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F Berkenbosch

Publications and source records attributed to F Berkenbosch.

64 records · Page 4Linked to original sources
PubMed1983

Vasopressin is not involved in the catecholamine-induced release of ACTH, alpha-MSH and beta-endorphin from the rat pituitary gland.

The effect of catecholamines on plasma levels of immunoreactive ACTH (ACTHi), alpha-MSH (alpha-MSHi), beta-endorphin (beta-ENDi), arginine-vasopressin (AVPi) and of corticosterone (B) was studied in female rats. Intravenous infusion of the specific beta-adrenoceptor-stimulating agent l-isoproterenol in Wistar rats under pentobarbital anesthesia resulted in a dose-dependent (dose range: 10-100 ng/kg . min) increase in plasma B. At higher concentrations, l-isoproterenol also caused a dose-dependent increase in plasma AVPi (dose range: 100-1,000 ng/kg . min). In addition to isoproterenol, also intravenous infusion of l-epinephrine caused a dose-dependent increase of plasma B (dose range: 100-1,000 ng/kg . min), whereas l-epinephrine was without effect on plasma AVPi, even at the highest dose tested (1,000 ng/kg . min). The effect of l-epinephrine or l-isoproterenol on plasma B was associated with a parallel and dose-related increase in plasma ACTHi, beta-ENDi and alpha-MSHi. The increase of plasma ACTHi, B and beta-ENDi in response to l-isoproterenol (300 ng/kg . min) was identical in Wistar, Long Evans and Brattleboro rats (Long Evans rats with a hereditary lack of vasopressin). Also the responses to l-epinephrine (1,000 ng/kg . min) were identical in Wistar and Brattleboro rats. We conclude that vasopressin does not mediate the catecholamine-induced release of ACTH, beta-endorphin and alpha-MSH.

Adrenocorticotropic Hormone↗
PubMed1982

Adrenergic mechanisms involved in the control of pituitary-adrenal activity in the rat: a beta-adrenergic stimulatory mechanism.

Epinephrine or isoproterenol was infused into a lateral tail vein of female Wistar rats under Nembutal anesthesia. After 20 min of diffusion, trunk blood was collected for the determination of plasma corticosterone (B) and ACTH immunoreactivity (ACTHi). Infusion of l-epinephrine resulted in a dose-related increase in plasma ACTHi and B. Maximal levels were similar to those observed during ether stress. The pituitary-adrenal system appeared more sensitive than the cardiovascular system to epinephrine, since the ED50 values of epinephrine for its effects on ACTHi and heart rate were 165 and 840 ng/kg . min, respectively. The effect of epinephrine on pituitary-adrenal activity could be mimicked by the beta-adrenergic agonist l-isoproterenol and could be blocked by the beta-adrenergic antagonist l-propranolol, whereas d-propranolol was ineffective. The response of the pituitary-adrenal system to epinephrine was not caused by effects on peripheral parameters such as the distribution or clearance of ACTH or B but was mediated by an increase in ACTH release. The pituitary-adrenal response to epinephrine and isoproterenol was not related to changes in heart rate, blood pressure, or vasopressin secretion. Infusion of epinephrine at a dose that induced a maximal increase in plasma ACTHi and B (1000 ng/kg . min) resulted in a circulating epinephrine concentration of 11 pmol/ml, which is within the physiological range. From these data we conclude that 1) circulating epinephrine can stimulate pituitary-adrenocortical activity, 2) this action is mediated by a beta-adrenergic receptor mechanism, and 3) such a mechanism may be involved in the response of the pituitary-adrenal axis during certain forms of stress.

Adrenal Cortex↗
PubMed1981

Hypothalamic deafferentation in the rat appears to discriminate between the anterior lobe and intermediate lobe response to stress.

Anterolateral deafferentation of the mediobasal hypothalamus prevented the increase of the plasma corticosterone concentration induced by ether, histamine and electric footshock. Hypothalamus deafferentation also prevented the ether stress-induced increase of the plasma levels of ACTH and beta-endorphin immunoreactivity (ACTHi, beta-ENDi). Infusion of isoproterenol evoked an increase of the plasma levels of corticosterone, ACTHi, beta-ENDi and alpha-MSH immunoreactivity (alpha-MSHi) in sham-operated rats. In rats with a deafferented hypothalamus, the responses of plasma corticosterone and ACTHi to isoproterenol were blocked but the responses of plasma beta-ENDi and alpha-MSHi remained intact. We conclude that circulating beta-ENDi after exposure to ether is of anterior lobe origin while circulating beta-ENDi after infusion of isoproterenol is of intermediate lobe origin.

Adrenocorticotropic Hormone↗
PubMed1981

Epinephrine as a potent releaser of immunoreactive beta-endorphin in rats.

The intravenous infusion of catecholamines to rats induced a dose dependent increase of immunoreactive beta-endorphin (beta-Endi) in plasma. The ED50 values of 1-epinephrine and 1-isoproterenol were 110 and 100 ng/kg X min respectively. 1-Propranolol, but not d-propranolol prevented the effect of 1-epinephrine. Infusion of 100 ng/kg X min of 1-epinephrine increased plasma epinephrine to 11 pmol/ml, a concentration that can occur during stress. We conclude that circulating catecholamines can stimulate beta-Endi secretion via a beta-adrenergic receptor mechanism and may play a role in the response of beta-Endi to stress.

