Search PubMed⌕ Search

Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 865 records · Page 48Linked to original sources
PubMed1982

Evaluation of the renin-angiotensin system in diabetes insipidus and psychogenic polydipsia.

The role of the renin-angiotensin system in polyuric patients was studied in 5 patients with pituitary diabetes insipidus, 1 patient with nephrogenic diabetes insipidus and 3 patients with psychogenic polydipsia by determining the plasma renin activity and infusing an angiotensin II analog, 1-Sar, 8-Ile angiotensin II. In all patients with diabetes insipidus, plasma renin activity was markedly increased and the blood pressure was reduced in 5 of 6 patients by the administration of the angiotensin II analog. In the other patient, the blood pressure remained unchanged. The plasma renin activity and response of blood pressure to the angiotensin II analog in a patient with nephrogenic diabetes insipidus were not significantly different from there of patients with pituitary diabetes insipidus. On the other hand, in all patients with psychogenic polydipsia, plasma renin activity was normal or low, and the blood pressure increased with the administration of the angiotensin II analog. These results suggest that evaluation of the renin-angiotensin system by determining plasma renin activity and infusing an angiotensin II analog is useful in differentiating between diabetes insipidus and psychogenic polydipsia.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1982

Measurement of plasma renin activity by a simple solid phase radioimmunoassay.

A solid phase RIA in which an antibody adsorbed onto polystyrene balls was developed to determine PRA. Complete inhibition of converting enzyme and angiotensinase during enzymatic reaction was achieved by phenyl methyl sulfonyl fluoride and EDTA combination. Pepstatin A was found to be an effective agent to block angiotensin I generation during the RIA, and the sample can be directly incubated at room temperature for RIA without any special treatment to inhibit renin activity. The intra- and interassay coefficients of variation (CV) were 5.5-6.9% and 3.7-8.2%, respectively. The recovery was 91.9-117% of added angiotensin I. The assay is sufficiently sensitive and reliable for routine use and correlates acceptably (r = 0.996) with an established RIA. The antibody-adsorbed balls were compared to the soluble antibody with respect to thermodynamic parameters. It was found that the apparent equilibrium constant of the antibody-adsorbed ball was reduced to approximately 1/2 sec of soluble antibody, which was predominately due to the decrease in unitary entropy change by adsorption.

Angiotensin I↗
PubMed1982

Responses of active and inactive plasma renin and changes in urinary kallikrein and plasma prekallikrein to various conditions in normal subjects.

Little is known about changes in inactive plasma renin in various conditions or the in vivo activation mechanism of inactive renin. The effects of various factors known to stimulate or suppress renin release on active and inactive PRA were examined in normal subjects. Inactive PRA was determined as the difference between the total PRA after trypsin activation and active PRA. Concurrent measurements of urinary kallikrein excretion and plasma prekallikrein activity were performed to assess the possible role of renal or plasma kallikrein in in vivo activation of inactive renin. Short term stimulation with iv furosemide and ambulation, infusion of isoproterenol, and administration of captopril increased active PRA, but had little or no effect on inactive PRA. Sodium restriction and sodium loading, each for 4 days, induced parallel changes in active and inactive PRA. The administration of propranolol for 4 days decreased active PRA but did not change inactive PRA. There were no significant correlations between the changes in urinary kallikrein excretion and those in active PRA or in the proportion of active to total PRA after any short term treatments, except furosemide administration. Plasma prekallikrein activity was correlated with the proportion of active renin only during the long term sodium balance study. The present data suggest that the mechanisms ofr the control of inactive and active renin are different. Neither renal nor plasma kallikrein seems to be consistently involved in the in vivo activation of inactive renin.

Adult↗
PubMed1982

Evaluation of hypotensive mechanisms of captopril in addition to its inhibition of the converting enzyme in spontaneously hypertensive rats.

In spontaneoulsy hypertensive rats (SHR), the hypotensive effect of captopril (30 mg/kg/day per os for 4 days), which inhibits the converting enzyme when given orally was significantly potentiated rather than suppressed by aprotonin (100,000 KIU/day s.c. for 7 days), but was not affected by indomethacin. These findings suggest that neither the kallikrein-kinin system nor the prostaglandin system is involved in any of the hypotensive actions of captopril in SHR other than the inhibition of the converting enzyme.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

The seasonal variation of blood pressure in patients with essential hypertension.

