Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to investigate the effect of several effectors on angiotensin II (A-II) receptors and steroidogenic responsiveness in cultured bovine fasciculata cells. Treatment of adrenal cells for 24 h with A-II (0.1 microM), corticotropin (1 nM), phorbol ester (PMA 0.1 microM), calcium ionophore A23187 (0.1 microM) and cyclic 8-bromoAMP (1 mM) produced a loss of A-II receptors whereas the A-II antagonist [Sar1-Ala8]A-II (0.1 microM) led to a small but significant increase. The extent of the down-regulation of receptors following maximal concentrations of A-II was greater than that produced by the other agents. The effects of A-II were dose-dependent with a ID50 of 3 nM. Since cycloheximide and actinomycin blocked the down-regulation of receptors, it seems likely that the effectors lead to the synthesis of certain proteins which inhibit the recycling of internalized receptors. Pretreatment of adrenal cells with A-II induced both homologous (90% decrease) and heterologous (corticotropin 83, PMA and ionophore 76% decrease) steroidogenic desensitization. However, the cAMP response to corticotropin of A-II-pretreated cells was higher (P less than 0.001) than for control cells. Pretreatment with PMA and A23187 also resulted in both homologous and heterologous steroidogenic refractoriness but to a lesser degree than that induced by A-II. In contrast, corticotropin-pretreated cells responded normally to further stimulation with corticotropin or A-II. Similarly pretreatment of bovine adrenal glomerulosa cells with A-II (1 nM and 0.1 microM) and corticotropin (1 nM) also induced A-II receptor loss and steroidogenic refractoriness. The present findings indicate that, in contrast to the results reported in vivo in the rat, where A-II leads to up-regulation of its own receptors on glomerulosa cells and increases steroidogenic responsiveness, this peptide results in both down-regulation and desensitization in cultured bovine fasciculata and glomerulosa cells. Our results also emphasize the absence of correlation between A-II receptor loss and steroidogenic responsiveness.
 ...
PMID:Regulation of angiotensin II receptors and steroidogenic responsiveness in cultured bovine fasciculata and glomerulosa adrenal cells. 283 Oct 60

The control of aldosterone secretion may be altered during acute changes in arterial blood gases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 +/- 2.0 ng.ml-1.h-1), ACTH (96 +/- 32 pg/ml), and ALDO (10 +/- 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 +/- 69 pg/ml) and ALDO (to 33 +/- 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 +/- 14 pg/ml) and ALDO (to 30 +/- 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 +/- 2 ng.ml-1.h-1), ACTH (to 397 +/- 114 pg/ml), and ALDO (to 41 +/- 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (less than 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (Po2 approximately 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.
 ...
PMID:Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats. 283 42

The release of adrenocorticotropic hormone (ACTH) from dispersed goldfish anterior pituitary cells was examined in order to determine whether human angiotensin II (AII) would potentiate the ACTH-releasing activity of urotensin I (UI) and ovine corticotropin-releasing factor (oCRF), peptides with a sequence homology of greater than 50%. In mammals, AII has a slightly enhancing or potentiating effect on CRF-stimulated ACTH release. In the present investigations, concentrations of AII (0.5 and 1 nM), and of UI (1 nM) or oCRF (3 nM), which elicit moderate increases in ACTH release, were tested alone and in combination. The ACTH-releasing activities of AII and UI combined, or of AII and oCRF combined, showed no potentiation and in fact were less than additive. It was concluded that AII does not potentiate the ACTH-releasing activity of either UI or oCRF observed with goldfish anterior pituitary cells in vitro.
 ...
PMID:Angiotensin II stimulation of teleost adrenocorticotropic hormone release: interactions with urotensin I and corticotropin-releasing factor. 283 58

Prolonged infusion with 120 micrograms/kg/day alpha-MSH significantly increased basal plasma level of aldosterone in the rat, as well as raised the acute aldosterone response to a bolus administration of a high dose of ACTH or angiotensin II. These findings suggest that chronic alpha-MSH treatment stimulates the steroidogenic capacity of rat zona glomerulosa.
 ...
PMID:Evidence that prolonged alpha-MSH infusion enhances the steroidogenic capacity of rat adrenal zona glomerulosa in vivo. 283 57

