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Biomedical subjects

N Yasuda

Publications and source records attributed to N Yasuda.

At least 361 records · Page 20Linked to original sources
PubMed1977

Demonstration of corticotrophin-releasing activity in rat and human peripheral blood.

Corticotrophin-releasing activity of rat or human peripheral blood was examined with a sensitive in vitro CRF bioassay, using cultured rat adenohypophyseal cells and ACTH measurement by radioimmunoassay. A dose-related ACTH secretion into the medium occurred in response to plasma or serum obtained from unstressed rats or humans. The minimum effective dose was 2.5 mul (0.1% of the medium concentration). No concomitant release of TSH occurred, indicating that cellular destruction was not the source of ACTH in the medium. As previously found with hypothalamic extract, 50% of the maximum ACTH secretion produced by a given quantity of plasma occurred within 1-5 min. Fifty per cent of CRF activity was retained after plasma was boiled for 5 min. CRF activity of serum was not different in intact, 1-10 min ether-stressed, adrenalectomized, hypophysectomized or dexamethasone-treated rats. There was no significant difference in CRF activity between serum from intact rats and those with complete forebrain removal and hypophysectomy, indicating that serum CRF originates from a source outside the forebrain or pituitary. Because of the lack of correlation of blood CRF activity with conditions in which there are marked differences in in vivo ACTH concentration, it is possible that the blood CRF activity we measure is non-specific.

Adrenalectomy↗
PubMed1977

Distribution of corticotrophin releasing factor activity within the hypothalamic-pituitary complex of rats and cattle.

An assay system involving cultured rat adenohypophysial cells from either intact or adrenalectomized donors was used to study the distribution of corticotrophin releasing factor (CRF) activity in the hypothalamic-pituitary complex of rats and cattle. In the rat hypothalamus, CRF activity was most concentrated in the median eminence, but CRF was present in the stalk and the posterior pituitary gland in much higher concentrations than in the median eminence in both species. The dose--response slopes for the median eminence, stalk and pars nervosa of the posterior pituitary gland were parallel to each other, suggesting a qualitative similarity between the CRF activity in these tissues. Rat posterior pituitary glands may also contain another CRF component which has a much flatter dose--response curve, but is detectable in smaller quantities of posterior pituitary tissue than is the other type of CRF.

Adrenalectomy↗
PubMed1976

Evidence of nycterohemeral periodicity in stress-induced pituitary-adrenal activation.

Plasma ACTH and corticosterone were measured under basal conditions and after ether or tourniquet stress during the nadir (a.m.) and zenith (p.m.) of the nycterohemeral pituitary-adrenal cycle. Exogenous ACTH was also given at these 2 times to assess adrenal sensitivity to ACTH and the maximal adrenal capacity for corticosterone secretion. Ether stress caused a greater rise in plasma ACTH in the a.m. than in the p.m., even though basal plasma ACTH and corticosterone concentrations were lower in the a.m. than in the p.m. When given in the p.m., pentobarbital anesthesia depressed plasma corticosterone and ACTH to the a.m. level; under these conditions the rise in plasma ACTH produced by tourniquet stress was the same in the a.m. and p.m. Both tourniquet and ether stresses caused maximal activation of adrenal corticosterone secretion, but ether produced a much greater rise in plasma ACTH. It is concluded that: (1) the greater ether-induced rise in plasma ACTH in the a.m. than in the p.m. is probably due to the lower plasma (and probably tissue) corticosterone concentration at that time; (2) the plasma ACTH concentration for inducing maximal adrenal activation is relatively low; and (3) the higher basal levels of plasma corticosterone in the p.m. than in the a.m. are due to a slight increase in basal ACTH secretion in the p.m.

Adrenocorticotropic Hormone↗
PubMed1976

Rat hypothalamic corticotropin-releasing factor (CRF) content remains constant despite marked acute or chronic changes in ACTH secretion.

Hypothalamic corticotropin-releasing factor (CRF) activity was only slightly increased by 1 min ether stress and was unaltered by 2.5-10 min ether stress, 15-day adrenalectomy, 11-day hypophysectomy or 3-day dexamethasone treatment. There was a slight tendency for the hypothalamic CRF activity to be higher in the p.m. than in the a.m. Basal hypothalamic deafferentation did not significantly affect hypothalamic CRF content in the a.m. or p.m. compared to intact controls. We conclude that hypothalamic CRF content maintains relative constancy under conditions of marked acute or chronic stimulation or suppression of ACTH secretion.

Adrenal Glands↗
PubMed1976

Studies on ACTH dynamics in cultured adenohypophyseal cells: effect of adrenalectomy or dexamethasone in vitro.

