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Biomedical subjects

F Oseko

Publications and source records attributed to F Oseko.

At least 55 records · Page 3Linked to original sources
PubMed1986

A case of adiposis dolorosa: lipid metabolism and hormone secretion.

The present report describes a 53-year-old non-obese man with adiposis dolorosa whose pain was dramatically relieved by the intravenous injection of lidocaine. The patient showed a paradoxical response of growth hormone to thyrotropin-releasing hormone. In addition, in-vitro studies on adipose tissue metabolism revealed the reduced glucose conversion to neutral glycerides in painful adipose tissue. These abnormalities may be related in some ways to the pathogenesis of this disorder.

Adipose Tissue↗
PubMed1985

Relative biological activities of Asn1-,Val5-angiotensin II, Ile5-angiotensin II and Sar1-angiotensin II in man.

Biological activities of asn1-,val5-angiotensin II (Hypertensin, Ciba, Asn1-,Val5-ANG II), ile5-angiotensin II (human angiotensin II, Ile5-ANG II) and sar1-angiotensin II (Sar1-ANG II) were compared in man. In 7 normal men 5 pmol/kg X min each of Asn1-,Val5-ANG II, Ile5-ANG II and Sar1-ANG II was infused iv from 0900 h to 0930 h at 1-week intervals. Average increments of blood pressure at the end of the infusions were 11/12, 23/20 and 36/30 mmHg, respectively (significant differences among the 3: P less than 0.001), average decrements of plasma renin activity were 0.30, 0.32 and 0.27 ng/ml X H, respectively (no significant difference among the 3), average increments of plasma aldosterone were 1.1, 2.3 and 4.4 ng/100 ml, respectively (significant difference between the former 2: P les than 0.001, between the latter 2: P less than 0.02), and durations of blood pressure rise after the cessation of these infusions (T) were 2-5 (average 5) min, 10-25 (average 20) min and 35-60 (average 40) min, respectively (significant difference between the former 2:less than P 0.01, between the latter 2: P less than 0.001). From these results it is evident that the pressor and steroidogenic actions of Ile5-ANG II are significantly stronger than those of Asn1-,Val5-ANG II and that the duration of pressor action of the former is much longer than that of the latter. Therefore, when the activities of angiotensin II (ANG II) derivatives are compared with those of ANG II in man, Ile5-ANG II--natural human ANG II--should always be used instead of Asn1-,Val5-ANG II. The pressor and steroidogenic actions and T of Sar1-ANG II are significantly stronger or longer than those of Ile5-ANG II. The reason for this is thought to be that Sar1-ANG II is bound tightly to the vascular and adrenal ANG II receptors and is not readily metabolized.

Adult↗
PubMed1985

Regional differences in carboxylesterase activity between human subcutaneous and omental adipose tissue.

Human adipose tissue was shown to contain carboxylesterase activity when measured by methylbutyrate as substrate. The enzyme has the same characteristics as carboxylesterase purified from rat epididymal adipose tissue. Like lipoprotein lipase, carboxylesterase activity was higher in large than in small fat cells. Both cell size and carboxylesterase activity were greater in human subcutaneous than in omental adipose tissue. However, the linear regression lines between the enzyme activity and cell volume in the two tissues were almost superimposable, suggesting that cell size is a determinant of enzyme activity. Although the physiological significance of adipose tissue carboxylesterase must await further clarification, it is possible that the enzyme is related to the hydrolysis of long-chain monoacylglycerols.

Adipose Tissue↗
PubMed1985

Influence of chronic hyperprolactinemia induced by sulpiride on the hypothalamo-pituitary-testicular axis in normal men.

