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Biomedical subjects

M A Greer

Publications and source records attributed to M A Greer.

At least 109 records · Page 6Linked to original sources
PubMed1978

Evidence that the hypothalamus mediates endotoxin stimulation of adrenocorticotropic hormone secretion.

The site of action of Escherichia coli endotoxin in inducing ACTH secretion was studied in vivo and in vitro. Hypophysectomized rats, bearing two to three transplanted pituitaries under the kidney capsule and "primed" with exogenous ACTH, responded to 2.0-7.5 microgram/100 g BW ip or iv endotoxin with a several-fold increase of plasma corticosterone. This response was markedly reduced by hypothalamic lesions and completely abolished by removing the entire forebrain. Endotoxin added directly to cultured rat adenohypophyseal cells in a concentration up to 10 microgram/ml did not induce significant ACTH secretion. We conclude that endotoxin-induced ACTH secretion from heterotopically transplanted pituitaries is mediated primarily by the hypothalamus, presumably through hypothalamic CRF that reaches the transplanted pituitaries via the systemic circulation.

Adrenocorticotropic Hormone↗
PubMed1978

Comparison of pituitary-thyroid maturation in the fetuses of rats fed an iodine-deficient or normal diet.

From the earliest detectable development of fetal pituitary-thyroid function (day 18-19 of gestation) through the first postnatal day, there was a higher degree of stimulation of the pituitary-thyroid axis in the fetuses of rats fed a low iodine diet (LID) than in those of rats fed a high iodine diet (HID). Significant differences between the two groups were consistently observed in relative thyroid size, plasma TSH, 4-h thyroid radioiodine uptake, and the labeled iodoamino acid composition of thyroid digests. Plasma T4 concentration was lower in both LID and HID fetuses and pups than in the HID mothers. Plasma T3 was not detectable (less than 20 ng/dl) in the fetuses of either group, nor was labeled T3 in the thyroid digests. Body weight, plasma T4, and pituitary TSH content were usually lower in the LID than the HID animals of comparable age; however, these differences were not consistently statistically significant (P less than 0.05). We conclude that iodine deficiency causes a marked stimulation of TSH secretion and, consequently, of thyroid growth and metabolism from the earliest development of fetal pituitary-thyroid function.

Animals↗
PubMed1978

Studies on the site of action of vasopressin in inducing adrenocorticotropin secretion.

Hypophysectomized rats bearing three transplanted pituitaries under the kidney capsule responded to synthetic lysine vasopressin or pitressin with a significant elevation of plasma corticosterone, whereas hypophysectomized rats with no grafts did not. This response was completely abolished by pretreatment of animals with dexamethasone but was unaltered by central hypothalamic destruction. Corticotropin-releasing factor content of the hypothalamic median eminence, hypophyseal stal-, or pars nervosa of the posterior pituitary of intact rats was unchanged 5 or 10 min after ip injection of vasopressin compared to the basal level. We conclude that vasopressin and dexamethasone act directly on the adenohypophysis in vivo to exert their stimulatory or inhibitory effect on ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1978

Lymphoid thyroiditis following immunization with group A streptococcal vaccine.

Severe lymphoid thyroiditis and associated hypothyroidism occurred in all of 7 male and 4 female F(7) derivatives (seventh generation) of rats immunized in each generation against Group A streptococci. This evidence of thyroiditis produced by immunization against a nonthyroidal antigen suggests that some cases of Hashimoto's thyroiditis in humans may result from nonspecific immune responses.

Animals↗
PubMed1977

Short-term antithyroid drug therapy for the thyrotoxicosis of Graves's disease.

We investigated whether thyrotoxic patients treated with short-term antithyroid therapy would achieve prolonged remissions. Thirty-one previously untreated and nine previously treated patients with thyrotoxic Graves's disease received a single daily dose of methimazole or propylthiouracil. The drug was stopped at, or shortly after, the time they became euthyroid. Twelve of the 31 previously untreated patients remained in remission for 29 +/- 3.5 months (mean +/- S.E.) after treatment for 4.5 +/- 0.3 months. Four of the nine previously treated have remained in remission of 13.0 +/- 2.1 months after treatment for 3.0 +/- 0.3 months. Of various possibilities analyzed, only a small goiter at the onset of therapy and tri-iodothyronine toxicosis were significantly favorable prognostic indicators that a remission would be maintained. The lasting remission rate is as good when antithyroid drugs are stopped as soon as the patient is euthyroid as when they are continued for one year or more.

Administration, Oral↗
PubMed1977

The effect of basal hypothalamic isolation on pituitary-thyroid activity and the response to propylthiouracil.

Basal hypothalamic deafferentation extending from the posterior border of the optic chiasm to the mid-mammillary bodies resulted in depression of plasma TSH, thyroxine (T4), and triiodothyronine (T3) concentration to 50% of normal controls within 7 days. Administration of 0.15% propylthiouracil (PTU) in the diet form postoperative day 26 caused a pronounced drop in the plasma T3 level and a rise in plasma TSH level within two days in the control animals, but had little effect during this interval in the deafferented animals. After 12 days of PTU, plasma T3 and T4 concentrations had dropped to undetectable concentrations in the control animals but both were still detectable in the deafferented animals. After 25 days of PTU, plasms T4 and T3 levels were undetectable and plasma TSH levels were significantly elevated above normal in all animals. Thyroid hypertrophy at that time was as great in the deafferented as in the control rats, although plasma TSH concentration was 50% lower in the former. Administration of 0.1 mug/100 g BW TRH iv on postoperative day 37, when plasma T4 and T3 were undetectable in the controls but still present in the deafferented animals, produced an equally high concentration of plasma TSH in all animals. We interpret these data to support the concepts that: 1) a major source of neural drive of that TRH which stimulates the secretion of TSH by the adenohypophysis lies outside the medial basal hypothalamus, 2) a decrease in TRH reaching the adenohypophysis causes a lower setting of the "thyrostat" sensitive to the concentration of circulating thyroid hormone, and 3) increased TSH secretion and resultant goitrogenesis is delayed in animals with impaired TRH secretion because of the slower rate of secretion of thyroid hormone than in intact controls and the longer time thus required to markedly reduce the concentration of circulating thyroid hormone.

Afferent Pathways↗
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↗