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Biomedical subjects

M Tanno

Publications and source records attributed to M Tanno.

At least 73 records · Page 4Linked to original sources

Renal vein plasma renin activity in patients with unilateral renovascular hypertension.

Plasma renin activity in the renal veins (V) or infrarenal inferior vena cavae (IVC) of 20 patients with unilateral renovascular hypertension (RVH) was measured to determine how renal vein renin ratio (RVRR) compares with renin index (V-IVC/IVC) as a predictor of curability of RVH. Although there was no significant difference between them in predicting curability, 3 out of 4 patients with hypersecretion of renin (V-IVC/IVC greater than or equal to 0.48) in the stenosed side with contralateral suppression (V-IVC/IVC less than or equal to 0) on the normal side were cured. In addition, 7 out of 11 patients with contralateral suppression irrespective of values of renin index in the stenosed side were also cured. On the other hand, only one out of 6 patients who had neither hypersecretion nor contralateral suppression was cured. These results reconfirm that significant renin secretion with or without contralateral suppression, or only contralateral suppression of renin is highly suggestive of curable RVH.

Adult↗

Role of the prostaglandin-thromboxane system in the development and maintenance of spontaneous hypertension in the rat.

In spontaneously hypertensive rats (SHR) between the ages of 6 and 8 weeks before the development of established hypertension, repeated daily subcutaneous administration of indomethacin, an inhibitor of cyclo-oxygenase, at a dose of 5 mg/kg/day enhanced significantly the development of spontaneous hypertension, but repeated daily subcutaneous administration of OKY 046, an inhibitor of thromboxane (TX)A2 synthetase, at a dose of 12 mg/kg/day did not alter the development of spontaneous hypertension. In SHR between the ages of 15 and 18 weeks with established hypertension, indomethacin or OKY 046 did not alter the high blood pressure as compared with the injection of vehicle. In both young and adult SHR, indomethacin decreased significantly urinary prostaglandin (PG)E2 and TXB2 excretion but not PGE2. These results indicate that cyclo-oxygenase products other than TXA2 may play a protecting role in the development of spontaneous hypertension in the rat whereas their contribution to the maintenance of hypertension may be unlikely. In addition, it is suggested that TXA2 may not be involved in the development and maintenance of spontaneous hypertension in the rat.

Animals↗

Characterization of hepatic and pulmonary cytochromes P-450 in 3-methylcholanthrene-treated hamsters.

Two major forms of hepatic cytochrome P-450 (hepatic P-450MCI and P-450MCII) were purified approximately 5-fold from liver microsomes in Syrian golden hamsters treated with 3-methylcholanthrene (MC). The purified preparations of hepatic P-450MCI and P-450MCII contained 9.6 and 8.3 nmol cytochrome P-450 (P-450) per mg protein, respectively, and were essentially free from NADPH-cytochrome c (P-450) reductase (fpT), NADH-cytochrome b5 reductase and cytochrome b5. By sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE), the molecular weights of hepatic P-450MCI and P-450MCII were estimated to be 56,000 and 53,500. Further, a major form of pulmonary P-450 (P-450MC) were purified from lung microsomes of MC-treated hamster, and contained 14.2 nmol P-450 per mg protein, and estimated to be 56,000 in monomeric molecular weight, indicating the similar molecular weight to hepatic P-450MCI in the hamster. From the absorption spectra the oxidized forms of hepatic P-450MCI and P-450MCII were high- and low-spin ferric hemoproteins, respectively, and pulmonary P-450MC was similar to hepatic P-450MCII in their hemoprotein spin state. No difference, however, was observed in the CO-reduced forms among hepatic P-450MCI, P-450MCII and pulmonary P-450MC, all exhibiting 446.5 nm Soret bands. In a reconstituted system containing fpT and dilauroylphosphatidylcholine (DLPC), pulmonary P-450MC efficiently catalyzed benzo[a]pyrene (BP) hydroxylation at a rate of 11.4 mol formed per min per mol P-450, but hepatic P-450MCI and P-450MCII both exhibited lower levels, e.g., 0.49 and 0.54, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Renal kallikrein activity in spontaneously hypertensive rats.

To assess possible roles of the renal kallikrein-kinin system in the development of spontaneous hypertension, we determined daily excretion of urinary total and active kallikrein in 6-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats for up to 2 weeks. We also evaluated the effect of aprotinin, a reversible inhibitor of kallikrein and other serine proteases, on the development of hypertension in the 6-week-old SHR on ordinary intakes of sodium or on sodium loading with 1% NaCl for up to 2 weeks. Active kallikrein was determined by its kininogenase activity, and the generated kinins were radio-immunologically measured. Total kallikrein was also determined by measuring kininogenase activity after inactive kallikrein had been activated with trypsin (200 micrograms/ml). Urinary active kallikrein excretion was significantly reduced in 7-week-old SHR (1.5 +/- 0.2 microgram/day compared to 2.8 +/- 0.3 micrograms/day in WKY, P less than 0.05) and in 8-week-old SHR (1.6 +/- 0.2 microgram/day compared to 3.2 +/- 0.4 micrograms/day in WKY, P less than 0.01). Urinary total kallikrein excretion was also reduced in the 7- and 8-week-old SHR whereas the ratio of active to total kallikrein did not change. In addition, renal contents of total and active kallikrein were significantly lower in the 8-week-old SHR than in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Long-term effects of aldosterone on kallikrein, prostaglandin E2 and sodium in rats.

