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Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 829 records · Page 46Linked to original sources
PubMed1984

Identification of 19-nor-deoxycorticosterone in normal rat serum by enzyme immunoassay and gas chromatography-mass spectrometry.

Recent reports on the isolation and identification of 19-nor-deoxycorticosterone from the urine of rats with adrenal regeneration hypertension give rise to the possibility of a role of this steroid in the pathogenesis of low renin essential hypertension. The present study was undertaken to investigate the presence of 19-nor-deoxycorticosterone in normal rat serum both by a sensitive enzyme immunoassay and by gas chromatography-mass spectrometry (GC/MS). 19-Nor-deoxycorticosterone in rat serum was separated from other steroids prior to enzyme immunoassay by using high performance liquid chromatography (HPLC). The average concentration of 19-nor-deoxycorticosterone in normal rat serum was 137 +/- 62 ng/dl (mean +/- SD, n = 32). Pooled normal rat serum (50 ml) was purified by HPLC and the purified sample was acetylated with acetic anhydride for GC/MS measurement. The retention time and m/z ions (358, 285, and 257) on the resulting mass fragmentogram coincided in position with those of authentic 21-acetoxy-19-nor-deoxycorticosterone and acetylated normal rat serum extract. The combined characteristics of HPLC elution, antigen-antibody reaction, GC retention and selected ion responses provided strongly evidence supporting the presence of 19-nor-deoxycorticosterone in normal rat serum.

Alkaline Phosphatase↗
PubMed1984

Responses of active and inactive plasma renin to insulin-induced hypoglycemia in normal subjects.

To examine the in vivo activation mechanism for the conversion of inactive to active renin in human plasma, we measured active, inactive and total plasma renin activity during an insulin tolerance test in normal subjects. Total renin was measured after trypsin activation of inactive renin. Inactive renin was calculated as the difference between total and active renin. With a decrease in the blood glucose level from 92 +/- 8 to 22 +/- 6 mg/dl (p less than 0.01), active renin increased significantly (p less than 0.01) from the basal level of 1.9 +/- 0.6 to 6.0 +/- 1.9 ng/ml.hr at 60 min after insulin injection. Total renin increased and inactive renin decreased slightly, but the changes were not statistically significant. The ratio of active to total renin showed a significant increase (p less than 0.01) at 60 min. These results suggest that stimulation of the endogenous sympathetic nervous system is involved in the in vivo activation of inactive renin.

Adult↗
PubMed1984

A new sensitive direct radioimmunoassay for human plasma renin and its clinical application.

We developed new sensitive direct radioimmunoassay for human plasma renin. Renin was purified from Haas' preparation utilizing a pepstatin-C6-Sepharose affinity chromatography. Antiserum, prepared by immunizing rabbits with the purified renin, was used for the direct radioimmunoassay at a final dilution of 1:30,000. The antibody was specific for human renal and plasma renin, but did not cross-react with cathepsin D, trypsin, or renins of mouse, dog, and rat. Radioimmunoassay was performed by the double antibody technique using the delayed tracer addition method. In this method, a standard curve was obtained over a range from 0.2 to 8.0 ng/ml. The values from our assay correlated well with total renin activity measured as the generation rate of angiotensin I after trypsin activation (r = 0.78, p less than 0.01), but correlated weakly with active renin activity. This finding disclosed that both active and inactive renin were detected by this method. In normal participants, plasma renin concentration determined by direct radioimmunoassay was increased by standing and furosemide injection. The plasma renin concentration determined by direct radioimmunoassay of patients with essential hypertension (0.7 to 1.7 ng/ml) was not significantly different from values in normal controls (0.8 to 1.9 ng/ml). The values were higher in patients with renovascular hypertension (1.6 to 2.7 ng/ml), malignant hypertension (2.8 to 3.4 ng/ml) and Bartter's syndrome (1.8 to 2.5 ng/ml), but lower in patients with primary aldosteronism (0.4 to 0.8 ng/ml) than in normal controls. This newly developed radioimmunoassay for human renin was sensitive enough to estimate the levels of renin in plasma of patients with low renin hypertension. It provides a new tool for the understanding of the renin-angiotensin system under various clinical conditions.

Adult↗
PubMed1984

Sensitive direct radio-immunoassay for human renin.

