bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cardiovascular and Steroid Responses to Graded Haemorrhage in Rats with Adrenal Regeneration Hypertension
Authors: Foulkes R. , Gardiner S. M. , Bennett T. 
Published: September 2006

AbstractBlood pressure (BP) and plasma steroid responses to haemorrhage (2 ml + 1 ml + 1 ml at 20‐min intervals) were assessed in sham‐operated (SO) rats and in rats with adrenal regeneration hypertension (ARH). Experiments were carried out between 0700 and 1000 h (a.m.) and between 1400 and 1700 h (p.m.), because rats with ARH have BPs that are higher a.m. than p.m. There were no differences in the BP responses following haemorrhage in SO or ARH rats either a.m. or p.m., although ARH rats were unable to increase their plasma steroid levels. Pretreatment with captopril alone, d(CH2)5 DAVP alone, or captopril and d(CH2)5DAVP augmented the early hypotensive responses to haemorrhage but did not influence the later compensated levels of BP in either group of rats. There were no clear‐cut a.m. to p.m. differences in the changes in BP in any of the drug‐treated groups of SO or ARH rats. Under all conditions studied, the compensated level of systolic BP in ARH rats, 20 min after the final bleed, remained higher a.m. than p.m., indicating that this difference was not dependent on the renin‐angiotensin system and vasopressin and suggesting that the sympathetic nervous system and/or other factors might be involved.
Interactions Between Opioid Peptides and Adrenaline‐Containing Neurons Modulate Luteinizing Hormone Secretion in Male Rats
Authors: Martensz N. D. , Goldstone A. P. , Stuart E. , Everitt B. J. 
Published: September 2006

AbstractThere is increasing evidence that the opioid inhibition of luteinizing hormone (LH) secretion is mediated, at least in part, by catecholaminergic mechanisms. This study determined the effects of selective manipulation of noradrenergic and adrenergic systems on the ability of opiate receptor blockade to induce the release of LH in adult male rats.Selective depletion of hypothalamic noradrenaline levels by 80% following 6‐hydroxydopamine infusions into the central tegmental tract did not alter the 2‐ to 3‐fold increase in serum LH levels following opiate receptor blockade with naloxone (2.5 mg/kg). In contrast, both selective depletion of hypothalamic adrenaline by prior treatment with the phenylethanolamine N‐methyltransferase inhibitor, LY134046 (2 × 50 mg/kg) and non‐selective depletion of all three catecholamines with α‐methyl‐p‐tyrosine (250 mg/kg), abolished the naloxone‐induced increase in LH.These results suggest that the inhibition of LH secretion by endogenous opioid peptides is influenced by catecholaminergic neurotransmission and further support the view that adrenaline rather than noradrenaline or dopamine is of importance in this context.
Biochemical and Immunocytochemical Assessment of Neural Progestin Receptors Following Estradiol Treatments that Eliminate the Sex Difference in Progesterone‐Facilitated Lordosis in Guinea‐Pigs
Authors: Olster Deborah H. , Blaustein Jeffrey D. 
Published: September 2006

AbstractA single injection of estradiol benzoate (10 μg), while highly effective in ovariectomized female guinea‐pigs, does not prime castrated males to display progesterone‐facilitated lordosis. In contrast, adult males and females exhibit the same, high degree of progesterone‐facilitated lordosis when primed with two, 2.0 μg injections of free estradiol‐17ß (pulse regimen). We compared neural progestin receptor induction after these different estradiol treatments by in vitro radioligand binding assays and immunocyto‐chemistry. Binding assays confirmed previous observations of lower concentrations of cytosol progestin receptors in the mediobasal hypothalamus‐preoptic area in estradiol benzoate‐treated males than in females. No such sex difference was observed in animals that had been exposed to the behaviorally effective estradiol pulse regimen; rather, hypothalamic‐preoptic area progestin receptor concentrations in these animals did not differ from the low levels observed in males treated with the behaviorally ineffective estradiol benzoate regimen. Immunocytochemical analysis revealed progestin receptor‐immunoreactivity in fewer cells in the medial preoptic nucleus‐anterior hypothalamic nucleus, periventricular preoptic area and arcuate nucleus of estradiol pulse‐ as compared to estradiol benzoate‐treated males and females. Estradiol benzoate treatment induced progestin receptor‐immunoreactivity in more cells in the medial preoptic area and ventrolateral hypothalamus than estradiol pulses in males, but not in females. Surprisingly, in these regions estradiol benzoate‐treated males had significantly more progestin receptor‐immunoreactive cells than females.These experiments yield two major findings: First, as has been shown in rats, the display of progesterone‐facilitated lordosis is not inflexibly differentiated according to sex in guinea‐pigs. Furthermore, reduced concentrations of estradiol‐induced progestin receptors in the hypothalamus and preoptic area cannot account for the lack of progesterone‐facilitated lordosis that is observed following priming with estradiol benzoate in males. Secondly, in the medial preoptic area and ventrolateral hypothalamus of female guinea‐pigs, estradiol pulses are as effective as estradiol benzoate in inducing progestin receptors. These observations, taken together with the finding of equal behavioral efficacy of the two estradiol treatments, are consistent with the hypothesis that estradiol‐induced progestin receptors in these regions of the brain are involved in progesterone‐facilitated lordosis in female guinea‐pigs.
Synchronous Pulsatile Release of Luteinizing Hormone and Immunoreactive Beta‐Endorphin from the Human Pituitary in vitro
Authors: Rossmanith W. G. , Yen S. S. C. , Rasmussen D. D. 
Published: September 2006

