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Biomedical subjects

J C Buckingham

Publications and source records attributed to J C Buckingham.

At least 91 records · Page 5Linked to original sources
PubMed1985

Influence of growth hormone, corticosterone, corticotrophin and changes in the environmental temperature on pituitary-ovarian function in the immature rat.

The influence of various endocrine and environmental factors on pituitary-ovarian function was studied in peripubertal rats treated with pregnant mare serum gonadotrophin (PMSG). Pregnant mare serum gonadotrophin induced ovulation in rats aged 27 days provided they weighed over 60 g. The response was preceded by a marked hypersecretion of LH which was detectable by radioimmunological and biological assay methods. In contrast, smaller rats of the same age did not ovulate in response to PMSG apparently because of the secretion of a pleiomorphic form of LH which, although immunoreactive, appeared to be biologically inactive. Ovarian function, assessed by response to exogenous gonadotrophins and by measurement of 125I-labelled human chorionic gonadotrophin binding, was normal despite the presence of the biologically inactive pleiomorph. Exposure of the small PMSG-treated rats to a high environmental temperature (39 degrees C) or treatment with corticosterone or GH altered the nature of the LH in the blood so that it was active in both assay systems and facilitated ovulation as also did ACTH. The results suggest that the abrupt change in the nature of the LH released by the pituitary gland essential for the initiation of ovulation may be affected by GH, corticosterone or a raised environmental temperature.

Adrenocorticotropic Hormone↗
PubMed1985

Salmonid melanin-concentrating hormone inhibits corticotrophin release.

Melanin-concentrating hormone (MCH) is a neural peptide associated with colour change in fishes. We show here that it also inhibits corticotrophin (ACTH) secretion. Synthetic salmonid MCH at a concentration of 100pmol/l reduced the in-vitro release of ACTH by pars distales (pDs) taken from stressed trout. At lower concentrations (10pmol/l) the peptide inhibited CRF-41-induced secretion of ACTH by pDs removed from unstressed trout, while at higher concentrations (10nmol/l) it reduced the corticotrophic response of rat pituitary tissue to CRF-41.

Adrenocorticotropic Hormone↗
PubMed1985

Two distinct corticotrophin releasing activities of vasopressin.

The effect of various corticotrophin releasing factors (CRFs) on the secretion of corticotrophin (ACTH) by segments of rat anterior pituitary tissue has been studied in vitro. ACTH release was stimulated by CRF-41 (5.0 X 10(-9) - 2.0 X 10(-7) M), hypothalamic extracts (0.2 - 1.6 HE ml-1) and arginine vasopressin (AVP, 5.0 X 10(-9) - 8.0 X 10(-7) M). The slopes of the dose-response lines of CRF-41 were greater than those of AVP, less than those of hypothalamic extracts from control animals and resembled those of hypothalamic extracts from Brattleboro rats. Simultaneous addition of AVP (10(-10) M) to the incubation medium enhanced the response to CRF-41 and increased the slope of its dose-response lines. The adrenocorticotrophic response to CRF-41 was enhanced similarly by pretreatment of the tissue with AVP (1.25 X 10(-11) - 2.0 X 10(-10) M) as also was the response to hypothalamic extracts. In contrast, pretreatment of the tissue with CRF-41 (2.3 X 10(-11) - 2.3 X 10(-8) M) depressed the subsequent response to CRF-41 and to hypothalamic extracts. The marked difference between the concentrations of vasopressin required to facilitate maximally the response to CRF-41 and those necessary to evoke ACTH release suggests that the two effects may be mediated by different types of vasopressin receptor.

Adrenocorticotropic Hormone↗
PubMed1984

Inhibition of corticotrophin releasing factor secretion in the pentobarbitone-morphine-treated rat.

The concentrations of ACTH in the plasma and adenohypophysis and corticotrophin releasing factor (CRF) in the hypothalamus were determined and the functional capacities of the adenohypophysis and hypothalamus assessed in male rats treated with pentobarbitone and morphine. A single injection of morphine increased markedly the concentrations of ACTH in both the plasma and the adenohypophysis and the CRF content in the hypothalamus. When the opiate was given to rats injected 10 min previously with sodium pentobarbitone its effects were substantially reduced and the hypothalamo-pituitary-adrenocorticotrophic response to stress was abolished. The functional activity in vitro of pituitary tissue removed from control rats was not affected by the addition to the incubation medium of pentobarbitone and/or morphine. Pituitary glands of drug-treated rats also responded normally both in vivo and in vitro, with respect to ACTH secretion, to hypothalamic extracts prepared from control animals, CRF-41 and arginine vasopressin (AVP). On the other hand, hypothalami removed from pentobarbitone/morphine treated rats showed a marked reduction in their ability to secrete CRF in response to acetylcholine or 5-hydroxytryptamine as also did hypothalami from control animals after preincubation with pentobarbitone and/or morphine. The results suggest that the hypothalamus is an important site of action of pentobarbitone and morphine in modulating the functional activity of the hypothalamo-pituitary-adrenocortical system and are in accord with the view that the pentobarbitone/morphine-treated rat is suitable for the detection and quantification of potential corticotrophin releasing factors.