Basal or hypothalamic extract-induced ACTH or TSH secretory capacity as well as intracellular ACTH content were assessed in cultured rat adenohypophyseal cells after various pretreatments of the donor animals. Medium and intracellular ACTH or TSH were measured by radioimmunoassay. Ten-day to 2-month adrenalectomy enhanced, whereas dexamethasone pretreatment suppressed, both synthesis and secretion of ACTH in the adenohypophyseal cells. Dexamethasone may also impair the replication of the adenohypophyseal cells in vivo, as indicated by the smaller number of cells obtained per animal in the dexamethasone-treated group. No significant increase in TSH secretion was observed when adenohypophyseal cells were derived from rats fed propyl-thiouracil (PTU) for 3 weeks instead of from intact rats.

Adrenal Glands↗
PubMed1976

Studies on the corticotrophin-releasing activity of vasopressin, using ACTH secretion by cultured rat adenohypophyseal cells.

CRF activity of synthetic vasopressins and pitressin was studied in an in vitro system of cultured rat adenohypophyseal cells using direct measurement of ACTH by radioimmunoassay. Pitressin (posterior pituitary extract) induced a dose-related secretion of ACTH whereas synthetic arginine or lysine vasopressin were devoid of CRF activity, even with the largest tested dose (4 mug/ml). No potentiation of the CRF activity of hypothalamic extract was observed with any vasopressin preparation studied. We concluded that: 1) the CRF activity of posterior pituitary extract is not due to vasopressin, and 2) the ACTH secretion induced by vasopressin administration in vivo is unlikely to be due to a direct effect of vasopressin on adenohypophyseal cells.

Adrenocorticotropic Hormone↗
PubMed1976

Distribution of corticotropin releasing factor(s) activity in neural and extraneural tissues of the rat.

Distribution and dose-response characteristics of corticotropin releasing factor(s) (CRF) activity in the central nervous and extraneural tissues of the rat were examined with a sensitive CRF bioassay using ACTH secretion by cultured rat adenohypophyseal cells. Dose-response curves for hypothalamus were steeper than and not parallel to those for cerebral cortex, liver, serum or human urine. The minimum effective dose was smallest for the posterior pituitary. CRF activity of the basal hypothalamus was considerably higher than that in other parts of the hypothalamus, and was unaltered by 2.5 or 10 min ether stress. Our data indicate that "specific" CRF is concentrated primarily in the basal hypothalamus and posterior pituitary and is not identical with widely distributed extrahypothalamic extraneurohypophyseal CRF.

Animals↗
PubMed1976

HLA antigens in Japanese populations.

HLA antigens in 841 healthy, unrelated Japanese from nine widely separated geographic localities were studied. The five most common antigens observed in order of decreasing frequency were for the HLA-A locus: HLA-A9, A2, A10, AW32 and A11; and for the HLA-B locus: HLA-'B5' (= HLA-B5+B17), BW40, B12, B14 and B8. The allelic frequency of undetected antigens of the HLA-A locus was .14-.37, and that of the HLA-B locus, .32-.67, indicating that there were serological difficulties in typing for Japanese antigens using antisera from Caucasians. Marked gene frequency clines were observed for HLA-A9 and HLA-A2 from south (Okinawa) to north (Nagoya). Two haplotypes, HLA-A9, B5 and HLA-A10, BW40 were shown to be in linkage disequilibrium in four of the nine subpopulations.

Alleles↗
PubMed1975

Changes in plasma thyroxine, triiodothyronine, and TSH during adaptation to iodine deficiency in the rat.

We have measured plasma thyroxine (T4), triiodothyronine (T3), and TSH with specific radioimmunoassays in rats during adaptation to severe iodine deficiency after they had previously received regimens supplying various quantities of iodine. Rats were maintained on a high-iodine diet (HID) containing 3 mg iodine/kg or a low-iodine diet (LID) containing 30 mug iodine/kg supplemented with 0.1, 0.2, or 0.4 mug iodine/ml of drinking water before swtiching to KID alone. Frequent serial blood samples were obtained up to 3 months, using 6 or more animals for each time interval. In animals originally fed HID, T4 remained at 4-6 mug/100 ml unitl the tenth day of LID, then rapidly decreased to a value of less than 0.4 mug/100 ml at 1 month. TSH was initially 50 muU/ml and increased linearly to 165 muU/ml on day 16. Thence there was a much more rapid rate of rise to 640 muU/ml at 38 days. The rats changed to LID alone after having been fed LID with iodine supplementation underwent similar qualitative hormonal changes. However, the decrease in plasma T4 and the increase in plasma TSH occurred sooner in the rats which had drunk water containing only 0.1 or 0.2 mug iodine/ml than in the previous experiment. Rats which had received 0.4 mug iodine/ml showed a pattern essentially identical to that of the animals which had been fed HID. plasma T3 did not change significantly in any of the experiments, remaining at 60-90 ng/100 ml, although there was a tendency for the values to be somewhat lower after several weeks of LID. There was a highly significant negative correlation of plasma T4 with plasma TSH. There was no significant correlation of plasma T3 with either plasma T4 or plasma TSH. It is concluded that the combined physiologic effect of plasma T4 and T3 concentration is more important in determining TSH secretion through negative feedback effects on the hypothalamus and/or pituitary than is the concentration of plasma T3.