We examined the role of dietary electrolytes and humoral factors in causing seasonal changes in blood pressure. Normal subjects had no seasonal difference in blood pressure, although urinary sodium and norepinephrine were significantly higher in winter than in summer. In patients with essential hypertension blood pressure, urinary sodium and norepinephrine excretion and plasma norepinephrine concentration were significantly higher in winter. Plasma renin activity, plasma and urinary aldosterone and urinary kallikrein excretion were not significantly different between the two seasons in both normal subjects and hypertensive patients. In conclusions, the blood pressure of patients with essential hypertension has a seasonal variation with higher pressures in the winter than in the summer. Increased sympathetic nervous activity and an increased load of sodium presented to the kidney for excretion may be contributing factors in the rise in blood pressure in winter in patients with essential hypertension.

Adult↗
PubMed1982

Release of prostaglandin I2 from hog kidney by propranolol.

Prostaglandin I2 (PGI2) decreases blood pressure. Perfusion of isolated hog kidney by propranolol in modified Krebs-Ringer solution resulted in a significant increase in 6-keto-prostaglandin F1 alpha, the major metabolite of PGI2. Prostaglandin E2 and renin activity remained unchanged. Because the concentration of PGI2-like substance in the renal vein has been shown to be greater than in the renal artery after bradykinin infusion, a contribution of PGI2 to the regulation of blood pressure was proposed. Isoproterenol has been shown to augment urinary kallikrein, but the effect of urinary kallikrein on propranolol is unclear. With a modified Krebs-Ringer solution free of plasma kininogen, a renin substrate, it was concluded that propranolol (1) induces PGI2 release from the kidney, which may contribute to a direct antihypertensive action of this beta-adrenergic blocking agent, and (2) decreases urinary kallikrein.

Animals↗
PubMed1982

Familial Bartter's syndrome.

Two sisters were found to have Bartter's syndrome. Both had hypokalemia, hyperreninemia, normal BPs, and decreased pressor responses to angiotensin II. During a water diuresis, patient 1 had an abnormally low distal tubular fractional reabsorption of chloride initially, but this normalized after hypokalemia was corrected for one year. Patient 2 had no demonstrable defect in chloride transport. Hypokalemia in Bartter's syndrome may be caused by some hereditary mechanisms other than defective reabsorption of chloride in the distal tubules.

Absorption↗
PubMed1981

[A simple solid phase radioimmunoassay for plasma renin activity (author's transl)].

A solid phase radioimmunoassay (RIA) in which plasma renin activity (PRA) can be measured in a single test tube throughout enzymatic reaction and determination of angiotensin-I (A-I) generated was developed. Two hundred micro 1 of plasma samples was incubated with phenylmethylsulfonyl fluoride (PMSF) and ethylenediamine tetraaceticacid (EDTA) at pH 6.0 or 7.4 at 37 degrees C for 1 hr, then the generated A-I was determined by solid phase RIA under 3 hr of incubation time at room temperature. An antibody absorbed onto polystyrene beads was used for B/F separation of RIA. The combination of PMSF and EDTA gave significant inhibition of angiotensinase and converting enzyme. Pepstatin A, proteolytic enzyme inhibitor, was found to be effective to block the renin activity during the incubation for RIA at room temperature. Recoveries of A-I added at two levels of 1.0 4.0 ng/ml to plasma sample incubated at 37 degrees C for 1 hr were 102 +/- 28.6% and 105 +/- 15.2%, respectively. Intra-assay precision (CV) ranged from 2.5 to 10.3% and inter-assay from 7.0 to 13.7% with four pooled sera. PRA obtained under enzymatic reaction of pH 6.0 showed approximately twice as much as that of pH 7.4. The assay correlated closely with the other established solid phase radioimmunoassay kit (r = 0.996). Normal values of PRA were 1.03 +/0 0.78 ng/mg/hr (n = 66) at supine position and 1.33 +/- 1.15 ng/ml/hr at upright position. The method for the measurement of PRA, described in this paper, can be clinically used as one of convenient methods froms its simplicity and reproducibility.

Female↗
PubMed1981

Hormonal responses to long-term converting enzyme inhibition in hypertensive patients.