For elucidation of the effects of hyperprolactinemia on the hypothalamic-pituitary-testicular axis, five healthy men were exposed to sulpiride (300 mg/day by mouth); four among the five maintained hyperprolactinemia (71.6 to 95.3 ng/ml) for 78 days. Clomiphene citrate (CC), luteinizing hormone (LH)-releasing hormone, and human chorionic gonadotropin tests were performed before and after sulpiride treatment. The CC test, given as a measure of hypothalamic function, was carried out in each of the five volunteers before sulpiride treatment (control) and on days 14 (2 weeks) and 60 (2 months) of sulpiride administration. Each value of plasma LH stimulated by CC was integrated and expressed as a ratio of the integrated value obtained after administering CC at 2 weeks and 2 months to that from each control experiment. The mean ratio in the four subjects at 2 months (mean +/- standard deviation, 0.769 +/- 0.121) was significantly lower than that at 2 weeks (0.942 +/- 0.073; P less than 0.05) and before sulpiride treatment (1.000; P less than 0.01). Impairment of LH responses to CC by 2-month long sulpiride-induced hyperprolactinemia suggests that chronic hyperprolactinemia in men partly suppresses LH secretion by its inhibitory action on the hypothalamus.

Adult↗
PubMed1985

Agonistic activities of isoleucine8-angiotensin II in man.

In order to clarify the importance of C-terminal phenylalanine in angiotensin II (ANG II) molecule, agonistic activities of a C-terminal substituted peptide, isoleucine8-angiotensin II (Ile8-ANG II), were studied in comparison with those of sarcosine1-, isoleucine8-angiotensin II (Sar1-, Ile8-ANG II) and isoleucine5-angiotensin II (Ile5-ANG II) in 5 normal men. When infused iv at a rate of 600 pmol/kg X min for 30 min, Ile8-ANG II and Sar1-, Ile8-ANG II raised the blood pressure to the same extent (15/15 mmHg on the average), while the average blood pressure increase was 21/21 mmHg after an iv infusion of Ile5-ANG II at a rate of 5 pmol/kg X min for 30 min. Duration of the pressor action after the cessation of each infusion was 50-90, 90-120 and 10-25 min, respectively. In each case plasma renin activity (PRA) decreased and plasma aldosterone (PA) increased. When infused iv at a rate of 10 pmol/kg X min (maximum non-pressor dose) for 120 min, both Ile8-ANG II and Sar1-, Ile8-ANG II lowered PRA and increased PA gradually, but 100 mg oral captopril given immediately before these infusions caused no significant increase in PRA or no significant decrease in PA but again a decrease in PRA and an increase in PA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Pressor activity of angiotensin II-(2-7)-hexapeptide in man.

Pressor activity and speed of metabolic degradation of angiotensin II-(2-7)-hexapeptide [ANG-(2-7)] were studied in 5 normal men. When infused iv at a rate of 72 nmol/kg X min for 7 min, ANG-(2-7) caused a very slight but statistically significant increase in blood pressure. Average blood pressure increases at 2, 5 and 7 min were 5/4, 8/10 and 8/9 mmHg, respectively, and the duration of the pressor action after the cessation of the infusion (T) was 5 min on the average. The pressor activity and T of this peptide were much less than or shorter than those of angiotensin II-(1-7)-heptapeptide [ANG-(1-7)] infused previously in the same 5 normal men at a rate of 18 nmol/kg X min, indicating that the pressor activity ratio of both the peptides in man is 1: greater than 7.2 which is similar to that of angiotensin II-(2-8)-heptapeptide (angiotensin III) and Ile5-angiotensin II (Ile5-ANG II) (1: greater than 5) and that the removal of N-terminal aspartic acid from ANG-(1-7) hastens the speed of metabolic degradation of the peptide as from Ile5-ANG II.

Adult↗
PubMed1985

Responses of patients with Bartter's syndrome to angiotensin III and angiotensin II-(3-8)-hexapeptide.

Studies were conducted to determine whether or not angiotensin III [AIII] and angiotensin II-(3-8)-hexapeptide [ANG-(3-8)] have their own specific arteriolar binding sites different from angiotensin II [AII] binding site(s) in man. Four patients with Bartter's syndrome were given asn1-,val5-AII by iv infusion at rates of 10, 20, 50 and 100 pmol/kg X min, each for 7 min. One hour later AIII was infused iv in the same 4 patients at rates of 50, 100, 250 and 500 pmol/kg X min, each for 7 min. After 100 or 150 mg/day of indomethacin treatment for 7 days, the same AII and AIII infusions were repeated. All patients showed blunted pressor responses to both AII and AIII before indomethacin and the responses were improved after indomethacin. Moreover, increment curves of blood pressure for AII were almost identical with those for AIII in individual patients both before and after indomethacin. ANG-(3-8) was infused iv in 3 normal men and 3 of the 4 patients with Bartter's syndrome at a rate of 3.500 pmol (2.838 ng)/kg X min for 15 min. Blood pressure rose in the normal men (12/12 mmHg on the average) but did not rise in the patients. These results suggest that AII, AIII and ANG-(3-8) have the same arteriolar binding sites in man.