Adrenocorticotropic Hormone↗
PubMed1984

Differences in hypothalamo-pituitary-adrenocortical activity in the rat after acute and prolonged treatment with morphine.

The influence of opioid substances on the secretion in vivo and in vitro of corticosterone, corticotrophin (ACTH) and corticotrophin releasing factor (CRF) in the rat was studied. Rats given a single injection of morphine exhibited a marked hypersecretion of ACTH and an exaggeration of the hypothalamo-pituitary-adrenocortical (HPA) response to stress. In contrast, animals rendered tolerant to morphine failed to release ACTH or corticosterone in response either to a subsequent injection of the opiate or to stress. The development of the inhibitory effect paralleled the development of tolerance to the analgesic actions of the drug. The production of ACTH by pituitary segments removed from control animals was not affected by the addition of opioid substances to the incubation medium. However, morphine, met-enkephalin and leu-enkephalin stimulated the secretion of CRF by hypothalami and their effects were competitively antagonized by naloxone. The secretory activity of hypothalami removed from rats treated acutely with morphine was enhanced. In contrast hypothalami from morphine-tolerant rats failed to secrete CRF in response to morphine, met-enkephalin, acetylcholine or 5-hydroxytryptamine. Neither the density nor the affinity of 3H-naloxone binding sites in the hypothalamus was influenced by the morphine treatment. The results suggest the opioid peptides and their receptors play a major role in the regulation of HPA function.

Adrenal Cortex↗
PubMed1983

A study of corticotrophic and melanotrophic activities in the pituitary and brain of the lamprey Lampetra fluviatilis.

Biological and radioimmunological assay methods were used in an attempt to detect and determine corticotrophic and melanotrophic activity in the pituitary gland and the central nervous system of the lamprey, Lampetra fluviatilis. The activities of various corticotrophin (1-39 ACTH)-related peptides in the cytochemical assay for ACTH could be readily distinguished on the basis of their dose-response lines. Extracts of the pituitary gland and brain but not of spinal cord were also active in this test. The dose-response lines of the pars distalis extracts were parallel with those of 1-39 ACTH; those of the neurointermediate lobe and the brain resembled des-Ac-alpha-MSH and alpha-MSH, respectively, although subsequent tests showed that the active molecules in the extracts differed from these standard peptides in other respects. Pituitary extracts were active in the Anolis bioassay for melanotrophin but not in a radioimmunoassay for alpha-MSH. Moreover, the electrophoretic Rf value of lamprey melanotrophic activity was distinct from both alpha-MSH and des-Ac-alpha-MSH. Brain extracts showed only low melanotrophic bioactivity and again no immunoreactivity. The results suggest that small amounts of corticotrophin occur in the pars distalis of the lamprey and that the melanotrophic factors in the neurointermediate lobe and brain are not identical to mammalian alpha-MSH and des-Ac-alpha-MSH.

Adrenocorticotropic Hormone↗
PubMed1983

Biological assay of luteinizing hormone-releasing hormone (gonadorelin).

The abilities of luteinizing hormone releasing hormone (LHRH) to stimulate the release of luteinizing hormone (LH) in vitro from dispersed pituitary cells or from segments of adenohypophysial tissue have both been exploited in an attempt to develop biological assays for its determination. Columns of dispersed adenohypophysial cells were highly sensitive to LHRH. The responses appeared to be specific, but the marked continual variation in their magnitude rendered the system nonprecise. Pituitary segments were less sensitive to LHRH than the dispersed cells. However, their responsiveness was increased by pretreatment ('priming') with the releasing hormone. Over a wide range of doses, there was a linear relationship between the LH released by 'primed' segments and the logarithm of the concentration of LHRH. The dose-response lines of hypothalamic extracts were parallel with those of the synthetic peptide. The method using segments is accurate, specific, and precise and fulfils the essential requirements of a biological assay.

Animals↗
PubMed1982

Secretion of corticotrophin and its hypothalamic releasing factor in response to morphine and opioid peptides.

