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Biomedical subjects

K Omata

Publications and source records attributed to K Omata.

At least 181 records · Page 10Linked to original sources
PubMed1982

Localization of active and inactive kallikrein (kininogenase activity) in the microdissected rabbit nephron.

Active and total (trypsin-activated) kallikrein were measured in discrete segments of the nephron by their kininogenase activity. The kinins generated were measured by radioimmunoassay and the amount of inactive kallikrein was calculated as the difference between total and active kallikrein. Single nephrons from collagenase-treated rabbit kidneys (N = 12) were microdissected and divided into eight segments: (1) glomerulus; (2) proximal convoluted tubule; (3) cortical thick ascending limb; (4) bright portion of distal convoluted tubule; (5) granular portion of distal convoluted tubule; (6) granular portion of cortical collecting tubule; (7) light portion of cortical collecting tubule; and (8) medullary collecting tubules. After pooled segments (approximately 50 nephron segments in each assay) were homogenized and treated with deoxycholic acid, active and total kallikrein were measured and inactive kallikrein was calculated. Active and inactive kallikrein were localized in granular portions of the distal and cortical collecting tubule, which contains more than 85% of the active and inactive kallikrein found in the total microdissected nephron. Little or no kallikrein was detected in other segments, including the bright portion of the distal segment which has the macula densa. The discrete localization of active and inactive kallikrein suggests a specific role for renal kallikrein in these nephron segments.

Animals↗
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↗
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

A report on the pathology of type A botulism.

An autopsy case of type A botulism, a sacrifice during the first outbreak in Japan, was presented. The patient exhibited typical neuromuscular symptoms and died on the 8th day from the onset of illness. Type A Clostridium botulinum was demonstrated from the stools and the toxin from the blood serum during the course of disease. The infection source of botulinus bacilli, however, was not clarified. The autopsy diagnoses were made as follows; 1) type A botulism, 2) bronchopneumonia, 3) respirator brain, 4) congestion, 5) hemorrhage in vagal nerve, myocardium and endometrium, 6) gastric erosion, 7) cloudy swelling of kidneys, 8) enterocolitis, 9) focal necrosis of liver and adrenals, 10) demyelination of cranial nerves, and 11) focal hyaline degeneration of striated and smooth muscles and myocardium. The botulinus toxin was confirmed from the samples of cardiac blood or autopsy.

Botulinum Toxins↗
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

Active and inactive renin after SQ 14225 (Captopril) administration.

The changes of active and inactive renin in plasma after the oral administration of 25 mg or 50 mg of SQ 14225 (Captopril) were studied in 29 hypertensive patients. Inactive renin was calculated as plasma renin activity (PRA) after cold storage minus PRA before cold storage. 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. These results suggest that inactive renin may be converted in vivo to active renin by Captopril.

Administration, Oral↗
PubMed1979

Change in plasma renin activity by cold storage of plasma in normal subjects and patients with essential hypertension and primary aldosteronism.

The time courses of change in renin activity after cold storage of human plasma at -5 degrees C and pH 7.4 were examined in 5 normal subjects, 6 patients with essential hypertension and one female patient with primary aldosteronism before and after extirpation of the adrenal tumor. In the 5 normal subjects and 6 essential hypertensives, the gradual increase in plasma renin activity was observed until 10 days of cold storage. The same result was obtained in the case of primary aldosteronism. However, there was no increase in renin activity despite of cold storage for 10 days in plasma which was sampled from this patient 45 days after operation. These data indicate that a period of 4 days for cryoactivation of human plasma renin as has been reported by Sealey et al. is not sufficient to accomplish activation of renin by cold storage.

Adolescent↗
PubMedDate not supplied

Well-differentiated hepatocellular carcinoma: findings of US, CT, and MR imaging.

BACKGROUND: To elucidate the imaging characteristics of well-differentiated hepatocellular carcinomas (HCCs) on ultrasonography (US), computed tomography (CT), and magnetic resonance (MR) imaging. METHODS: Ultrasonograms, CTs, and MR images of 18 histopathologically proven well-differentiated HCCs in 15 patients were reviewed. The findings of these images were correlated with histopathologic findings. RESULTS: On US, seven tumors were depicted as a hyperechoic area and eight as a hypoechoic area. Three tumors were not visualized. On precontrast CT, four tumors were depicted as a low-density area, but 14 were not visualized. On conventional contrast-enhanced CT, 12 tumors were depicted as a low-density area but six were not visualized. On T1-weighted MR images, 10 tumors had high signal intensity and two had low signal intensity. Six tumors were not visualized. On T2-weighted MR images, five tumors had high signal intensity and two had low signal intensity. Eleven tumors were not visualized. Tumors with fatty change and/or clear cell formation were frequently hyperechoic on US and hyperintense on T1-weighted MR images. CONCLUSIONS: Well-differentiated HCCs show different findings on US, CT, and MR imaging. Therefore, reliable diagnosis of well-differentiated HCCs by these imaging techniques may be difficult.

Aged↗
PubMedDate not supplied

Vasodilation mediated by angiotensin II type 2 receptor is impaired in afferent arterioles of young spontaneously hypertensive rats.

Renal vasoconstrictor action of angiotensin II (Ang II) is exaggerated in the spontaneously hypertensive rat (SHR) before development of hypertension. We have recently demonstrated that in the rabbit afferent arteriole (Af-Art) activation of the AT2 receptor causes vasodilation, which modulates the vasoconstrictor action of Ang II mediated by the AT1 receptor. In this study, we tested the hypothesis that vasoconstrictor action of Ang II is exaggerated in SHR Af-Arts due to an impaired function of the AT2 receptor before development of hypertension. Af-Arts were microdissected from the superficial cortex of 4- to 5-week-old SHR or age-matched Wistar Kyoto rats (WKY), and perfused at 60 mm Hg in vitro. Ang II (10(-11) to 10(-8) M) decreased the luminal diameter of Af-Arts of both strains in a dose-dependent manner. However, the constriction was stronger in SHR; at 10(-10) M, the diameter decreased by 34 +/- 4% in SHR (n = 6) compared to 18 +/- 3% in WKY (n = 6; p < 0.01). Pretreatment with PD123319 (PD), an AT2 receptor antagonist, significantly augmented Ang II-induced constriction in WKY but not SHR Af-Arts; at 10(-10) M, the diameter now decreased by 41 +/- 5 and 37 +/- 1% in SHR (n = 6) and WKY (n = 6), respectively. Thus, blockade of the AT2 receptor abolished the difference in Ang II action on Af-Arts between strains. Moreover, with the AT1 receptor blockade Ang II caused dose-dependent dilation of preconstricted Af-Arts only in WKY (27 +/- 5% at 10(-8) M, n = 5), and the dilation was abolished by simultaneous treatment with PD. In contrast, no such dilation was observed in SHR Af-Arts. These results suggest that activation of the AT2 receptor modulates AT1 receptor vasoconstriction in WKY Af-Arts, while impaired modulatory function of AT2 receptor may play a role in the exaggerated vasoconstrictor action of Ang II on the Af-Art of prehypertensive SHR.

Angiotensin II↗