PubMed Health⌕ Search

Biomedical subjects

M Tanno

Publications and source records attributed to M Tanno.

At least 109 records · Page 6Linked to original sources
PubMed1985

Decreased urinary active and inactive kallikrein by chronic infusion of vasopressin in conscious rats.

To assess possible interactions of circulating vasopressin with the synthesis or activation of renal kallikrein, we studied the effect of chronic infusion of vasopressin (7.2 U/kg/day i.p.) for 6 days on the urinary excretion of total and active kallikrein in conscious rats. We determined urinary total, active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after the treatment with trypsin (200 micrograms/ml). Chronic infusion of vasopressin induced sustained decreases in urinary total, active and inactive kallikrein excretion, but did not affect the ratio of active to total kallikrein. The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1 +/- 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5 +/- 14.6 pg/ml in vehicle-infused rats (n = 7), p less than 0.001) and in weight gain (39.6 +/- 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 +/- 3.3 g in vehicle-infused rats (n = 7), p less than 0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Circulating levels of angiotensin II was decreased by chronic infusion of vasopressin. Thus, the present study suggests that the elevation of circulating vasopressin levels induces a decrease in the synthesis of renal kallikrein.

Animals↗
PubMed1984

Renal prostaglandin E in the hypotensive mechanism of MK-421 in conscious rats.

To assess the role of renal prostaglandin E in the hypotensive mechanism of MK-421, we evaluated the effects of chronic infusion of MK-421 (6 mg/kg/day i.p.) on systolic blood pressure and urinary prostaglandin E excretion in conscious rats in states of sodium repletion or depletion and also during chronic infusion of norepinephrine (1.8 mg/kg/day i.p.) or vasopressin (7.2 U/kg/day i.p.). The hypotensive effect of MK-421 was greater in sodium depleted than in sodium repleted rats. The hypertensive effect of norepinephrine or vasopressin was inhibited by the simultaneous administration of MK-421. MK-421 induced an increase in the excretion of urinary prostaglandin E, in both sodium repleted and depleted rats. However, simultaneous administration of MK-421 had no influence on the increase in urinary prostaglandin E excretion induced by norepinephrine or vasopressin. In addition, the combined administration of MK-421 with indomethacin (10 mg/kg/day s.c.) still abolished the hypertensive effect of norepinephrine or vasopressin. The disparate effect of MK-421 on urinary prostaglandin E excretion suggests that the renal prostaglandin system is not essential for the mechanism of the hypotensive effect of MK-421.

Angiotensin I↗
PubMed1984

Responses of the kallikrein-kinin system to angiotensin converting enzyme inhibitors in the rat.

Three structurally different drugs, MK421, SA446 and captopril, are angiotensin converting enzyme inhibitors. They induced a significantly greater fall in systolic blood pressure in sodium depleted rats than in sodium repleted ones. The combined administration of vasopressin or norepinephrine with MK421 eliminated the hypertensive effect of vasopressin or norepinephrine. Urinary kallikrein and kinin excretion were increased by MK421, SA446 or captopril in the sodium depleted rats whereas any significant changes in them were not observed in the sodium repleted rats. The combined administration of norepinephrine with MK421 induced further increases in urinary kallikrein and kinin excretion when compared to rats infused with norepinephrine alone, whereas the combined administration of vasopressin with MK421 did not induce any changes in them when compared to rats infused with vasopressin alone. Chronic infusion of captopril for up to 6 days in the rats induced a reduction of the vascular response to exogenous bradykinin; the blood pressure fall was less than that of the controls by 17% on Day 2 and by 18% on Day 6. These results indicate that the hypotensive response to angiotensin converting enzyme inhibitors was in part associated with the enhanced renal and vascular smooth muscle kallikrein-kinin system.

3-Mercaptopropionic Acid↗
PubMed1984

Renal kallikrein-kinin system and the depressor effect of angiotensin converting enzyme inhibitors MK 421, SA 446, and captopril in rats.