The influence of morphine and enkephalins on the functional activity of the hypothalamo-pituitary-adrenocortical system in the rat was studied by investigating their effects on the secretion in vivo and in vitro of corticotrophin (ACTH) by the pituitary gland and corticotrophin-releasing factor (CRF) by the hypothalamus. A single injection of morphine caused a rise followed by a fall in hypothalamic CRF content and increases in the concentrations of ACTH in the plasma and adenohypophysis. In addition, the stress-induced increments in hypothalamic CRF and pituitary and plasma ACTH were exaggerated in morphine-treated rats. The production of ACTH by pituitary segments in vitro was not affected by the addition to the incubation medium of morphine, met-enkephalin, leu-enkephalin or naloxone. However, morphine and the enkephalins stimulated the secretion of CRF by isolated hypothalami and their effects were antagonized by naloxone. The results indicate that morphine and the enkephalins evoke hypothalamo-pituitary-adrenocortical activity by stimulating specific receptors in the hypothalamus and raise the possibility that opioid peptides and their receptors are physiologically important in the control of the secretion of CRF.

Adrenocorticotropic Hormone↗
PubMed1982

Effects of adrenocortical and gonadal steroids on the secretion in vitro of corticotrophin and its hypothalamic releasing factor.

The effects of adrenocortical and gonadal steroids on the secretion in vitro of ACTH by adenohypophysial segments and corticotrophin releasing factor (CRF) by isolated hypothalami were studied in the rat. Corticosterone (1.25 X 10(-6) mol/l), betamethasone (2.5 X 10(-8) mol/l) and progesterone (2.5 X 10(-7) mol/l) reduced the hypothalamic extract-induced secretion of ACTH by pituitary tissue in vitro but aldosterone (2 X 10(-7) mol/l), testosterone, androsterone, androstenedione (2 x 10(-7) mol/l), oestradiol, oestriol, and oestrone (10(-6) mol/l) did not. Corticosterone (2.5 +/- 10(-9) mol/l), aldosterone (2 X 10(-8) mol/l) and betamethasone (2 X 10(-10) mol/l) inhibited and oestradiol, oestriol and oestrone (10(-8) - 10(-6) mol/l) potentiated the production of CRF by isolated hypothalami which occurred when acetylcholine or 5-hydroxytryptamine were added to the incubation medium but progesterone (2.5 X 10(-7) mol/l), testosterone, androsterone and androstenedione (2 X 10(-7) mol/l) had no effects. The results indicate that hypothalamo-pituitary-adrenocorticotrophic activity may be modified not only by glucocorticoids but also by other steroids.

Adrenocorticotropic Hormone↗
PubMed1981

A cytochemical bioassay method for the determination of luteinizing hormone in biological fluids and tissues.

1 The ability of luteinizing hormone (LH) to alter the reducing activity of corpora lutea in rat ovarian sections has been exploited to develop a new cytochemical bioassay for the hormone. 2 Sections of ovaries, removed from mature rats during the second day of dioestrus, were incubated with either standard LH or samples diluted for assay, stained immediately for reducing potential and the intensity of the stain measured by scanning and integrating microdensitometry. 3 An inverse linear relationship existed between the density of the stain and the logarithm of the concentration of standard LH (68/40) and the dose-response lines of serial dilutions of rat or human plasma were parallel with those of the standard. 4 The method was found to be accurate, specific, sensitive, precise and suitable for the determination of LH in the rat and in man.

Adult↗
PubMed1981

The influence of vasopressin on hypothalamic corticotrophin releasing activity in rats with inherited diabetes insipidus.

1. The corticotrophin releasing activity of hypothalamic extracts from rats congenitally lacking vasopressin (Brattleboro strain) has been studied in the presence and absence of arginine vasopressin and its antiserum. 2. Hypothalamic extracts from Brattleboro rats stimulated the production of corticotrophin by pituitary segments in vitro but both their potency and the slopes of their dose-response lines were significantly less than those of controls. Arginine vasopressin also stimulated pituitary-adrenocorticotrophic activity in vitro but only in concentrations considerably greater than those present in hypothalamic extracts from normal rats. 3. In low, physiological concentrations arginine vasopressin did not affect the corticotrophin releasing activity of hypothalamic extracts from controls but potentiated markedly the activity of extracts from Brattleboro rats and rendered the slopes of their dose-response lines parallel with those of the controls. 4. The antiserum to arginine vasopressin did not affect the corticotrophin releasing activity of Brattleboro extracts but reduced the activity of control extracts and rendered the slopes of their dose-response lines parallel with those of Brattleboro extracts. 5. The results suggest that vasopressin acts synergistically with the corticotrophin releasing factor and is essential for the full expression of pituitary-adrenocorticotrophic activity.

Animals↗
PubMed1980

Hypothalamo-pituitary-adrenocortical function in rats with inherited diabetes insipidus.

