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Biomedical subjects

S Harvey

Publications and source records attributed to S Harvey.

At least 253 records · Page 14Linked to original sources

Mechanisms of release of prolactin from fowl anterior pituitary glands incubated in vitro: effects of calcium and cyclic adenosine monophosphate.

Fowl anterior pituitary glands were bisected and each half was pretreated in either Medium 199 or medium containing EGTA to deplete endogenous calcium (Ca2+) stores, after which they were incubated in Medium 199, or Ca2+-free medium, containing prolactin release-stimulating agents and verapamil, a Ca2+ channel blocker. High K+ concentrations, hypothalamic extract, synthetic thyrotrophin-releasing hormone (TRH) and dibutyryl cyclic AMP (dbcAMP) all stimulated release of prolactin from control (non EGTA-treated) hemianterior pituitary glands. The effects of TRH and dbcAMP were not additive, but the response to submaximal concentrations of TRH was augmented by theophylline, a phosphodiesterase inhibitor. Reduction of Ca2+ availability with EGTA or verapamil reduced basal release of prolactin, prevented the prolactin-stimulating effects of high K+ concentrations and TRH, and markedly attenuated responses to hypothalamic extract and dbcAMP, EGTA being more effective than verapamil. Increasing the Ca2+ concentration of the medium did not augment basal or stimulated release of prolactin. These results suggest that both Ca2+ and cyclic AMP may act as intracellular mediators in the release of prolactin. Both basal and stimulated release of prolactin depend upon the presence of Ca2+. Although influx from the medium may be the major source of Ca2+, endogenous stores of Ca2+, perhaps mobilized by dbcAMP, may be able to maintain some release of prolactin. The prolactin-stimulating effects of TRH may be mediated by cyclic AMP.

Animals↗

Physiological control of growth hormone secretion by thyrotrophin-releasing hormone in the domestic fowl.

Immature cockerels (4- to 5-weeks old) were passively immunized, with antiserum raised in sheep, against thyrotrophin-releasing hormone (TRH). The administration of TRH antiserum (anti-TRH) at doses of 0.5, 1.0 or 2.0 ml/kg lowered, within 1 h, the basal concentration of plasma GH for at least 24 h. The administration of normal sheep serum had no significant effect on the GH concentration in control birds. Although the GH response to TRH (1.0 or 10.0 micrograms/kg) was not impaired in birds treated 1 h previously with anti-TRH, prior incubation (at 39 degrees C for 1 h) of TRH (20 micrograms/ml) with an equal volume of anti-TRH completely suppressed the stimulatory effect of TRH (10 micrograms/kg) on GH secretion in vivo. These results suggest that TRH is physiologically involved in the hypothalamic control of GH secretion in the domestic fowl.

Animals↗

Control of plasma levels of growth hormone, glucagon and insulin in ducklings: roles of free fatty acids and somatostatin.

The effects of plasma free fatty acids (FFA) and somatostatin-14 (S-14) on concentrations of plasma GH, glucagon and insulin were investigated in juvenile ducks. Oleic acid, S-14 or both were infused into 4- to 7-week-old birds and plasma GH, glucagon-like immunoreactivity (GLI), immunoreactive insulin (IRI) and FFA were measured. An increase in plasma GH and a decrease in GLI but no change in IRI was observed after infusion of 9 mg oleic acid/kg per min. A decrease in plasma GH, FFA and IRI and an increase in plasma GLI was seen after infusion of 800 ng S-14/kg per min. These effects of S-14 on IRI and GLI were abolished when S-14 was infused simultaneously with oleic acid. It is concluded that FFA have a direct stimulatory effect on GH secretion and an inhibitory effect on glucagon secretion. Somatostatin-14 directly inhibits the secretion of GH and its stimulatory effect on the secretion of glucagon is mediated by a depression in concentrations of plasma FFA. Finally, S-14 has no effect on plasma insulin when basal levels of plasma FFA are maintained.

Animals↗

Endocrine changes in the fowl during infection with Eimeria maxima.

Plasma concentrations of thyroxine (T4), triiodothyronine (T3), prolactin, growth hormone and corticosterone were measured in immature domestic fowl which were infected with Eimeria maxima, uninfected but given the same amount of food as those infected (pair-fed) or fed ad libitum. Infection with E maxima caused a decrease in plasma T4 concentration whereas pair feeding caused an increase when food intake was minimal. Plasma T3 concentrations were decreased similarly in both infected and pair-fed birds. Infection caused an increase in plasma prolactin concentration, whereas pair-feeding did not. The plasma concentration of growth hormone was not affected by any of the treatments. Plasma corticosterone concentration was markedly increased on days 5 and 6 in pair-fed birds but was not affected by infection with E maxima.