To assess the long-term effects of mineralocorticoids on the regulation of the synthesis or release of kallikrein and prostaglandin E2 in the renal kallikrein-kinin-prostaglandin E system, we studied the effects of chronic infusion of aldosterone (50 micrograms/kg/day) on urinary excretion of total and active kallikrein, and prostaglandin E2 for 10 days in conscious rats on regular intakes of sodium and on sodium loading with 1% NaCl as a drinking water. Chronic infusion of aldosterone induced a prompt and transient decrease in the ratio of sodium to potassium and a sustained increase in urinary prostaglandin E2 excretion in rats on regular diets, whereas urinary total and active kallikrein excretion did not increase significantly until the 4th day of aldosterone infusion. In rats loaded with sodium, aldosterone did not induce any changes in urinary total and active kallikrein excretion, whereas it induced similar changes in the ratio of sodium to potassium and urinary prostaglandin E2 excretion to those in rats on regular diets. Thus, the present results suggest that aldosterone might stimulate the synthesis or release of renal prostaglandin E2 independent of sodium balance. Furthermore, it is also suggested that aldosterone might stimulate the synthesis or release of kallikrein, at least partly, via the same pathway as sodium loading does.

Aldosterone↗

The clinicopathological significance of changes of ganglioside patterns in the cirrhotic liver: a study of 11 cases.

Unique ganglioside components including GM2 and spots No. 1 and 2 designated tentatively were increased in content in some cases of cirrhotic liver as well as in all cases of hepatocellular carcinoma (HCC). Tissues of cirrhotic liver in which these components were increased were examined histologically. These components were increased in cirrhotic liver showing many foci of dysplastic nodules and in cirrhotic nodules at the matrix of multicentric HCC. These findings, thus, indicate that the unique ganglioside components are probably related to the histological findings of the cirrhotic liver.

Aged↗

No evidence on significant roles of the prostaglandin-thromboxane and kallikrein-kinin system in the antihypertensive effect of MK 421 in rats made hypertensive by norepinephrine or vasopressin.

Inhibition of angiotensin converting enzyme by MK 421 (6 mg/kg/day ip) induced a significant increase in urinary kinin excretion in norepinephrine-infused rats (1.8 mg/kg/day ip), whereas it had no effect on urinary prostaglandin E2 excretion. In contrast, MK 421 did not induced any significant changes in urinary kinin and prostaglandin E2 excretion in vasopressin-infused rats (7.2 U/kg/day ip). The simultaneous administration of indomethacin (10 mg/kg/day sc), OKY 046 (12 mg/kg/day sc) or aprotinin (100,000 units/kg/day sc) did not affect the antihypertensive effect of MK 421 in rats made hypertensive by chronic infusion of norepinephrine or vasopressin. The present results suggest that the hypotensive effect of MK 421 may depend on a reduced sensitivity of the vasculature to vasoconstrictor substances. In addition, it is also suggested that neither the prostaglandin-thromboxane or kallikrein-kinin systems are essential for the antihypertensive effect of MK 421 in these models of hypertension.

Animals↗

Effects of angiotensin converting enzyme inhibitors MK 421, SA 446 and captopril on renal prostaglandin E and kinins in conscious normotensive rats.

Angiotensin converting enzyme inhibition by MK 421, SA 446 or captopril (6 mg/kg/day ip) for up to 6 days induced significant fall in systolic blood pressure and plasma angiotensin II concentration. The hypotensive effect was greater in sodium depleted rats than in sodium repleted rats. The hypotensive effect was also accompanied by increased excretion of urinary prostaglandin E2, however the levels of urinary prostaglandin E2 in sodium repleted rats were not different from those in sodium depleted rats. Urinary kinin excretion was increased during infusion of MK 421, SA 446 or captopril in sodium depleted rats, whereas no significant change was found in sodium repleted rats. Thus the present results suggest that renal prostaglandin E system may not be essential for the hypotensive effect of these inhibitors. In addition, the greater hypotensive effect of these inhibitors in sodium depleted rats may be in part due to stimulated renal kinin system.

3-Mercaptopropionic Acid↗

[Clinical evaluation of gallium-67 scintigraphy in comparison with autopsy findings in the elderly, with particular reference to histological findings and classification of pulmonary cancer].

A correlative study of autopsy findings and retrospective review of gallium scintigrams were performed in 106 elderly patients. Of the cases studied, 57% demonstrated positive gallium study in the present series. Histological correlation was undertaken in cases of lung cancer. Among them, squamous cell carcinoma showed the highest incidence of positive results (83%), whereas adenocarcinoma was the lowest (35%). There is no apparent correlation between subtypes of histological classification of adenocarcinoma and abnormal accumulation of gallium. However, abnormal accumulation of the nuclide seems to be rather related with interstitial reactions, namely fibrotic changes, lymphocyte infiltration and vascularization.

Adenocarcinoma↗