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Biomedical subjects

T Naka

Publications and source records attributed to T Naka.

At least 109 records · Page 6Linked to original sources
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↗
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

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