Animals↗

Stress and adrenal function.

The natural environment is composed of various potentially hostile stressors. It is a basic requirement of life that the cells of an organism must be maintained within closely defined physiological limits. The maintenance of a constant interior mileu results from physiological and behavioural homeostatic adaptations. The physiological regulation of homeostatis is achieved by complex endocrine interactions, principally by the hormones secreted from the adrenal glands. In this brief review the responses of the avian adrenal glands to stressful stimuli, the mechanism of adrenal activation, and the function of the adrenal responses will be considered.

Adaptation, Physiological↗

Adrenocortical and adrenomedullary responses of fowl to treadmill exercise.

Adrenomedullary and adrenocortical responses of 40-day-old cockerels to treadmill exercise (0.4 km/hr, 0 degrees incline) were determined. Plasma concentrations of adrenaline were increased above both resting and control levels (P less than 0.001) after 30 min exercise and continued to increase (P less than 0.01) until the cessation of exercise. Plasma noradrenaline and dopamine levels were increased after 60 min of exercise (P less than 0.01 and 0.05, respectively). The adrenaline component of the plasma catecholamine response increased significantly above that of noradrenaline (P less than 0.001). Plasma corticosterone levels were also increased (P less than 0.001) during exercise and were closely correlated with plasma adrenaline concentrations. Exercise depleted (P less than 0.01) adrenal stores of adrenaline, which were inversely proportional to plasma adrenaline concentrations (P less than 0.001). Neither adrenal noradrenaline nor dopamine were significantly correlated with their plasma levels. These results suggest that adrenocortical (corticosterone) and adrenomedullary (adrenaline) responses during exercise may occur in response to similar stimuli or may be interrelated.

Adrenal Cortex↗

Stimulation of growth hormone secretion in dwarf chickens by thyrotrophin-releasing hormone (TRH) or human pancreatic growth-hormone-releasing factor (hpGRF).

The basal plasma growth hormone (GH) level in adult sex-linked dwarf hens was elevated in comparison with autosomal dwarf hens and with control (Cornell K strain) laying hens. The iv administration of thyrotrophin-releasing hormone (TRH) (10 micrograms/kg) had no effect on GH secretion in control hens but slightly (1.2-fold) and transiently (for 10 min) increased the GH level in the autosomal dwarfs and greatly (8.7-fold) increased the GH level in the sex-linked dwarfs, in which it remained elevated for at least 30 min after injection. The iv administration of human pancreatic GH-releasing factor (hpGRF) (10 micrograms/kg) stimulated GH release in each strain. The response in the sex-linked dwarfs was greater than that in the autosomal dwarfs and the control hens but less than that elicited by TRH. These results suggest that the increased basal GH level in the sex-linked dwarfs results from an increased responsiveness to provocative stimulation.

Animals↗

Stimulation of growth hormone secretion by human pancreatic growth-hormone-releasing factor and thyrotrophin-releasing hormone in anaesthetized chickens.

Sodium pentobarbitone anaesthesia depressed the concentration of growth hormone (GH) in the plasma of young (6 weeks of age) and old (22-30 weeks of age) domestic fowl. In both cases the concentration was reduced (P less than 0.05) within 10 min and had declined (P less than 0.001) to stable low levels (less than 5 ng/ml) within 50 min. The intravenous administration of synthetic human pancreatic growth-hormone-releasing factor (hpGRF) (10 micrograms/kg) (2 X 10(-9) mol/kg) increased (P less than 0.01) the GH concentration in both the young and old birds. This effect was observed irrespective of whether the birds were conscious or anaesthetized. The magnitude of the response in conscious young birds (164 ng/ml) was, however, greater (P less than 0.01) than that in anaesthetized chicks (64 ng/ml). The response in anaesthetized adult fowl (18.8 ng/ml) was also less (P less than 0.05) than that in their conscious counterparts (42.8 ng/ml). The GH response in conscious and anaesthetized 6-week-old birds to hpGRF was greater (P less than 0.01) than that in the corresponding adult birds. Thyrotrophin-releasing hormone (TRH) (10 micrograms/kg (2.8 X 10(-8) mol/kg); iv) also provoked (P less than 0.01) GH secretion in conscious and anaesthetized young birds and in anaesthetized (but not conscious) adults. Anaesthesia blunted (P less than 0.01) the GH response to TRH in the immature cockerels, although the response was greater (P less than 0.05) than that in anesthetized adults.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

Comparative effects of somatostatin-28 and somatostatin-14 on basal growth hormone release and pancreatic function in immature ducks (Anas platyrhynchos).

