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K Masuo

Publications and source records attributed to K Masuo.

At least 55 records · Page 3Linked to original sources
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

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↗
PubMed1982

Effect of prostacyclin infusion on active and inactive renin release in the isolated perfused kidney.

The effect of prostacyclin infusion into the renal artery of the isolated perfused hog kidney on the release of active and inactive renin was investigated. Infusion of prostacyclin at a rate of 0.1 microgram/min resulted in a significant increase (p less than 0.01) in active renin and a significant fall (p less than 0.01) in inactive renin. Prostacyclin also increased urinary kallikrein excretion (p less than 0.05). The results indicate that the kidney secretes not only active renin but also inactive renin, and suggest that prostacyclin stimulates the conversion of inactive renin to the active form through the activation of the renal kallikrein system.

Animals↗
PubMed1982

[Urinary epinephrine and norepinephrine excretion in patients with medullary thyroid carcinoma and their relatives].

Medullary thyroid carcinoma can arise as a component of multiple endocrine neoplasia (MEN) syndrome which includes adrenal pheochromocytoma. Familial medullary thyroid carcinoma with no association of other components of MEN syndrome is also reported. Epinephrine and norepinephrine excreted in 24 hour urine and/or randomly voided urine were measured for screening of pheochromocytoma in patients with medullary thyroid carcinoma of either the hereditary or sporadic type and in their relatives. Six patients with clinical symptoms and signs suggesting pheochromocytoma had a markedly increased epinephrine and epinephrine/norepinephrine (E/N) ratio and a less dominant increase of norepinephrine in 24 hour urine. The diagnosis of pheochromocytoma was proved later at surgery. Among 10 patients with hereditary medullary thyroid carcinoma without any clinical symptoms and signs for pheochromocytoma, 6 patients had increased epinephrine and E/N ratio and normal norepinephrine, and the remaining 4 had normal epinephrine, norepinephrine and E/N ratio in 24 hour urine. The six patients with increased epinephrine and E/N ratios were regarded as having latent adrenal medullary hyperfunction. The mean ages of the 6 patients with proved pheochromocytoma, the 6 with latent adrenal medullary hyperfunction and the 4 with normal urinary catecholamine fractions were 51.3, 42.5 and 28.5 years, respectively. At least one patient in each family with hereditary medullary thyroid carcinoma had proved pheochromocytoma or latent adrenal medullary hyperfunction, leaving no family with hereditary medullary thyroid carcinoma only. Urinary epinephrine, norepinephrine and E/N ratios in patients with sporadic medullary thyroid carcinoma and relatives of patients with medullary thyroid carcinoma were not higher than those in normal subjects. Measurements of epinephrine and norepinephrine in randomly voided urine are also a valuable and convenient method for the screening of pheochromocytoma in patients with medullary thyroid carcinoma and their relatives, because they gave results similar to those in 24 hour urine.

Adolescent↗
PubMed1982

[Plasma norepinephrine variation with dietary sodium intake in normotensive subjects and patients with essential hypertension].

Sympathetic nervous system may play an important role in the pathogenesis of essential hypertension. The present study was undertaken to evaluate the interaction between sodium intake and sympathetic nervous activity in the patients with essential hypertension. Plasma and urinary catecholamines (CA) were measured in 38 hypertensive patients (WHO 1-2 stage) and 24 age-matched normal subjects on regular (urinary sodium excretion (UNaV): 133 +/- 8 mEq/day; mean +/- SEM), high (UNaV 317 +/- 90 mEq/day), and low (UNaV 67 +/- 28 mEq/day) sodium diets for each 5 days at random. CA were analyzed by THI methods after HPLC separation. Twenty-four hour urinary norepinephrine (NE), epinephrine (E), and electrolytes (Na+, K+) excretion on the 5th day of each regimen were determined. In the 6th day morning supine and 5 min upright plasma NE(PNE), plasma E (PE), and plasma renin activity were determined after blood pressure and pulse rate measurement. The results were also analyzed according to the difference between salt-sensitive and non-salt-sensitive type of hypertensive patients. Plasma NE was 1.1 +/- 0.4 p mol/ml (supine), 1.5 +/- 0.4 p mol/ml (upright) in normotensive subjects and 1.8 +/- 1.1 p mol/ml (supine), 2.5 +/- 1.1 p mol/ml (upright) in the patients with essential hypertension, 24 hr urinary NE excretion were 116 +/- 54 micrograms/day in normotensive subjects and 138 +/- 88 micrograms/day in the patients with essential hypertension on regular sodium intake. Mean plasma NE levels in patients with essential hypertension were always higher than those in normotensive subjects on any sodium diets. Plasma NE and urinary NE were significantly reduced by high sodium intake and increased by low sodium intake in both normotensive subjects and the patients with essential hypertension. Percentile decrease in PNE when the diet was changed from low sodium to high sodium was much greater in normotensive subjects than the patients with essential hypertension. These tendency was observed in both salt-sensitive and non-salt-sensitive hypertensive patients. However, PNE in non-salt-sensitive hypertensive subjects tended to be higher than those in salt-sensitive hypertensive subjects. These results suggest that abnormal relationship between sodium intake and sympathetic nervous system may play an important role in the pathogenesis of essential hypertension.

Adult↗
PubMed1982

Effect of three angiotensin II antagonists, [Sar1, Thr8]-, [Sar1, Ile8]- and [Sar1, Ala8]angiotensin II on blood pressure and endocrine factors in normal subjects.

The biological effects of 1-Sarcosine, 8-Threonine angiotensin II ([Sar1, Thr8]ANG II) on blood pressure, plasma aldosterone concentration (PAC) and plasma renin activity (PRA) were investigated in six normal subjects on an unrestricted diet, and compared with those of 1-Sarcosine, 8-Isoleucine ANG II ([Sar1, Ile8]ANG II) and 1-Sarcosine, 8-Alanine ANG II ([Sar1, Ala8]ANG II). All three ANG II analogues (AIIA) showed agonistic pressor activity, that of [Sar1, Ile8]ANG II being greater than that of [Sar1, Thr8]ANG II or [Sar1, Ala8]ANG II. The antagonistic effect of [Sar1, Thr8]ANG II on blood pressure was less than [Sar1, I1e8]ANG II or [Sar1, Ala8]ANG II. Both [Sar1, Ile8]ANG II and [Sar1, Ala8]ANG II increased PAC and blocked the steroidogenic action of ANG II, while [Sar1, Thr8]ANG II showed little effect on PAC. All three AIIA caused similar suppression of PRA and showed no inhibitory effect on the decrease in PRA produced by ANG II. These results indicate that [Sar1, Thr8]ANG II is an AIIA with weak agonistic pressor action and that it has vascular selective properties. It is also suggested that ANG II receptors in a variety of target organs are heterogeneous.

1-Sarcosine-8-Isoleucine Angiotensin II↗
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

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↗
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↗