intake were 2.9, 5.1 and 13.0 micrograms/ml in Group A, B and C, respectively, and mean elimination half-life was about 60 h. Mean concentrations of AD-810 in erythrocytes were higher than those in plasma. The unchanged AD-810 and a major metabolite, the glucuronide of the N-O cleft compound, were excreted at 48.7% and 12.4% of the given dose in the urine for 2 weeks in Group C, respectively. The results suggest that AD-810 would induce no severe adverse effects in man at plasma concentrations over 10 micrograms/ml, the therapeutic concentrations predicted from animal experiments.

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

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↗