A sensitive direct human renin radio-immunoassay has been developed for clinical use. The antigen source was human renal renin purified from Haas' preparation by pepstatin-C6-sepharose affinity chromatography, this was used to prepare a specific human renin antibody. The radio-immunoassay was performed by the double antibody technique using the delayed tracer addition method. Standard curves were obtained over the range 0.2-8.0 ng/ml. Dilution curves of human renal renin and human plasma were superimposable on the standard curve. Both active and inactive renin were detected by this method, and measurements correlated well with total renin activity after trypsin activation. Intra- and inter-assay coefficients of variance were 4.6% and 5.1%, respectively. Renin concentration was higher in patients with renovascular hypertension (1.97 +/- 0.38 ng/ml, mean +/- s.d., n = 10, P less than 0.01), but lower in primary aldosteronism (0.66 +/- 0.16 ng/ml, n = 13, P less than 0.01) compared with essential hypertension (1.38 +/- 0.34 ng/ml, n = 12). This method provides a new tool for the investigation of the renin-angiotensin system in man.

Humans↗
PubMed1984

A new orally active hypotensive peptide, N-(dibenzyloxyphosphinoyl)-L-alanyl-L-prolyl-L-proline (PAPP).

The antihypertensive effects and mechanisms of a newly developed orally active tripeptide, N-(dibenzyloxyphosphinoyl)-L-alanyl-L-prolyl-L-proline (PAPP), were investigated. When PAPP (1-30 mg/kg orally) was administered to spontaneously hypertensive rats (SHR), systolic blood pressure (SBP) reached a maximum reduction after 8 h and this effect lasted over 24 h. In two-kidney, one clip hypertensive rats (2KIC rats) and DOCA-salt hypertensive rats, PAPP also reduced SBP. In normotensive Wistar rats, however, PAPP did not have a hypotensive effect. PAPP showed low toxicity in Sprague-Dawley rats. The depressor response to bradykinin (BK) was potentiated, but the pressor response to angiotensin I (ANG I) was not inhibited by PAPP. PAPP significantly relaxed isolated SHR aortic strips treated with KC or norepinephrine. Angiotensin converting enzyme (ACE) inhibition by PAPP was relatively low in vivo and in vitro.

Administration, Oral↗
PubMed1983

Effect of captopril on renal vascular resistance, renin, prostaglandins and kinin in the isolated perfused kidney.

Vasodilatory and natriuretic effects of captopril were studied in the isolated hog kidney perfused with modified Krebs-Ringer solution. Renal arterial infusion of captopril caused increases in releases of renin, prostaglandins (PGE2, 6-keto-PGF1 alpha and PGF2 alpha) and kinin, and was accompanied by a decrease in the renal vascular resistance and an increase in urinary sodium excretion. Indomethacin administered with captopril diminished the saluretic effect of captopril and evoked an increase in kinin, but was associated with a marked decrease in prostaglandin and renin releases, while renal vascular resistance remained decreased. Indomethacin alone did not alter vascular resistance and kinin; however, renin and prostaglandin releases were decreased. Aprotinin administered with captopril showed a decrease in releases of prostaglandins, renin and kinin without any change in vascular resistance. These results suggest that increased release of kinin induced by captopril contributes to a reduction in renal vascular resistance. Increased prostaglandin release after captopril administration may be caused by an increase in kinin without direct involvement of captopril in prostaglandin synthesis. Renal prostaglandins may enhance sodium excretion and mediate renin secretion in captopril perfusion.

Animals↗
PubMed1983

[A simple and direct radioimmunoassay for serum and urinary metanephrine].

A simple, direct and specific radioimmunoassay for serum and urinary metanephrine was developed, in which we used 125I-Synephrine and specific antiserum generated in rabbits by injecting with metanephrine conjugated with bovine serum albumin as described by Grota and Brown. The sensitivity of the assay was 2 pg/tube. Intra- and inter-assay coefficients of variation were 2.6 approximately 7.8% and 5.0 approximately 9.6%, respectively. The recoveries of metanephrine added at two levels of 250 pg/ml and 500 pg/ml to ten serum samples and ten urine samples (hydrolyzed and diluted) were 96.7 and 108% in serum, and 94.8 and 103% in urine, respectively. Normal values of serum metanephrine were 40.3 +/- 25.8 pg/ml (mean +/- SD) from 20 normal subjects. Normal values of 24 hour urinary metanephrine excretion were 12.5 +/- 6.7 ug/day from 24 normal subjects. Serum metanephrine values for 7 patients with pheochromocytoma were 210 approximately 628 pg/ml. Urinary metanephrine values for 9 patients with pheochromocytoma 8.7 approximately 302 ug/day.

Adrenal Gland Neoplasms↗
PubMed1983

[Effect of aging on blood catecholamine under 3 conditions of sodium intake--comparison between normal subjects and patients with essential hypertension].