The 30-min infusion of somatostatin (SRIF)-14 or SRIF-28 (800 ng/kg/min) in 7- to 8-week-old ducklings reduced the basal level of plasma growth hormone (GH). The magnitude of the GH suppression induced by SRIF-14 was similar to that elicited by SRIF-28. "Rebound" GH secretion was observed 30 min after infusion, the GH concentration being elevated above the basal level. The increase in GH secretion after SRIF-14 infusion was greater than that induced by SRIF-28. Plasma insulin and free fatty acid (FFA) levels were similarly reduced after 10 and 30 min of SRIF-14 or SRIF-28 infusion. Following infusion the FFA levels returned to the pretreatment concentration, whereas the insulin concentration in both groups remained suppressed 30 min after infusion. The insulin level was still suppressed 60 min after SRIF-14 infusion, but not after SRIF-28 infusion. The infusion of SRIF-14 resulted in a marked, progressive increase in the glucagon concentration, which was reduced in birds infused with SRIF-28 and accompanied by hypoglycaemia. Following SRIF-28 infusion a "rebound" in the glucagon concentration occurred and remained elevated for at least 60 min. These results demonstrate comparative effects of SRIF-14 and SRIF-28 on the basal release of pituitary GH and pancreatic insulin and glucagon, and in particular they suggest that SRIF-28 is more potent in inhibiting pancreatic A cell activity.

Animals↗

Oestradiol 17 beta modifies fowl pituitary prolactin and growth hormone secretion in vitro.

Chicken pituitary glands were incubated in medium containing oestradiol 17 beta (E2), alone or together with single whole hypothalami. E2 stimulated prolactin release from the pituitary and increased the prolactin releasing activity of the hypothalamus, but did not affect growth hormone release. Preincubation of pituitaries with E2 dramatically stimulated subsequent prolactin release. Pituitaries primed with E2 were more responsive to the prolactin-stimulating effects of hypothalamic extract (HE) and thyrotrophin-releasing hormone (TRH) and more sensitive to the prolactin-inhibiting effect of dopamine. E2-primed pituitaries were much less sensitive to the growth hormone releasing activity of TRH and HE. These results show that E2 may regulate pituitary function by direct effects on hormone release by modifying pituitary sensitivity to stimulatory or inhibitory influences and by altering hypothalamic releasing activity.

Animals↗

Dietary sodium and adrenocortical activity in ducks (Anas platyrhynchos) and chickens (Gallus domesticus).

Immature chickens and ducks were maintained on synthetic diets containing normal (0.4%), low (0.018%), or high (1.9%) sodium for 8 days, with freshwater available ad libitum. Food intake was similar in both species regardless of the diet but weight gain was depressed in birds fed the low-sodium diet. In both species the circulating aldosterone concentration was increased within 24 hr of dietary sodium depletion, although maximal levels were not attained until after 5 days. The magnitude of adrenocorticotrophin (ACTH)-induced aldosterone secretion was also increased in sodium-deprived chickens and ducks. The basal aldosterone level was slightly suppressed by excess dietary sodium, which blunted the aldosterone response to exogenous ACTH. The transfer of chickens and ducks from low- to high-sodium regimes reduced the aldosterone levels (within 24 hr) to those in their respective controls. The transfer of birds from high- to low-sodium diets resulted in a prompt increase in the aldosterone concentration, although of reduced magnitude when compared with control birds transferred to low sodium. In both species alterations in the dietary sodium content had no effect on basal or ACTH-induced corticosterone secretion. The plasma prolactin levels in chickens were also unrelated to their sodium status. These results suggest that homeostatic adaptations in electrolyte balance during sodium depletion or excess are principally mediated by alterations in aldosterone secretion.

Adrenal Cortex↗

Brain testosterone metabolism in thyroidectomized and thyroxine-treated chickens.