Adolescent↗
PubMed1984

Effects of mazindol on lipid metabolism of human adipose tissue in vitro.

The interaction of mazindol with catecholamine in regulating peripheral lipid metabolism was studied in vitro. Noradrenaline-induced and adrenaline-induced glycerol release was augmented by addition of 50 ng mazindol. On the other hand, isoproterenol-induced glycerol release was suppressed by addition of 50 ng mazindol. Basal and dopamine-induced glycerol release was not altered by addition of 50 ng mazindol. These results suggest that mazindol may interact with alpha 2-adrenergic receptors in adipose tissue.

Adipose Tissue↗
PubMed1983

Improvement of ejaculatory incompetence with bromocriptine in a man with prolactin-secreting pituitary tumor.

We report a case of a prolactin-secreting pituitary tumor in a man whose characteristic findings were ejaculatory incompetence and no response of gonadotropin to clomiphene. After treatment with bromocriptine ejaculation was normal, gonadotropin responded slightly to clomiphene and the high level of plasma prolactin returned to normal. A Hardy operation was performed to remove the pituitary tumor. The patient continues to receive 2.5 mg. bromocriptine daily to maintain normal ejaculation.

Adult↗
PubMed1982

Effects of a new angiotensin-converting enzyme inhibitor, MK 421, in normal men and patients.

Effects of MK 421, a new angiotensin-converting enzyme inhibitor, were studied in normal men and patients. MK 421 was given at 0900 h as a single oral dose of 20 mg, to 5 normal men and 2 patients with essential hypertension and 10 mg to a patient with Bartter's syndrome, in the recumbent position. In all of them blood pressure (BP) fell, plasma angiotensin I (Pl AI) and plasma renin activity (PRA) increased, and plasma aldosterone (PA) decreased from 2 h to 6 h. Maximum effects were observed at 4 or 6 h. Then the effects attenuated gradually but still remained at 24 h. In the same 5 normal men angiotensin I (AI) was infused iv at a rate of 20 ng/kg . min from 0900 h to 1500 h, from 2030 h to 2100 h, and the next morning from 0830 to 0900 h. At first the BP rose and PA increased. The onset of the BP fall was at 35, 55, 60, 70 and 85 min in each subject, respectively. Then the BP and PA began to decrease and the Pl AI and PRA began to increase. The maximum effects were observed at 4 or 6 h. Then these inhibitory effects on the AI were attenuated but still remained at 24 h. The 2 patients with essential hypertension and a patient with malignant hypertension was treated with MK 421 at a daily doses of 5 to 40 mg for 2 to 6 months. They all showed a fall in BP and no side-effects were noted. From these results it is concluded that MK 421 is a strong and long-acting antihypertensive drug and its clinical application seems very useful for the treatment of hypertension.

Adult↗
PubMed1982

Biological activity of des-asp1-des-arg2-angiotensin II in man.

The biological activity of des-asp1-des-arg2-angiotensin II (3-8AII) was studied in man. When 3-8AII was infused iv at rates of 22 and 308 pmol (17.5 and 250 ng)/kg . min separately into 5 normal men each for 120 min, blood pressure showed no change, plasma renin activity (PRA) decreased gradually and plasma aldosterone showed a gradual slight increase. The lower dose of 3-8AII partially inhibited captopril-induced PRA increase and plasma aldosterone decrease in the same 5 normal men and the higher dose of the hexapeptide completely abolished them. In one of the 5 normal men blood pressure rose in response to doses of 3-8AII greater than 2220 pmol (1750 ng)/kg . min. When 3-8AII was infused iv at 308 pmol/kg . min into 2 patients with Bartter's syndrome for 60 min, it caused marked decrease in PRA and plasma aldosterone but no change in blood pressure. This decrease in plasma aldosterone is thought to be secondary to the decrease in PRA. From these results it is evident that 3-8AII has a minimal pressor action, a weak aldosterone-stimulating action and a significant renin-suppressing action in man and this PRA-lowering action is thought to be due to direct inhibition of renin release by its whole molecule or a smaller part of the molecule.