Increased sympathetic nervous activity may play an important role in the pathogenesis of essential hypertension. It is well-known that both dietary sodium intake and age influence plasma norepinephrine (P-NE). There are many reports on comparative studies of P-NE in patients with essential hypertension and normotensive controls. However, there are few studies on changes in plasma catecholamines in both the aging and salt intake states. The present study was undertaken to evaluate the effect of age on sympathetic nervous activity in patients with essential hypertension and normal controls under low (UNa V 29 +/- 3 mEq/day), regular (UNa V 133 +/- 8 mEq/day) and high (UNa V 324 +/- 12 mEq/day) sodium regimens. The catecholamine levels were analyzed by THI methods after HPLC separation. Twenty-four hour urinary norepinephrine, epinephrine and electrolyte (Na+, K+) excretion on day 5 of each regimen was also determined. On day 6 morning, supine and upright P-NE, plasma epinephrine and plasma renin activity were determined after blood pressure and pulse rate measurement. Subjects were separated according to age as follows: young (less than 40 y.o.), middle-aged (40 approximately 60 y.o.) and old (greater than 60 y.o.). P-NE in hypertensives was significantly higher than in normals under any three sodium intakes. There was a significantly positive correlation between age and P-NE, but only in normal controls under three sodium intakes and not in hypertensive patients under any three sodium regimens. In the young group of hypertensive patients, P-NE was significantly higher than that of normal controls. These results suggest that the increased sympathetic nervous activity plays an important role in the pathogenesis and maintenance of essential hypertension, and this is particularly obvious in young patients.

Adolescent↗
PubMed1983

A novel purification method of human renin.

Human renal renin was isolated from a partially purified preparation, Haas' preparation step 5 material, with a remarkably high yield of 28% by a newly developed method. This method consisted of only four steps including affinity chromatography on pepstatin-aminohexyl-agarose, chromatofocusing, gel filtration and DEAE-chromatography after the initial extraction and concentration. This method enabled us to obtain pure human renin without another affinity column used by other investigators. Pure human renin had a molecular weight of 40,000 daltons as estimated by gel filtration and sodiumdodecylsulfate-polyacrylamide gel electrophoresis. The pI of purified renin was 5.6.

Chromatography, Affinity↗
PubMed1983

Decreased serum 19-nor-deoxycorticosterone (21-hydroxy-19-nor-4-pregnene-3, 20-dione) level in adrenal regeneration hypertensive rats.

An enzyme immunoassay of 19-nor-deoxycorticosterone in rat serum was established. The normal value of 19-nor-DOC in rat serum obtained from 9:00 am to 10:00 am was 148 +/- 30 ng/dl (mean +/- SE,n = 10). Serum levels of this steroid decreased in rats with adrenal regeneration hypertension during the course of the experiment up to 8 weeks, while systolic blood pressure rose progressively. We concluded that this mineralocorticoid is not involved at least as a circulating hormone in the pathogenesis of adrenal regeneration hypertension in rats.

Adrenal Glands↗
PubMed1983

Levels of plasma 6-keto-PGF1 alpha in normotensive and essential hypertensive males with and without a family history of hypertension.

Prostacyclin may act physiologically as an antihypertensive hormone. It remains uncertain, however, whether prostacyclin may be involved in the etiology of primary hypertension. As an index of prostacyclin production, we measured the levels of venous plasma 6-keto-PGF1 alpha by specific radioimmunoassay after silicic acid column chromatographic purification in 31 normotensive and 36 hypertensive males. The subjects were grouped according to the presence or absence of a family history of hypertension, and matched for age and blood pressure. Levels of 6-keto-PGF1 alpha in normotensive males with a family history of hypertension (12.0 +/- 1.7 pg/ml; mean +/- SEM; n = 18) were lower than in normotensive males without a family history of hypertension (17.7 +/- 2.0 pg/ml; n = 13) (p less than 0.01). Levels of plasma 6-keto-PGF1 alpha in hypertensive males with a family history of hypertension (10.2 +/- 1.2 pg/ml; n = 15) were lower than in hypertensive males without a family history of hypertension (20.5 +/- 1.5 pg/ml; n = 21) (p less than 0.005). The levels of plasma 6-keto-PGF1 alpha in males with a family history of hypertension may be decreased genetically. The decrease in production of prostacyclin in males with a family history of hypertension may be a factor in the etiology of hypertension.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Plasma inactive renin in patients with hyperthyroidism.

