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Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 883 records · Page 49Linked to original sources

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

The effect of age on active and cryoactivatable inactive plasma renin levels was examined in 58 normal subjects and 58 patients with essential hypertension during recumbency and after stimulation with furosemide and ambulation. Active renin levels declined with age in both supine subjects and patients. Inactive renin levels did not change with age in normal subjects, while in hypertensive patients they decreased with age. Following stimulation with furosemide and ambulation, the levels of active renin increased but its responsiveness to the stimulus decreased with age in both groups. In contrast, inactive renin was not significantly influenced by furosemide administration and ambulation. These data show that an acute stimulation with furosemide and ambulation affects mainly the active form of plasma renin, and that the effect of age on inactive plasma renin in normal subjects may be different from that in patients with essential hypertension.

Adolescent↗

A case of normoreninemic, normotensive primary aldosteronism associated with essential hypertension and nephrocalcinosis.

A 36-year-old female case of normotensive normoreninemic primary aldosteronism with persistent hypokalemia and nephrocalcinosis is reported. She was referred to us for episodes of sudden muscle weakness during 8 years prior to admission. On the first day of admission, her blood pressure was 174/104 mmHg. On the second day of admission blood pressure normalized to 120/80 mmHg. Both of her parents were hypertensive. Arterial blood gas analysis showed metabolic alkalosis. Except an impaired urine concentration ability, renal functions were normal. Intravenous pyelogram showed numerous granular calcifications. Basal plasma renin activity was 1.0 approximately 1.5 ng/ml/hr and increased by sodium depletion. Plasma aldosterone concentration was 70 approximately 80 ng/dl and did not respond to various stimulations. Blood pressure was dependent on sodium balance. It fell on salt restriction and rose on salt loading. Blood pressure responses to vasoactive hormones were normal. Circulating plasma volume was within normal range. After removal of an adrenal adenoma, there was mild fall of blood pressure, serum potassium returned to normal level and plasma renin activity increased slightly. Histologically, there was renal tubular calcifications, and juxtaglomerular apparatus was normal. Blood pressure was elevated to 160/100 mmHg when patient was followed at out-patient clinic after discharge. We concluded that she had essential hypertension associated with primary aldosteronism. Although sodium loss and an increase in urinary kallikrein were found, they did not seem to be the cause of normoreninemic normotensive state of this patient, and the pathogenesis remains to be elucidated.

Adrenal Gland Neoplasms↗

Reserpine, hydrochlorothiazide and pituitary-gonadal hormones in hypertensive patients.

Sex histories and serum samples were obtained from 27 hypertensive men before and after 3 months of therapy with either 100 mg of hydrochlorothiazide or 0.25 mg of reserpine daily. Sera were analyzed for testosterone, dihydrotestosterone, estradiol, luteinizing hormone and prolactin. Both drugs effectively lowered pressure. The incidence of impaired sexual performance was low and insignificantly different in the two treatment groups. There were no significant changes in serum hormone concentrations as a result of drug therapy.

Adult↗

Effects of two angiotensin II analogues on blood pressure, plasma aldosterone concentration, plasma renin activity and creatinine clearance in normal subjects on different sodium intakes.

Two angiotensin II analogues (AIIA), 1-sarcosine, 8-isoleucine angiotensin II ([Sar, Ile]-AII) and 1-sarcosine, 8-alanine angiotensin II ([Sar, Ala]-AII), were infused in six normal volunteers on high, regular and low sodium diets. The agonist and antagonist activities of these AIIA on blood pressure (BP), plasma aldosterone concentration (PAC), creatinine clearance and plasma renin activity were examined. Both AIIA had agonistic pressor activities in subjects on high and regular sodium diets, [Sar, Ile]-AII being more potent than [Sar, Ala]-AII. Both AIIA caused similar elevation of PAC in subjects on high and regular sodium diets, and an equally fall in PAC in subjects on a low sodium diet. Both AIIA strongly antagonized the rise in BP, the increase in PAC and the reduction of Ccr induced by AII administration in subjects on all three sodium diets. The results indicate that both AIIA can be used to examine the activity of the renin-angiotensin system in patients with hypertension, and they also suggest that AII interaction with its receptors differs in different target tissues.

1-Sarcosine-8-Isoleucine Angiotensin II↗

Long-term effects of captopril in hypertension.

Captopril was given for treatment of hypertension alone or in combination with diuretics to 32 patients for 1- to 4-mo periods. The decrement of mean blood pressure after 1 and 2 mo correlated with pretreatment plasma renin activity (PRA) and the response of blood pressure to infusion of an angiotensin II antagonist. These correlations were no longer apparent after 4 mo of treatment. When subjects with a decrement of mean blood pressure that exceeded 13 mm Hg were compared with nonresponders, responders not only had higher control PRA and higher PRA at 1 mo of treatment, but also had decreased plasma aldosterone levels, decreased urinary aldosterone excretion, and increased serum postassium levels that persisted over the 4 mo of observation. The reduction of plasma aldosterone correlated with the fall of mean blood pressure. Urinary kallikrein, catecholamines, electrolytes, and endogenous creatinine clearance did not change in response to treatment. These findings indicate that the antihypertenisve activity of captopril on long-term administration probably depends in part on the blockade of angiotensin II, but other mechanisms cannot be excluded.