Responses in urinary kallikrein and kinin excretion and systolic blood pressure to MK 421, SA 446 or captopril were studied in normotensive rats fed on a regular or a low sodium diet to assess the role of renal kallikrein-kinin system in their hypotensive effect. MK 421, SA 446 or captopril were infused at a rate of 6 mg/kg/day by osmotic minipump implanted intraperitoneally for up to 6 days. The magnitude of fall in systolic blood pressure was greater on a low sodium diet when compared to on a regular diet, whereas the pattern of the fall was similar on both diets. The magnitude of falls in plasma angiotensin II and aldosterone concentration induced by MK 421, SA 446 and captopril was not significantly different between both regular and low sodium diets. Urinary kallikrein and kinin excretion and sodium excretion were increased during infusion of MK 421, SA 446 or captopril on a low sodium diet, however any significant changes were not found in each of them on a regular diet. The present results suggest that on a low sodium diet the augmented hypotensive response to angiotensin converting enzyme inhibitors in the rats might be due to the enhanced renal kallikrein-kinin system in addition to suppressed renin-angiotensin system.

3-Mercaptopropionic Acid↗
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↗
PubMed1984

[Quality control of radioimmunoassay by bivariate analysis].

Automatic calculation of control charts for precision and accuracy of radioimmunoassay was reported by Faure, et al. Duplicate control samples independently measured was assumed to have a bivariate normal distribution. In this case they assumed that the correlation coefficient between each value of the pairs of control samples is zero. Our experience using this method revealed that a considerable number of assayed samples distributed outside the calculated control limits in case of "accuracy control". It was considered that this happened because in radioimmunoassay the between-assays precision is usually larger than the within-an-assay precision and there is a significant correlation between values of duplicates. We also found equal probability density did not make a true circle but a long circle. Therefore in the present paper we proposed for control charts of radioimmunoassay an equal probability long circle calculated by bivariate analysis of Mahalanobis' generalized distance. It was found that a Mahalanobis' long circle could explain the density distribution of radioimmunoassay with a reasonable percent of samples outside the calculated control limits. What happened here can be interpreted by a large between-assays variability shown by some commercial kits. This automatic calculation method could be applied not only for quality control but also for evaluation and comparison of radioimmunoassay system or commercial kits. Control survey could also be analyzed by such a method.

Analysis of Variance↗
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

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

[Laboratory and clinical studies on latamoxef in the field of obstetrics and gynecology].

Latamoxef (LMOX) is a new antibiotic synthesized by Shionogi Research Laboratory. Chemically LMOX is especially unique with a sulfur atom replacing the oxygen atom in the 1 position of the conventional cephalosporin nucleus, and in addition, this antibiotic has a cephamycin-like structure. The antibacterial activity of LMOX shows high potency against Gram-negative bacteria, but tends to be weak against Gram-positive bacteria. The tissue levels of LMOX in humans after intravenous injection of 1 g were examined. The levels in uterine and adnexa uteri tissue at 1 hour after administration were 25.4 and 27.4 micrograms/g respectively. LMOX was administered to 147 cases in infections of obstetric and gynecological field. The clinical effect according to disease was 94.6% for intrauterine infections, 95.0% for adnexitis, 87.0% intrapelvic infections, and 100% for external genital organ infections, making a total of 92.5%. The rate of occurrence of side effects or abnormal laboratory findings was similar to or slightly less than that seen with other beta-lactam antibiotics.

Adult↗
PubMed1983

[Factors affecting the serum thyroid hormone concentration during fasting in rats--with special reference to the relation with temperature].

The present studies examine the effect of starvation together with cold or hot exposure on thyroid hormone levels in rats. At 23 degrees C starved for 5 days, serum thyroid hormone levels decreased significantly compared with fed rats, averaging 3.6 +/- 0.5 micrograms/dl of thyroxine (T4), 47 +/- 11 ng/dl of triiodothyronine (T3), 1.4 +/- 0.3 ng/dl of free T4 and 39.6 +/- 5.1 pg/ml of reverse T3, respectively. At 15 degrees C rats starved for 5 days, serum free T4 level significantly more increased than that of 23 degrees C starved rats, while serum T4 level and T3 did not increase significantly. At 30 degrees C rats whether concomitant starvation or not, serum thyroid hormone levels of both group markedly more decreased than control rats. These experiment provide additional evidence that thyroid gland and the peripheral metabolism of thyroid hormone respond to variety situations such as cold or hot exposure together with starvation or not.

Animals↗