Animals↗
PubMed1981

Release of beta-lipotropin and beta-endorphin from rat hypothalami in vitro.

Hypothalamic tissue extracts of rats were chromatographed and beta-endorphin immunoreactivity (beta-Endi) was measured. The two major peaks of beta-Endi co-eluted with beta-lipotropin (beta-LPH) and beta-End respectively. Hypophysectomy caused a local decrease of beta-LPH and beta-End concentrations in the mediobasal hypothalamus. During superfusion of hypothalamic tissue blocks in vitro, membrane depolarization by electric stimulation or 45 mM k+ induced a Ca2+-dependent release of both beta-LPH and beta-End.

Animals↗
PubMedDate not supplied

Beta-adrenoceptor activation mediates stress-induced secretion of beta-endorphin-related peptides from intermediate but not anterior pituitary.

Recently, we reported that adrenaline can stimulate the secretion of immunoreactive beta-endorphin in the rat. This response is mediated by beta-adrenoceptors and requires circulating adrenaline concentrations which are known to occur during stress. We therefore studied whether catecholamines are implicated in the stress-induced secretion of immunoreactive beta-endorphin from the pituitary gland. We report here that in rat the beta-adrenoceptor antagonist (-)propranolol reduces or abolishes the rapid increase of immunoreactive beta-endorphin levels during some stress stimuli (footshock, passive avoidance, restraint) but not during others (ether, formalin, laparotomy). The propranolol-sensitive response is largely prevented by extirpation of the neurointermediate lobe of the pituitary gland but is unaffected by dexamethasone, which inhibits peptide secretion from the corticotroph cells of the anterior lobe. These results suggest that catecholamines activate the release of immunoreactive beta-endorphin from the intermediate lobe but not from the anterior lobe of the pituitary gland during certain stress conditions.

Animals↗
PubMedDate not supplied

ACTH response to a low dose but not a high dose of bacterial endotoxin in rats is completely mediated by corticotropin-releasing hormone.

In experimental animals and humans, bacterial endotoxin activates the hypothalamus-pituitary-adrenal (HPA) axis. The pathways by which endotoxin stimulates adrenocorticotropic hormone (ACTH) and corticosterone secretion are uncertain. In the present study we compared the role of hypothalamic corticotropin-releasing hormone (CRH) in the activation of the HPA axis by a low (2.5 micrograms/kg) and a high (2.5 mg/kg) dose of bacterial endotoxin. Two experimental models were applied using chronically cannulated male Wistar rats. In the first model, rats were subjected to lesions of the hypothalamus that interrupted dorsal, lateral and frontal input to the median eminence (anterolateral deafferentation) or to sham operation and rats were used 7 days later. Before and at hourly intervals after endotoxin (2.5 micrograms/kg i.p.), blood samples were taken for the determination of plasma ACTH and corticosterone concentrations. Deafferentation of the hypothalamus strongly attenuated the elevations in plasma ACTH and corticosterone concentrations by a low dose of endotoxin compared to the responses in sham-operated animals. The second model involved passive immunization to CRH using a monoclonal antibody to rat/human CRH (PFU83). PFU83 (90 nmol/rat) abolished the elevation of plasma ACTH concentrations and attenuated corticosterone responses to a low dose of endotoxin (2.5 micrograms/kg i.p.) compared to that in control IgG-treated rats. Since the corticosterone responses to endotoxin were less effectively inhibited by the antibody than the ACTH responses, we postulate that non-ACTH-dependent mechanisms may contribute to the corticosterone response to endotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMedDate not supplied

Tumor necrosis factor-alpha: specific binding sites in rodent brain and pituitary gland.

Specific binding sites for TNF-alpha in mouse and rat brain, spleen and pituitary gland have been visualized and characterized, using quantitative autoradiography. Mouse recombinant 125I-TNF-alpha has been used as a radioligand. In the spleen, TNF-alpha binding sites were highly concentrated in the white pulpe of mouse and rat spleen. The IG50, as determined by displacement of radioligand by the unlabelled peptide, was 0.3 x 10(-9) M for both species. In the mouse brain, a weak specific binding was observed on the entire surface of the brain tissue. However, none of the nervous or vascular structures were specifically labelled above this signal. No specific binding was detectable in the rat brain tissue. In sharp contrast, in the anterior lobe of the pituitary gland of both mouse and rat, high concentrations of specific binding sites were detectable. Displacement curves in the mouse pituitary gland revealed the presence of two classes of binding sites with respective IC50 values of 10(-9) and 5 x 10(-11) M. A single class of TNF binding site was demonstrated in the rat with an IC50 of 10(-9) M. The presence of TNF binding sites in the anterior pituitary gland underlines the existence of regulatory pathways between the immune and neuroendocrine system.

Animals↗