Active and inactive PRA were measured after 1 h at rest in 16 normal controls and 20 patients with hyperthyroidism. In some of the patients these measurements were repeated after they had become euthyroid or received 90 mg propranolol for 1 week. Inactive PRA was determined as the difference between total PRA after trypsin activation and active PRA. Active PRA was significantly higher (P less than 0.01) in untreated patients than in normal subjects; however, the inactive PRA of patients was not different compared with that of normal subjects. Active PRA was normalized, and inactive PRA did not change after achievement of euthyroidism. The proportion of active of total PRA was significantly correlated with the levels of serum thyroid hormones (T3 and T4) in hyperthyroid patients (r = 0.46; P less than 0.05 and r = 0.55; P less than 0.01, respectively). The administration of propranolol reduced active PRA (P less than 0.05) and increased inactive PRA slightly but not significantly. These results indicate that in hyperthyroidism, the in vivo conversion of inactive renin to active renin is probably facilitated by increased sympathetic activity.

Adult↗
PubMed1983

Effect of aging on 6-keto-PGF1 alpha levels in normotensive and essential hypertensive males.

Prostacyclin (PGI2) is produced in the vessel wall and acts as a vasodilator hormone. Measurement of plasma 6-keto-PGF1 alpha is considered to be an index of PGI2 production. In the present study the effects of aging on the plasma 6-keto-PGF1 alpha levels were studied in 64 normotensive and 48 essential hypertensive males. The subjects were divided into 3 groups, i.e., young (24-39 years), middle-aged (40-55 years) and elderly (over 56 years) groups. Plasma 6-keto-PGF1 alpha was measured by specific radioimmunoassay after silicic acid column chromatographic purification. The 6-keto-PGF1 alpha levels were lower in elderly normotensive males (10.3 +/- 1.4 pg/ml, mean +/- SE, n = 12) than in normotensive young males (15.3 +/- 2.3, n = 30, p less than 0.05). The plasma 6-keto-PGF1 alpha levels in hypertensive elderly males (10.6 +/- 1.3 pg/ml, n = 10) is lower than in hypertensive young males (19.8 +/- 2.2, n = 17, p less than 0.01). These results indicate that the plasma 6-keto-PGF1 alpha levels decreased with age in both normotensive and hypertensive groups. Thus, PGI2 production may decrease with age.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Plasma inactive renin in diabetic patients with neuropathy: a role for the sympathetic nervous system in the conversion in vivo of inactive renin.

Plasma levels of active and trypsin-activatable inactive renin and catecholamines were measured in 6 diabetic patients with neuropathy (group 1), 8 diabetic patients without neuropathy (group 2) and 8 age-matched normal subjects. The effect of insulin administration on plasma active and inactive renin and plasma catecholamine levels in diabetic patients was also investigated. The levels of inactive renin were calculated as the difference between the levels of total renin after trypsin activation and those of active renin. The levels of plasma catecholamines were determined by the trihydroxyindole method. The levels of active renin were significantly lower and inactive renin was increased slightly in group 1 when compared with controls. Group 1 showed a significant reduction in plasma norepinephrine levels. Group 2 showed slightly reduced active renin, normal inactive renin and normal norepinephrine values. There was no significant difference in the levels of epinephrine between the 3 groups. After insulin injection, active renin levels were increased in groups 1 and 2. The mean increment in active renin levels was less in group 1 than in group 2. Inactive renin levels were slightly decreased in both groups. Significant increases in epinephrine and norepinephrine levels were observed following insulin administration. The mean increment in norepinephrine levels was less in group 1 than in group 2. There was a positive correlation between the mean increment in active renin and in norepinephrine levels in diabetic patients. These results suggest that the impaired conversion of inactive renin into an active form is responsible in part for the low levels of active renin in diabetics with neuropathy.

Diabetes Mellitus↗
PubMed1983

Effects of angiotensin I converting enzyme inhibitors on the renal excretory function, hemodynamics and renin release in isolated perfused rat kidney.

Direct renal effects of angiotensin I converting enzyme inhibitors (CEIs), captopril, SA446 and MK421, were examined in isolated rat kidneys perfused with a renin-substrate-free medium. Among three CEIs, only captopril induced a significant natriuresis, whereas SA446 and MK421 did not. UKV, renal vascular resistance and creatinine clearance were not affected by any of these CEIs. Renin release from perfused rat kidneys were not influenced by CEIs under the present experimental conditions. These results suggest that among three different types of CEIs, only captopril possesses natriuretic action in the isolated perfused rat kidney and that this action may be independent of its inhibitory action on angiotensin converting enzyme. It is also suggested that these three CEIs themselves do not have a direct effect on the renal vascular bed.

3-Mercaptopropionic Acid↗