The metabolism of testosterone to reduced derivatives was studied in the pituitary gland, the hypothalamus, and the hyperstriatum dorsale of thyroidectomized, sham-operated, and thyroxine (T4)-injected immature cockerels. The levels of plasma thyroid hormones were markedly reduced (P less than 0.001) in thyroidectomized cockerels whereas thyroidectomized or sham-operated birds injected daily with 100 micrograms/kg thyroxine had significantly elevated (P less than 0.001) levels in comparison with sham-operated control birds. Each tissue was found to produce significant amounts of 5 beta-androstane-17 beta-ol-3-one (5 beta-DHT), 5 beta-androstane-3 alpha, 17 beta-diol (5 beta-3 alpha-diol), and androstenedione. Irrespective of thyroid state 5 beta-DHT and 5 beta-3 alpha-diol were produced to the greatest extent by the hyperstriatum dorsale whereas androstenedione was maximally produced in the pituitary gland. In comparison with the hyperstriatum dorsale and the hypothalamus only small quantities of 5 beta-DHT were produced in the pituitary gland. In the hyperstriatum dorsale of thyroidectomized birds both 5 beta-DHT (P less than 0.05) and 5 beta-3 alpha-diol (P less than 0.1) were formed to a greater extent than in sham-operated birds. This effect was reversed by administration of T4 to the operated birds which reduced the levels to those measured in the sham-operated controls. Similarly, injection of T4 into sham-operated birds decreased (P less than 0.05) the production of 5 beta-DHT in the hypothalamus while in the pituitary gland injection of T4 into thyroidectomized birds reduced the production of androstenedione (P less than 0.05). It was concluded that in the cockerel thyroid hormone is likely to play a role in the metabolism of testosterone. The physiological significance of 5 beta-reductase activity in the neuroendocrine tissues is discussed.

Androstane-3,17-diol↗

Stimulatory and inhibitory effects of prostaglandin E2 on prolactin release in the domestic fowl.

In vivo prolactin secretion was increased in immature cockerels 20-30 min after the intravenous administration of prostaglandin (PG) E2 at a dose of 200 micrograms/kg. The addition of PGE2 to incubation medium had no direct effect on the release of pituitary prolactin during short-term (3-hr) culture, but augmented the stimulatory effect of hypothalamic tissue on prolactin secretion. The stimulatory effect of serotonin, noradrenaline, acetylcholine, and histamine on hypothalamus-induced prolactin release was also increased when pituitaries were coincubated with 10(-7)M PGE2, as was the stimulatory effect of thyrotrophin-releasing hormone (TRH) and hypothalamic extract (HE). The long-term (24-hr) preincubation of pituitaries with 10(-7)M PGE2 reduced the responsiveness of the prolactin-secreting cells to TRH or HE stimulation. PGE2 treatment also reduced the stimulatory effect of hypothalamic tissue on prolactin release and diminished the stimulatory effect of serotonin on hypothalamus-induced prolactin secretion. A 24-hr preincubation of hypothalamic tissue with 10(-7)M PGE2 also reduced its stimulatory effect on prolactin release when subsequently incubated with control pituitary glands. These results demonstrate that PGE2 initially stimulates in vivo and in vitro prolactin secretion in the fowl, possibly by increasing the release of hypothalamic prolactin-releasing activity and/or by increasing pituitary sensitivity to provocative stimuli. Chronic PGE2 stimulation appears to result in a reduction in pituitary responsiveness to stimulatory influences and in the release of hypothalamic-releasing activity.

Acetylcholine↗

Muscle development in thyroidectomised chickens (Gallus domesticus).

The metabolic and contractile activity of muscle was determined in immature cockerels made hypothyroid by surgical thyroidectomy at 6 weeks of age. Four weeks after thyroidectomy the activity of Mg2+-activated myofibrillar ATPase and total phosphorylase was reduced in the fast-phasic, posterior latissimus dorsi (PLD) and scapulotriceps (ST) muscles. The activities of these enzymes were unaffected in the slow-tonic, anterior latissimus dorsi (ALD) muscle. Thyroidectomy had no effect on length of the muscles studied but reduced the weight of the ALD and ST muscles. These results suggest that hypothyroidism results in a "slowing down" of fast-phasic muscles, although it does not affect the activity of slow-tonic muscles.