Sodium uptake by rat adrenal glomerulosa cells was stimulated by intracellular acidosis evoked by Na+-propionate. This process was inhibited by 5-(N,N-hexamethylene) amiloride (HMA), a known inhibitor of the Na+-H+ exchange. These experiments demonstrate the existence of the Na+-H+ exchange in glomerulosa cells. Although amiloride inhibited the angiotensin II- and adrenocorticotropic hormone (ACTH)-induced aldosterone response, HMA, a more specific inhibitor of Na+-H+ exchange, failed to do that. 45Ca2+ influx and efflux were dependent on intra- and extracellular Na+ concentrations. Amiloride analogues, known to inhibit Na+-Ca2+ exchange, reduced basal 45Ca influx. Although we could not reveal the activation of Na+-Ca2+ exchange by angiotensin II, inhibitors of Na+-Ca2+ exchange also inhibited the angiotensin- and ACTH-induced aldosterone response of glomerulosa cells. Our results suggest that Na+-Ca2+ exchange supports the maintenance of basal Ca2+ level in the cytoplasma of glomerulosa cells, and amiloride derivatives inhibit aldosterone production by reducing Ca2+ level below resting values.
 ...
PMID:Na+-H+ and Na+-Ca2+ exchange in glomerulosa cells: possible role in control of aldosterone production. 283 93

The aim of the present study was to examine the effects of corticotropin-releasing factor (CRF) in conscious dogs and to determine whether the stimulation of adrenocorticotropic hormone (ACTH) release by angiotensin II (ANG II) results from potentiation of the action of CRF. In addition, the possible role of CRF in the stimulation of vasopressin released by ANG II was investigated. The following experiments were performed: 1) intravenous saline infusion; 2) ANG II (10 ng.kg-1.min-1) alone; 3) vasopressin (1 ng.kg-1.min-1) alone; 4) CRF (0.001, 0.01, or 0.1 microgram/kg iv) bolus; 5) vasopressin (1 ng.kg-1.min-1) and CRF (0.1 microgram/kg) together; 6) CRF (0.001, 0.01, or 0.1 microgram/kg) and ANG II (10 ng.kg-1.min-1) together; 7) ANG II (10 ng.kg-1.min-1) followed 15 min later with CRF (0.001, 0.01, or 0.1 microgram/kg). Each dose of CRF was tested on a different day. Infusion of ANG II alone stimulated the release of ACTH, cortisol, and vasopressin. Administration of CRF produced dose-dependent increases in plasma ACTH and cortisol concentrations, and the highest dose of CRF increased plasma vasopressin concentration. CRF given together with ANG II did not potentiate the stimulation of ACTH release by CRF. Vasopressin at the dose tested did not stimulate ACTH release but potentiated the ACTH response to CRF. ANG II stimulated vasopressin release but did not potentiate the AVP response to CRF. These results show that, in conscious dogs, ANG II and CRF each increase plasma ACTH concentration and that the ACTH response to CRF is potentiated by vasopressin but not by ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of CRF and ANG II on ACTH and vasopressin release in conscious dogs. 283 38

In this paper we provide evidence to show that the pathways by which adrenocorticotropic hormone (ACTH) and angiotensin II (AII) stimulate steroidogenesis in bovine fasciculata cells are only partially independent. Both hormones have the same intrinsic activity but a 500-fold higher dose of AII is required to achieve 50% stimulation of steroidogenesis. Whereas ACTH acts by way of cAMP, AII appears to operate through protein kinase C. The phorbol ester, 12-O-tetradecanoylphorbol-13 acetate (TPA), and the calcium ionophore, A23187, each stimulate steroidogenesis and, when added together, act synergistically. To test the relationship between the ACTH and AII pathways, we added the two hormones simultaneously and measured steroid production. When the hormones were present at submaximal concentrations, their effects were additive. At maximal doses, steroid production was 40% above that elicited by either hormone alone. In contrast to the action of AII in the glomerulosa cell where it inhibits ACTH-stimulated cAMP formation, AII causes no inhibition in the fasciculata. Cycloheximide inhibits steroidogenesis stimulated by AII or a mixture of TPA and A23187. Scatchard analysis of the binding of 125I-AII to particulates from adrenal cortical fasciculata indicates the presence of a single class of binding sites (Kd = 0.6 X 10(-8) M). Binding is not inhibited by ACTH. Biotin-containing AII analogs that bind specifically to the particulates have been evaluated as potential tools for avidin-biotin affinity chromatography of the receptor. One of these, [N epsilon-6-(biotinylamido)hexyllys1, Val5] AII, is a promising candidate for receptor isolation.
 ...
PMID:Angiotensin stimulation of adrenal fasciculata cells. 284 22