AbstractAn in vitro perifusion system employing very frequent (30 s) perifusate collectionswas utilized to investigate the relationship between pulsatile release of luteinizing hormone (LH) and immunoreactive β‐endorphin (iβ‐END) during individual perifusions of adult human anterior hemipituitaries. Each of six hemipituitaries released LH and iβ‐END in a distinctlypulsatile fashion, with pulses occurring approximately every 3.2 min for each. Power spectral analysis revealed that pulsatile release of both LH and iβ‐END occurred in a rhythmic pattern, with a periodicity of 3.1 and 3.2 min, respectively, and that the periodicity of pulsatile LH and iβ‐END release was correlated within individual perifusions. Moreover, the relative amplitudes (% change) of the synchronous LH and iβ‐END pulses were correlated. The effluent fractions from two of the perifusions were also assessed for thyrotropin, and it was determinedthat thyrotropin pulses were synchronized to both LH and iβ‐END pulses. These studies confirm that LH and iβ‐END are released from human anterior pituitaries in vitro in an intrinsically pulsatile fashion, and demonstrate that the LH and iβ‐END pulses tend to occur rhythmically and in synchrony and proportion with each other. Furthermore, correlation of thyrotropin pulses to both the LH and iβ‐END pulses suggests a common fundamental intrapituitary pulse generating mechanism.
Large Molecular Weight Immunoreactive Corticotrophin‐Releasing Hormone has Bioactivity on Superfused Ovine Pituitary Cells
Authors: Chan E‐C. , Thomson M. , Madsen G. , Boettcher B. , Falconer J. , Smith R. 
Published: September 2006

AbstractHuman placental extracts fractionated with Sephadex G‐50 produced three peaks of corticotrophin‐releasing hormone immunoreactivity, a large molecular weight peak (Mr30,000), an intermediate peak (4,758 < Mr < 10,000) and a low molecular weight peak coeluting with the 41‐residue hormone. All three peaks of immunoreactivity stimulated the release of β‐endorphin‐like immunoreactivity from ovine pituitary cells superfused in vitro. No response was observed from unstimulated cells superfused in parallel. Gel chromatography indicated that intermediate and small molecular weight forms of human corticotrophin‐releasing hormone immunoreactivity remained intact after contact with the ovine pituitary cells, whereas the large molecular weight material dissociated to produce 41‐residue hormone immunoreactivity. The secreted β‐endorphin immunoreactivity was shown by gel chromatography to comprise both β‐lipotrophin‐like and the 31‐residue β‐endorphin‐like immunoreactivity. The data show that the intermediate and low molecular weight forms of placental corticotrophin‐releasing hormone immunoreactivity are bioactive and suggest that the intermediate form is a hormone precursor, possibly procorticotrophin‐releasing hormone125–196, and the small form is identical to the hypothalamic hormone. The results with the larger molecular weight material indicate that it is likely to be a complex of the mature 41‐residue hormone and a binding protein.
Estrous Cycle Variations in Gonadotropin‐Releasing Hormone, Substance P and Beta‐Endorphin Contents in the Median Eminence, the Arcuate Nucleus and the Medial Preoptic Nucleus in the Rat: A Detailed Analysis of Proestrus Changes
Authors: Parnet P. , Lenoir V. , Palkovits M. , Kerdelhué B. 
Published: September 2006