1. Hypothalamo-pituitary-adrenocortical activity in male homozygous and heterozygous Brattleboro rats was compared with that in normal (Long Evans) controls in an attempt to elucidate the role of vasopressin the control of the secretion of corticotrophin. 2. The concentrations of corticosterone and corticotrophin in the plasma, corticotrophin in the adenohypophyses and corticotrophin releasing factor in the hypothalami were lower in the heterozygotes than in the controls and lower still in the homozygotes. 3. The capacities of adenohypophyses and hypothalami to secrete in vitro corticotrophin and corticotrophin releasing factor respectively in response to trophic stimuli were also reduced in the heterozygotes and, to an even greater extent, in the homozygotes. 4. The results suggest that vasopressin is not the corticotrophin releasing factor but they do not exclude the possibility that it may be involved in the sequence of events which leads to the secretion of corticotrophin in the rat.

Adrenocorticotropic Hormone↗
PubMed1979

Suppression of plasma ACTH concentration by angiotensin II infusion in normal humans and in a subject with a steroid 17 alpha-hydroxylase defect.

Six healthy subjects were infused with angiotensin II and plasma concentrations of angiotensin, ACTH and cortisol were measured before, during and after the infusion. In all cases the plasma ACTH concentration fell as plasma angiotensin increased and rose again, sometimes to higher than basal levels, when the angiotensin infusion was terminated. These effects were most marked at the highest rate of infusion (8 pmol/kg/min) and, at the lower rates (2 and 4 pmol/kg/min), there was some recovery of ACTH levels during the infusion period in some subjects. Plasma ACTH concentrations also fell when angiotensin was infused into a patient with high ACTH levels due to a steroid 17 alpha-hydroxylation defect. The inhibition of ACTH secretion is not due to a rise in plasma cortisol operating a negative feedback inhibition. It could be a direct effect of the infused angiotensin on the brain-hypothalamus-pituitary complex or an effect on the metabolism of ACTH.

Adrenal Hyperplasia, Congenital↗
PubMed1979

The influence of corticosteroids on the secretion of corticotrophin and its hypothalamic releasing hormone.

1. The effects of stress, adrenalectomy and corticosterone treatment on the functional activity of the hypothalamo-pituitary-adrenocortical system have been studied using highly sensitive and precise bio-assay methods for the determination of ACTH and CRH.2. Adrenalectomy resulted in a rise and corticosterone treatment a fall in the hypothalamic CRH content and the plasma ACTH concentration.3. Stress caused a fall followed by a rise in the hypothalamic CRH content, a rise in the pituitary and plasma ACTH concentrations and an increase in the plasma corticosterone concentration.4. The stress-induced changes in hypothalamic CRH content and pituitary and plasma ACTH were exaggerated in adrenalectomized rats but normal in adrenalectomized rats treated with corticosterone. They were also normal in animals injected I.P. with corticosterone 15 min before the stress but inhibited in those similarly treated 60 min previously.5. The ability of adenohypophyses and hypothalami to synthesize and release in vitro ACTH and CRH respectively in response to trophic stimuli was exaggerated in glands removed from adrenalectomized rats and reduced in those removed from corticosterone-treated rats.6. Addition of corticosterone to the pre-incubation medium reduced the capacities of adenohypophyses and hypothalami removed from untreated rats to synthesize and release ACTH and CRH respectively.

Adrenalectomy↗
PubMed1979

Hypothalamic receptors influencing the secretion of corticotrophin releasing hormone in the rat.

1. The production of corticotrophin releasing hormone (CRH) by the rat hypothalamus in vitro was studied in the presence and absence of various neurotransmitter substances and drugs which mimic or antagonize their actions.2. Acetylcholine, nicotine and bethanechol increased, in a dose-related manner, hypothalamic CRH release and content but the maximal responses to bethanechol or nicotine were less than those to acetylcholine.3. The actions of acetylcholine were antagonized by atropine, pempidine and hexamethonium but were completely inhibited only when atropine and pempidine were given together. The effects of nicotine were abolished by pempidine but not by atropine while those of bethanechol were abolished by atropine but not by pempidine.4. Acetylcholine-induced hypothalamic CRH activity was also antagonized by cyproheptadine but not by methysergide.5. 5-Hydroxytryptamine caused dose-related increases in hypothalamic CRH release and content. Its effects were antagonized by cyproheptadine and methysergide but not by atropine, pempidine or hexamethonium.6. Acetylcholine-induced increases in hypothalamic CRH production were reduced by GABA, noradrenaline, adrenaline, methoxamine and phenylephrine but not by isoprenaline. The actions of GABA were antagonized by bicuculline and those of noradrenaline by phentolamine but not by atenolol.7. The results suggest the presence of nicotinic and muscarinic cholinoceptors, 5-hydroxytryptamine receptors, alpha-adrenoceptors and GABA-receptors within the hypothalamus all of which may be important in the control of CRH secretion.

Animals↗