1. Physical effort involves, along with an increase in the plasma concentration of beta-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h). 2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone. 3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone. 4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.
 ...
PMID:Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise. 284 14

Vasopressin (VP) and angiotensin II (AT II) stimulate the production of inositol phosphates (IP) in rat glomerulosa cells. Guanosine 5'-[gamma-thio]triphosphate (GTP[S]), but not VP or AT II, stimulates IP production in a myo-[3H]inositol-prelabelled glomerulosa-cell membrane preparation. In combination with GTP[S], these hormones potentiate the response to GTP[S], indicating the existence of a G-protein involved in the coupling of the VP and AT II receptor with the phospholipase C. ADP-ribosylation with pertussis toxin (IAP) revealed the specific labelling of a single molecule of 41 kDa. No significant inhibition of VP- or AT II-stimulated IP accumulation was detected in intact cells when the whole 41 kDa molecule was endogenously ADP-ribosylated by IAP treatment. On the contrary, when glomerulosa cells were infected with cholera toxin (CT), both the VP- and AT II-stimulated IP accumulations were inhibited in a dose-dependent manner. Yet these effects were partial even at high concentrations of CT, and could not be related to the ADP-ribosylation of 'alpha s' molecules. Similarly, when the cells were infected with 1 microgram of CT/ml, the specific binding of VP and AT II decreased by 50-60%. Such results may signify that the treatment primarily affects the densities of the hormone receptors. When glomerulosa cells were incubated for 15 h in the presence of 10 nM-corticotropin (ACTH), a condition in which the intracellular concentration of cyclic AMP was increased 3-fold, the maximum IP response to 0.1 microM-VP or -AT II was decreased by 50%. When similar experiments were carried out only after a 15 min incubation period with the same concentration of ACTH, the increase in cyclic AMP was more pronounced, but no inhibition of hormone-induced IP accumulation was observed. Altogether, these results may suggest that CT exerts its action on the VP- or AT II-sensitive phospholipase C systems via a prolonged increase in intracellular cyclic AMP.
 ...
PMID:Cholera-toxin and corticotropin modulation of inositol phosphate accumulation induced by vasopressin and angiotensin II in rat glomerulosa cells. 284 33

This study examined the effects of angiotensin II (ANG II) and mammalian adrenocorticotropin hormone (ACTH) on adrenal corticosteroid secretions in the freshwater turtle, Pseudemys scripta. Synthetic turtle ANG II ([Asp1, Val5] ANG II) was infused at rates of 1, 10, and 100 ng/kg/min in conscious turtles while monitoring blood pressure (BP). One 60-min saline (0.6%) infusion preceded the ANG II infusions; two followed. Blood samples were collected at 30- and 60-min intervals and the plasma was frozen at -20 degrees until assay. Mammalian ACTH was infused at doses of 0.1 and 1.0 IU/min; the procedures were followed as delineated above. The plasma was assayed for corticosterone, cortisol, and aldosterone utilizing radioimmunoassay techniques. Infusions of exogenous, native ANG II at subpressor and pressor rates elicited dose-dependent increases in BP, which rose from a control mean of 22.6 +/- 5.8 mm Hg to a maximum mean value of 38.2 +/- 11.0 mm Hg (P less than 0.05 compared to control), and plasma corticosterone concentrations, which rose from a control mean of 6.6 +/- 2.8 ng/ml to a maximum mean value of 27.2 +/- 2.6 ng/ml (P less than 0.05 compared to control). Furthermore, both BP and corticosterone levels returned toward control levels during the final saline recovery period, suggesting that neither physical stress suffered by the animal nor blood volume changes due to infusions and blood sampling affected these parameters. ACTH failed to alter either BP or corticosterone. Neither ANG II nor ACTH had any effect on plasma cortisol or aldosterone concentrations--which fell below the minimal detection levels for these assays.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The effects of adrenocorticotropin hormone and angiotensin II on adrenal corticosteroid secretions in the freshwater turtle Pseudemys scripta. 284 7


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>