Animals↗
PubMed1975

Acute effects of thyroxine, triiodothyronine, and iodide on thyrotropin secretion.

Rats fed a Purina or low-iodine diet (LID) for varying periods were serially sampled before and after a single iv injection of T4, T3, iodide or saline. Suboptimal replacement doses of T4 and T3 were given to rats fed LID for 2 months or 1 year (basal TSH, approximately 1000 and 2000 muU/ml, respectively). Both 1 mug T4 and 0.25 mug T3/100 g BW dropped plasma TSH to 70% of the initial level at 15 min and to 10--20% at 4 h. By 12 h TSH had begun to rise in 2-month LID rats, followed by a secondary decline 3--5 days after injection. Statistical comparison of the slopes of the initial TSH decline indicated there was no significant difference between the effect of T4 and T3. There effect of graded doses of T3 (0.01--0.3 mug/100 g) was also examined. There was a highly significant correlation of the magnitude of TSH suppression with the dose of T3 administered. Saline had no effect but 0.65 mug iodide/100 g BW (equal to that in 1 mug T4) had a delayed effect, depressing TSH to a minimum of 25% of the initial value at 48 h in 2-month LID rats. There was no difference in the effect of these doses of T4, T3, or saline in purina-fed rats (basal TSH, 170 muU/ml). T4 or T3 in physiologically equivalent doses thus produces an identical prompt rate of decrease in plasma TSH, indicating that both hormones possess intrinsic hormonal activity. The delayed effect of iodide is presumably because it must first be incorporated into T4 and T3 and secreted by the thyroid gland. The similarity of depression of plasma TSH by thyroid hormones or saline injection in Purina-fed rats is believed due to a nonspecific stress effect in these animals with a low basal rate of TSH secretion. The non-specific inhibition of TSH secretion is minimal in the iodine-deficient rats with a much higher basal rate of TSH secretion, presumably because of relative vectorial influences.

Animals↗
PubMed1975

Changes in plasma thyrotrophin, thyroxine, and triiodothyronine after acute or chronic administration of iodide to iodine-deficient rats.

The effect of chronic oral or acute iv administration of small graded doses of iodide was studied in severely iodine-deficient rats. Drinking water supplemented with 0.1, 0.2, or 0.4 mug 127I-/ml was given for up to 42 days. Plasma T3, which was initially in the normal range, increased 2--3-fold on days 1 and 2 after initiation of iodide supplementation, then dropped to approximately the intial concentration at day 3. Plasma T4, initially undetectable, was calculated to increase approximately 20-fold within one day after beginning iodide supplementation, but was still climbing into the normal range at day 3. In all groups, the initially high plasma TSH fell significantly by day 1 and was in approximately the normal range for iodine-sufficient rats by day 3. At 42 days, thyroid weight and 131I uptake were significantly elevated in all groups and inversely correlated with the dose of iodide, even though the thyroidal labeled T3/T4 ratio and plasma TSH, T4, and T3 were within the normal range. Intravenous injection of 0.1 or 0.5 mug 125I-/100 g caused an approximately 2-fold increase in plasma T3 within 24 h, which was not statistically different between the 2 groups. Plasma T4 rose to the normal range 24 h after 0.5 mug and was slightly, but significantly, elevated after 0.1 mug; it then declined in both groups. Twenty-four hours after injection of 2.5 mug 125I-/100 g, there was a significant fall in plasma T3, no change in plasma TSH, and no detectable plasma T4. Thereafter, there was a dramatic increase in plasma T4 and a fall in plasma TSH. The duration and degree of suppression of plasma TSH was related to the dose of iodide injected. We conclude that, under the conditions of our experiments, plasma T3 derives primarily from thyroidal secretion rather than from extra-thyroidal conversion of T4 to T3. Severely iodine-deficient rats secrete maximum quantities of TSH which are not increased by a further transient drop in plasma thyroid hormone concentration.

Administration, Oral↗
PubMed1975

A sensitive and simple in vitro assay for corticotropin-releasing substances utilizing ACTH release from cultured anterior pituitary cells.

Graded doses of rat hypothalamic extract (HE) were added to dishes containing dispersed, pooled rat adenohypophyseal cells cultured for several days. ACTH secretion into the medium gave a linear log-dose response curve over a 100-fold range between 0.01 and 1 mg of NIH-HE (0.0125-1.25 rat hypothalamus). Forty percent of the maximal ACTH secretion in response to a given dose of HE occurred within 3 min. No decrease in intracellular ACTH occurred at any time or with any dose of HE, indicating that secretion was always balanced by production. ACTH secretion stopped as soon as HE-containing medium was replaced by medium without HE. The same cultured cells could be satisfactorily used in repetitive assays performed on the same or different days.

Adrenocorticotropic Hormone↗