AbstractThe concentrations of gonadotropin‐releasing hormone, substance P and β‐endorphin were measured in the median eminence, the arcuate nucleus and the medial preoptic nucleus of 4‐day cycling female rats. Very well marked estrous cycle‐related fluctuations were registered for these neuropeptides in these areas. The largest variations in concentrations of peptide levels were observed in the median eminence. Substance P concentration was highest throughout the day of proestrus as compared to the three others days of the cycle. At the time of the preovulatory luteinizing hormone surge, on the afternoon of proestrus, there was a marked increase in gonadotropin‐releasing hormone concentration and a marked decrease in β‐endorphin concentration.
The Biosynthesis of Melanin‐Concentrating Hormone in a Fish
Authors: Bird David J. , Baker Bridget I. , Eberle Alex , Swann Ray W. 
Published: September 2006

AbstractThis work investigated the biosynthesis of a neurohypophysial hormone, melanin‐concentrating hormone (MCH), in the trout. Sephadex G‐75 chromatography showed the presence of several large MCH‐immunoreactive molecules in hypothalamic and pituitary gland extracts, with different retention times on high‐performance liquid chromatography from the mature MCH1–17. About 10% of the total MCH‐immunoreactivity in the hypothalamus was attributable to large molecular weight forms but these contributed less than 1% to the immunoreactivity in the neurointermediate lobe. Both [35 S]methionine and [3 H]leucine were injected into the hypothalamus near the MCH perikarya (nucleus lateralis tuberis region) of anaesthetized fish, after which the fish were killed at intervals of up to 8 h post‐injection and the basal hypothalami, pituitary pars distales and neurointermediate lobes were extracted in acid. MCH‐related immunoprecipitates from these extracts were fractionated by sodium dodecyl sulphate polyacrylamide gel electrophoresis or by Sephadex G‐50 chromatography. The results show the incorporation of radiolabel into 15.3 K and 11.3 K precursors within 0.75 h, and their conversion, via several smaller intermediates, to a molecule resembling MCH1–17. The results are discussed in relation to the known cDNA sequence of salmon MCH. Labelled MCH first appeared in the neurointermediate lobe 4 h after injection, giving an estimated transit rate of 0.4 mm/h.
The Effect of Anteroventral Third Ventricular Lesions on the Changes in Cholecystokinin Receptor Density in the Rat Supraoptic Nucleus Following Saline Drinking
Authors: Blackburn R. E. , Dayt N. C. , Leng G. , Hughes J. 
Published: September 2006

AbstractAutoradiography and computerized image analysis were used to study the density of Cholecystokinin binding sites in the supraoptic nucleus of sham‐lesioned and anteroventral third ventricle (AV3V)‐lesioned animals in which the magnocellular system had been activated by salt‐loading with 2% saline for 48 h. Rats were maintained in metabolic cages for 5 to 7 days prior to a sham‐ or AV3V‐lesioning procedure, and the ratio of sodium intake:urinary sodium output used as a measure of sodium excretion. Following the sham or lesion procedure half of the rats had their drinking water replaced with 2% saline and the other half were maintained on normal drinking water. Neurohypophysial hormone levels were measured by specific radioimmunoassay in trunk blood samples taken 48 h after the saline or water treatment. The AV3V‐lesioned group of animals were characterized by an inability to excrete the excess sodium load and by a failure to increase secretion of both oxytocin and vasopressin into the general circulation in response to the salt‐stimulus. Despite this inappropriate response, [125 l]cholecystokinin octapeptide binding in the oxytocin‐rich dorsal portion of the supraoptic nucleus was similarly elevated in both sham‐ and AV3V‐lesioned rats following 2 days of saline treatment. These results suggest that the magnocellular oxytocin system is capable of responding to an osmotic stimulus even when the release of hormone has been severely impaired.
Effects of Different Opioid Receptor Antagonists on the Electrically‐Evoked Release of Endogenous Dopamine from the Isolated Neural Lobe of the Rat Pituitary Gland in vitro
Authors: Racké K. , Hering B. , Weber I. 
Published: September 2006