Adolescent↗

Urinary catecholamine response to glucagon in young and elderly patients with essential hypertension.

The role of the sympathetic nervous system (SNS) in essential hypertension was evaluated by examining the response of urinary catecholamines to the intramuscular injection of glucagon in both young and elderly normal subjects (total 16) and in both young and elderly patients with essential hypertension (total 16). Urine was collected for 2 hours before glucagon injection and for 2 and 4 hours after injection, for determination of adrenaline and noradrenaline. The increments of urinary adrenaline and noradrenaline after glucagon injection were significantly higher in young hypertensive than in young normotensive subjects or in normotensive and hypertensive elderly subjects. The observation that the reactivity of the SNS is increased in young patients with essential hypertension lends support to the hypothesis that the SNS is more important in the maintenance of hypertension in the young than in the elderly.

Adult↗

Blood pressure response to an angiotensin II antagonist in thyrotoxic patients with and without high blood pressure.

An angiotensin II antagonist, [sacrosine1, isoleucine8] angiotensin II, was infused into thyrotoxic patients. Blood pressure was monitored before and during the infusions to investigate whether the renin-angiotensin-aldosterone system was involved in the maintenance of blood pressure in normotensive and hypertensive thyrotoxic patients. Five out of 17 normotensive patients with hyperthyroidism showed more than a 10 mmHg decrease in mean blood pressure in response to the infusion (responders), while the remaining 12 patients showed no substantial change in blood pressure (non-responders). The infusion caused little change in blood pressure in 8 hyperthyroid patients with systolic hypertension. The mean levels of serum thyroxine, triiodothyronine, plasma renin activity and plasma aldosterone concentration in the normotensive responders were significantly higher than the values in the normotensive non-responders. There were no significant differences in these laboratory values between the hypertensive patients and the normotensive non-responders except that serum triiodothyronine levels were significantly higher in the hypertensive patients. The present study indicates that increased activity of the renin-angiotensin-aldosterone system is involved in the maintenance of blood pressure in most normotensive patients with severe hyperthyroidism, while hypertension in patients with hyperthyroidism is not angiotensin II dependent.

1-Sarcosine-8-Isoleucine Angiotensin II↗

The effect of 5 alpha-dihydrocortisol on the blood pressure of rats treated with deoxycorticosterone acetate and salt.

5 alpha-dihydrocortisol has been reported to amplify the mineralocorticoid activity of aldosterone. In this study 5 alpha-dihydrocortisol was administered to unilaterally nephrectomized rats treated with 11-deoxcorticosterone acetate (DOCA) and sodium chloride to examine its potentiating effect on the elevation of blood pressure in these animals. Subcutaneous administration of DOCA at two dose levels (40 microgram and 100 microgram/100 g of body weight 3 times a week) resulted in a significant rise in blood pressure when compared with controls given no DOCA. However, concomitaut injection of 5 alpha-dihydrocortisol (300 microgram/100 g of body weight 3 times a week) with both doses of DOCA did not accelerate the development or potentiate the severity of the hypertension in a 4 week period. Furthermore, administration of 5 alpha-dihydrocortisol did not cause a further decrease in plasma renin activity or a greater increase in urinary kallikrein excretion than those observed after DOCA alone. Thus, 5 alpha-dihydrocortisol does not potentiate DOCA in the production of low renin hypertension in unilaterally nephrectomized salt-loaded rats.

Animals↗

Is normoreninemic essential hypertension caused by disordered central dopaminergic regulation?

Some investigators have reported that plasma prolactin levels are elevated in hypertensive men and that both their hyperprolactinemia and hypertension were controlled by bromocriptine, a dopamine agonist. They concluded that reduced central dopaminergic activity may be a factor in maintaining essential hypertension. We examined the serum prolactin and thyrotropin (TSH) responses to thyrotropin releasing hormone (TRH), metoclopramide (a dopamine antagonist) and bromocriptine in 10 normal and 10 hypertensive normoreninemic men. TRH caused significant increase of both prolactin and TSH and metoclopramide caused significant increase of prolactin in both normals and hypertensives. Bromocriptine suppressed prolactin and TSH significantly in both groups. There were no significant differences in prolactin and TSH levels between the normal and hypertensive groups before or during the tests. These results provide no support for the hypothesis that alterations in the activity of central dopaminergic neurons are involved in the maintenance of the elevated blood pressure of normoreninemic men with essential hypertension.

Bromocriptine↗