Adult↗
PubMed1981

Interaction of prolactin and testosterone in the human prostate.

Three experiments were performed to determine whether human prolactin (hPr) affects prostatic uptake and metabolism of testosterone (T). 1) Patients with prostatic cancer were infused twice with radio-labelled androgens, the first time with basal hPR, the second time with oral thyrotrophin-releasing hormone (TRH)-elevated hPr. In 5/7, significant increases in metabolic clearance of dihydrotestosterone (DHT) and in conversion of T to DHT accompanied increased hPR. 2) The incorporation of labelled T into minced benign prostatic hypertrophy (BPH) tissue from subjects with high (40 ng/ml) hPR was measured and was found to be more than twice the uptake into tissue from those with low hPR (6.5 +/- 1.9 ng/ml). 3) Uptake and metabolism in vivo of a bolus of 3H-T by BPH and carcinomatous prostates was measured and was far greater in subjects whose hPR was elevated by chlorpromazine than in untreated controls. It is concluded that prolactin increases prostatic uptake and metabolism of T. It is suggested that the best management of prostatic cancer should include depletion of prolactin as well as androgen.

Dihydrotestosterone↗
PubMed1981

Suppression of captopril-induced increase in plasma renin activity by des-Asp1-,Ileu8-angiotensin II in man.

One hundred milligrams of oral captopril (SQ 14225) caused a significant increase in PRA and a significant decrease in plasma aldosterone (PA) in five normal men and five hypertensive patients. Blood pressure (BP) showed no change in the normal men, but it fell significantly in the patients. An iv infusion of 200 ng/kg.min des-Asp1-,Ileu8-angiotensin II (AIIIA) for 2 h caused a significant decrease in PRA and a slight but significant increase in PA, but caused no change in BP in the normal men. When 100 mg captopril were given orally immediately before the start of the AIIIA infusion, BP showed no change in the normal men, but fell in the patients. However, PRA showed a significant decrease and PA showed a slight but significant increase in both the normal men and the patients, except for one patient with renovascular hypertension who showed a decrease in PA. Thus, this suppression of captopril-induced PRA increase by AIIIA, a derivative of angiotensin II, is not related to BP change, and it suggests that the principal cause of the PRA increase after captopril is a disappearance of endogenous angiotensin II.

Adult↗
PubMed1981

Normotensive primary aldosteronism: report of a case.

A 23-yr-old male patient with normotensive primary aldosteronism is reported. He complained of muscle weakness, polydipsia, and polyuria. His blood pressure was generally 118/60 to 124/70 mm Hg. Serum sodium, potassium and chloride were 152.2.2, and 108 meq/liter, respectively. Arterial blood pH, glomerular filtration rate, renal plasma flow and circulating plasma and blood volumes were normal, and plasma bicarbonate was normal or elevated. PRA was 0.16 ng/ml.h and did not increase significantly after sodium deprivation, ambulation, and iv furosemide injection. Plasma aldosterone was 64.1 ng/100 ml. He showed pressor responses to infused angiotensin II and norepinephrine which were similar to those in normal men. Adrenal scintiscanning after iv injection of [131I]6 beta-iodomethyl-19-nor-cholesterol during dexamethasone administration showed dense uptake on the right adrenal and minimal uptake on the left. Intravenous infusion of angiotensin III at a rate of 20 ng/kg. min for 30 min did not cause an increase in plasma aldosterone. Serum electrolytes became normal after spironolactone but not after dexamethasone. At surgery, the right adrenal, bearing a benign adenoma, was removed. After surgery, blood pressure was unchanged, but all biochemical abnormalities disappeared. The cause of this normotension remains to be elucidated, but the diagnosis criteria of primary aldosteronism should now be partly modified.

Adenoma↗