AbstractIsolated neural lobes of the rat pituitary gland were incubated in Krebs‐HEPES solution which contained the dopamine uptake inhibitor GBR 12921 and in some experiments additionally pargyline. The release of endogenous dopamine evoked by electrical stimulation of the pituitary stalk was determined by high‐performance liquid chromatography with electrochemical detection. (±)‐ Naloxone increased the evoked dopamine release maximally by 440% (EC50 209 nM). The (+)‐enantiomer of naloxone (up to 10 μM) did not affect the release of dopamine. The preferential κ‐opioid receptor antagonist MR 2266 increased the evoked dopamine release maximally by 135% (EC50 7 nM). MR 2267, the inactive (+)‐enantiomer of MR 2266, had no effect on dopamine release. The δ‐opioid receptor selective antagonist ICI 174864 increased the release of dopamine maximally by 120% (EC50 10 nM). The non‐selective opioid receptor agonist etorphine up to 10 μM had no effect on the evoked dopamine release. In conclusion, endogenous opioids in the neurohypophysis strongly inhibit the release of endogenous dopamine from this gland. Activation of κ‐ and δ‐opioid receptors appears to be involved in the inhibitory action of the endogenous opioids on the neurohypophysial release of dopamine.
Dose‐Related Effects of Progesterone and 5 Alpha‐Dihydroprogesterone upon Estrogen‐Induced Prolactin Release
Authors: Brann Darrell W. , Putnam Carla D. , Mahesh Virendra B. 
Published: September 2006

AbstractPrevious work from our laboratory has shown that progesterone causes a rapid reduction of pituitary nuclear estrogen receptors. This effect is accompanied by a loss of estrogen action such as estrogen‐induced progesterone receptor synthesis and prolactin release. Recent work has demonstrated that the effect of progesterone on estrogen receptor depletion is dose‐related. Therefore the purpose of this study was to examine the effect of different doses of progesterone upon estrogen‐induced prolactin release. Progesterone exhibited a multiphasic effect on estrogen‐induced prolactin release. The 0.8 mg/kg body wt and 3.2 mg/kg body wt doses of progesterone significantly inhibited estrogen‐induced prolactin release, whereas the intermediate dose, 2.0 mg/kg, was without effect. Progesterone is rapidly metabolized to 5α‐dihydroprogesterone in the pituitary, and this metabolite has recently been shown to deplete pituitary estrogen receptors similar to progesterone. Thus the effect of 5α‐dihydroprogesterone onstrogen‐induced prolactin release was also examined. 5α‐dihydroprogesterone was found to exhibit a multiphasic effect similar to progesterone in inhibiting estrogen‐induced prolactin release. The 0.4 mg/kg and 2.0 mg/kg doses of 5α‐dihydroprogesterone significantly inhibited estrogen‐induced prolactin release, whereas the 0.8 mg/kg dose was ineffective. The effect of 5α‐dihydroprogesterone required estrogen priming and was blocked by the antiprogestin, RU486, suggesting progesterone receptor mediation.
Evidence for a Short Feedback of Prolactin on the Tubero‐Infundibular Endings: Differential Effect on the Release of [3 H]Gamma‐Aminobutyric Acid and [3 H]Dopamine from Superfused Median Eminence
Authors: Felman K. , Tappaz M. 
Published: September 2006

AbstractRelease experiments were undertaken on the tubero‐infundibular terminals of the hypothalamic median eminence. Isolated median eminences were preloaded with [3 H]y‐aminobutyric acid (GABA) or [3 H]dopamine in such conditions that non‐specific uptake was pharmacologically impaired. Each median eminence was continuously superfused with Krebs bicarbonate medium and tritium releases were evoked with high potassium solutions. The evoked release was estimated by measuring the total radioactivity of which actual dopamine and GABA represented more than 60% and 80%, respectively. The experiments were done by applying two successive 5‐min pulses of potassium, the second in the presence of prolactin. These stimulations were submaximal: for each, a KCl concentration was chosen that gave about half the maximal response (45 mM for GABA and 30 mM for dopamine); the responses were suppressed by calcium‐free medium. Rat prolactin induced a significant increase of dopamine‐evoked release in a dose‐dependent manner with a maximum (30%) at 25 μg prolactin/ml of medium. Over the same range of concentration a significant but still weak (10%) increase of evoked GABA was observed only with the highest prolactin concentration (25 μg prolactin/ml). At the same concentrations, ovine prolactin induced a markedly reduced effect on dopamine release and had no effect on GABA release. Spontaneous releases of dopamine and GABA were not affected by prolactin. These results show that prolactin enhances acutely and directly, but differently, the evoked release of GABA and dopamine by the median eminence. This differential effect may reflect either a differential regulation or a greater heterogeneity of GABAergic endings. Our data give support for a short feedback exerted by prolactin directly on the tubero‐infundibular neurons.
Source of Stress‐Induced Increase in Plasma Met‐Enkephalin in Rats: Contribution of Adrenal Medulla and/or Sympathetic Nerves*
Authors: Barron B. A. , Pierzchala K. , Van Loon G. R. 
Published: September 2006