Captopril was given alone and in combination with diuretics to 49 patients with hypertension for 1 to 12 mol Within 2 mo blood pressure reduction correlated with pretreatment plasma renin activity and response to the infusion of angiotensin II antagonist, but these effects were not present at 4 mo. Plasma and urinary aldosterone were suppressed but serum converting enzyme activity, plasma bradykinin, kallikren, and prostaglandins (E and F) were in the normal range effect of captopril. Despite sustained reduction of blood pressure, plasma catecholamines were not elevated and urinary catecholamines were suppressed in patients on captopril alone. It is concluded that another mechanism, such as enhancement of renal or local kinin-prostaglandin system, as well as suppression of the renin-angiotensin-aldosterone system may be involved in the long-term efficacy of captopril. Sympathetic activity may also be depressed and contribute to the hypotensive effect.

Adolescent↗
PubMed1981

Effect of age on active and inactive plasma renin in normal subjects and in patients with essential hypertension.

The effect of age on the levels of active and trypsin-activatable inactive plasma renin was examined in 41 normal subjects and 54 patients with essential hypertension, during recumbency and after stimulation with furosemide and ambulation. Active renin levels in supine subjects and patients decreased with age. Inactive renin levels did not change with age in normal subjects, whereas in hypertensive patients they decreased with age. Following stimulation with furosemide and ambulation, the levels of active renin increased but the responsiveness to stimulus decreased with age in both groups. In contrast, inactive renin levels slightly increased after furosemide administration and ambulation, resulting in increased proportion of active to total renin. These data show that an acute stimulation with furosemide and ambulation affects mainly the active form of plasma renin, and the effect of age on inactive plasma renin in normal subjects may be different from that in patients with essential hypertension.

Adult↗
PubMed1981

The effect of aging on urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension.

The effect of aging on urinary kallikrein excretion (UkalV) was investigated in 54 normal subjects, 11-88 yr old, and 37 patients with essential hypertension, 17-82 yr old. Urinary sodium, potassium, and aldosterone excretion (U(Ald)V) were also measured in these subjects. Urinary sodium and potassium excretion in both normal subjects and hypertensive patients did not significantly change with aging. In normal subjects, U(kal)V (r = 0.45; P less than 0.001) and U(Ald)V (r = 0.58; P less than 0.01) significantly decreased with increasing age. U(kal)V was positively correlated with U(Ald)V (r = 0.44; P less than 0.001). In contrast, the hypertensive patients had a significant decrease with age in U(Ald)V (r = -0.36; P less than 0.05), but no significant age-related change in U(kal)V. No significant correlation between U(kal)V and U(Ald)V was observed in the hypertensive patients. In individuals less than 60 yr old, there was no significant difference in U(kal)V values between normal subjects and hypertensive patients. Hypertensive patients more than 60 yr old excreted more urinary kallikrein than normal subjects of the same age group (P less than 0.05). In conclusion, the age-related decrease of U(kal)V in normal subjects may be due to the reduced activity of the renin-angiotensin-aldosterone system. It remains to be elucidated whether the absence of the age-related decrease in U(kal)V in hypertensive patients is related to the pathogenesis or pathophysiology of essential hypertension.

Adolescent↗
PubMed1981

Central and peripheral effects of dopamine on the renin-angiotensin-aldosterone system in conscious rats.

To investigate the role of the central and peripheral dopaminergic systems in the control of the renin-angiotensin-aldosterone system in conscious rats, dopamine or its antagonist, metoclopramide, was injected intravenously (i.v.) and intracerebroventricularly (i.c.v.). Dopamine (100 micrograms/kg), when injected i.c.v., decreased plasma renin activity (PRA) and plasma aldosterone concentration (PA), while metoclopramide (50 micrograms/kg, i.c.v.) increased both of them. Intravenous administration of dopamine (1 microgram/kg/min) did not produce significant changes in either PRA or PA. In contrast, metoclopramide (500 micrograms/kg, i.v.) increased PA, which was not accompanied by any change in PRA. Blood pressure was decreased by i.c.v. administration of dopamine and increased by i.c.v. injection of metoclopramide, whereas no change in blood pressure was observed when these compounds were administered i.v. Dopamine and metoclopramide, injected i.v. or i.c.v., did not produce significant changes in plasma sodium, potassium and corticosterone concentrations. These results suggest that the dopaminergic system in the brain regulates renin secretion, thereby changing PA. In contrast, dopamine receptors of the adrenal glands may inhibit aldosterone secretion, which is not mediated by changes in the renin-angiotensin system, plasma potassium and ACTH.

Aldosterone↗