Adenosine Triphosphatases↗

Thyroid and adrenal responses of ducks (Anas platyrhynchos) during saline adaptation.

Fresh water-reared Aylesbury ducklings were given 0.1 or 0.2 M NaCl drinking water and variations in the plasma concentrations of thyroxine (T4), triiodothyronine (T3), corticosterone, and aldosterone were determined. Within 24 hr of being transferred to 0.2 M NaCl the corticosterone concentration was increased, whereas the levels of plasma T3 and aldosterone were reduced. The increase in corticosterone secretion persisted for at least 7 days, but the T3 and aldosterone concentrations had returned to control levels within 5 days. The concentrations of plasma aldosterone and T3 were similarly affected in birds transferred to 0.1 M NaCl, although corticosterone levels increased only after the birds were maintained on 0.1 M NaCl for 7 days. Plasma concentrations of T4 were increased in 1- to 2-week-old (but not 7-week-old) birds 7 days after their transfer to 0.1 and 0.2 M NaCl. In birds maintained on saline for 6 weeks the basal concentration of each hormone was not significantly different from that in fresh water-reared controls. When saline-reared birds were returned to freshwater conditions the plasma aldosterone and T3 concentrations were increased over a 5-day period. Transfer to saline consistently reduced body weight and food intake, whereas the transfer of saline-reared birds to fresh water stimulated body weight gain. Consequently, although these endocrine responses during saltwater adaptation might be expected to minimise the loss of body reserves and to facilitate the extra renal excretion of sodium, these alterations in endocrine function may be partly due to salt water-induced changes in food intake.

Adaptation, Physiological↗

Growth hormone and prolactin secretion in water-deprived chickens.

The deprivation of water for 12 or 24 hr increased the prolactin concentration in the plasma of immature chickens but had no effect on the circulating growth hormone (GH) level. The increase in plasma prolactin level reflected an increase in the basal rate of prolactin release from incubated hemipituitary glands and an increase in the responsiveness of the pituitary gland to hypothalamic releasing factors. The deprivation of water had no effect on basal level of pituitary GH release in vitro but abolished the stimulatory effect of the hypothalamus on in vitro GH secretion.

Animals↗

Neurotransmitter effects on in vitro prolactin and growth hormone release from fowl pituitary glands: dopamine and noradrenaline.

Pituitary glands and hypothalami from broiler fowl heads were incubated alone or together with dopamine, noradrenaline or monoaminergic drugs (apomorphine, pimozide, phentolamine, isoproterenol and propranolol). The basal release of both prolactin and growth hormone was not affected by any of these amines or aminergic drugs. The co-incubation of pituitary glands with whole hypothalami consistently stimulated prolactin and growth hormone secretion. Apomorphine inhibited hypothalamus-induced prolactin and growth hormone release and the response was blocked by pimozide. Noradrenaline markedly stimulated hypothalamus-induced prolactin release, an effect antagonised by phentolamine. Thyrotrophin-releasing hormone (TRH) stimulated the release of prolactin and this stimulation was reversed, in a dose-related manner, by dopamine. TRH also increased the release of growth hormone, in the presence or absence of dopamine. These results demonstrate inhibitory dopaminergic effects on prolactin and growth hormone secretion and stimulatory noradrenergic effects on prolactin release. These aminergic effects may be mediated at pituitary and/or hypothalamic sites.

Animals↗

Plasma concentrations of luteinising hormone, follicle stimulating hormone, androgen, growth hormone, prolactin, thyroxine and triiodothyronine during growth and sexual development in the cockerel.

Changes in concentrations of plasma luteinising hormone (LH), follicle stimulating hormone (FSH), androgen, growth hormone (GH), prolactin (Prl), thyroxine (T4) and triiodothyronine (T3) were measured during growth and sexual maturation in broiler cockerels reared in continuous light to 7 weeks and 14 h light/d thereafter. Concentrations of LH and FSH began to increase between 13 and 15 weeks, while those of androgens increased between 16 and 17 weeks. FSH concentration increased faster than that of LH. Concentrations of GH and Prl were high at 3 weeks; that of GH decreasing progressively between 3 and 14 weeks of age and thereafter remaining low, while that of Prl was low between 5 and 9 weeks, relatively high between 10 and 13 weeks, and then temporarily decreasing before increasing progressively during sexual maturation. Concentrations of T3 and T4 were higher in juvenile than in adult birds.

Androgens↗