AbstractThe contribution of the adrenal medulla and/or the sympathetic nerves to the plasma levels of Met‐enkephalin was investigated. Rats were divided into four groups: sham‐operated/saline, sham‐operated/guanethidine, adrenal‐demedullated/saline, demedulla‐ted/guanethidine. After 4 weeks of injection with either saline or guanethidine (25 mg/kg/day), animals were cannulated in the left carotid artery for blood sampling. Three days later, blood samples were taken before and at 2 and 30 min of restraint stress. Adrenal demedullation lowered basal plasma epinephrine levels markedly and prevented entirely the increase induced by restraint stress. Chronic guanethidine treatment lowered basal plasma norepinephrine levels and decreased the response to stress. Guanethidine treatment increased the basal plasma epinephrine level without affecting the response to stress. The combination of guanethidine plus adrenal demedullation lowered basal plasma concentrations of all three catecholamines and further attenuated the norepinephrine response. Restraint stress increased plasma native and peptidase‐derivable Met‐enkephalin. Adrenal demedullation, resulting in greater than 95% depletion of adrenal catecholamines and significant depletion of adrenal Met‐enkephalin, did not inhibit the stress‐induced increase in plasma Met‐enkephalin, and in fact, was associated with a potentiated response to stress. Guanethidine treatment with or without demedullation increased baseline plasma native Met‐enkephalin and abolished the stress‐induced increase in plasma native and peptidase‐derivable Met‐enkephalin. Thus, the stress‐induced increase in plasma Metenkephalin results from release from sympathetic nerves, rather than adrenal medulla. However, the sympathetic nerves and adrenal medulla together do not appear to account entirely for basal concentrations of circulating Met‐enkephalin. Hepatic portal vein plasma concentration of native Met‐enkephalin was greater than that in the carotid artery, suggesting contribution from the gastrointestinal tract; however, evisceration did not decrease plasma native Met‐enkephalin. Some compensatory mechanism results in elevation of basal plasma native Met‐enkephalin in sympathectomized rats. Also, in the absence of the adrenal medulla there is a compensatory increase in the amount of Met‐enkephalin released into the circulation in response to stress.
Kappa‐Selective Opioid Receptor Agonists Leumorphin and Dynorphin Inhibit Supraoptic Neurons in Rat Hypothalamic Slice Preparations
Authors: Inenaga K. , Imura H. , Yanaihara N. , Yamashita H. 
Published: September 2006

AbstractTo clarify the effects of opioid peptides, and in particular the effects of kappa‐receptor agonists on the activity of supraoptic neurons, extracellular recordings were made from 71 spontaneously firing neurons in the rat hypothalamic slice preparation. Of 71 neurons, 28 showed a phasic firing pattern (phasic neurons: putative vasopressin neurons). The mean firing rate of phasic neurons was 2.6 spikes/s (intraburst firing rate 5.4 ± 2.2 spikes/s). The mean firing rate of neurons classified as non‐phasic neurons (putative oxytocin neurons) was 4.5 spikes/s. Following bath application of leumorphin (LM) at 10−7 M, which has potent opioid activity at kappa‐receptors, 17 (61%) of 28 phasic neurons were inhibited and 22 (51%) of 43 non‐phasic neurons were inhibited. Excitation was observed in only one non‐phasic neuron. The dose‐dependence of the response to LM was tested in five supraoptic neurons. There was an inverse relationship between LM concentration and percent change in firing rate. The threshold concentration of LM was approximately 10−8 M. The relatively selective kappa‐receptor antagonist, MR‐2266, completely blocked the LM‐induced responses. Its effects were long‐lasting and only partial recovery was observed 2 h after the application of MR‐2266. Dynorphin had similar inhibitory effects on supraoptic neurons to those obtained with LM when tested on the same neurons. In another series of experiments the mu‐receptor agonist morphine and the delta‐receptor agonist [D‐Ala, D‐leu]‐enkephalin (DADLE) were applied to 28 supraoptic neurons (12 phasic and 16 non‐phasic neurons) at 10−7 M and their actions compared directly with that of LM. Only two of 12 phasic neurons tested were inhibited by DADLE and none of five phasic neurons tested was inhibited by morphine, while eight of the 12 neurons tested were inhibited by LM. By contrast the non‐phasic neurons tested were inhibited by application of each of the peptides; seven of 16 neurons tested were not only inhibited by LM, but also five of 11 neurons by DADLE and seven of 15 by morphine. The magnitude of the responses varied from cell to cell. These results suggest that LM acts at the same receptors as dynorphin, and that opioids acting preferentially at kappa‐receptors inhibit both vasopressin and oxytocin neurons while delta‐ and mu‐receptor agonists inhibit primarily oxytocin neurons.