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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous angiotensin II and ether stress were found to produce a rapid, transient increase in the corticotropin-releasing hormone (CRH) content of the median eminence as measured by a radioimmunoassay employing an antibody against rat CRH(1-41). This confirms previous reports of transient increases in CRH measured by bioassay. The increase did not occur in the paraventricular region or in other parts of the brain. It occurred along with an increase in plasma adrenocorticotropic hormone (ACTH) when a second ether stress was administered 1 h after the first, and it also occurred when rats that had been adrenalectomized for 5 days were exposed to ether. The increases in CHR and the ACTH responses to ether were reduced or abolished by dexamethasone and pentobarbital. Four days after semicircular knife cuts in the posterior hypothalamus, resting CRH in the median eminence was increased but there was no further rise after ether stress. Plasma ACTH was normal at rest after the cuts, but the increase produced by ether was reduced. The ACTH responses to angiotensin II and immobilization were also reduced. Because the posterior knife cuts reduced hypothalamic catecholamine content, the effects of reducing hypothalamic norepinephrine and epinephrine by administration of the dopamine-beta-hydroxylase inhibitor diethyldithiocarbamate (DDC) were tested. Five hours after DDC, plasma ACTH was elevated but there was no further increase with ether stress. The median eminence CRH content was normal but failed to increase after exposure to ether.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation between the stress-induced transient increase in corticotropin-releasing hormone content of the median eminence of the hypothalamus and adrenocorticotropic hormone secretion. 254 56

Systemic hypoxia has been reported to inhibit selectively aldosterone secretion in vivo. The mechanism of this inhibition has not been elucidated. We hypothesized that decreased tissue PO2 directly inhibited aldosteronogenesis. To test this hypothesis, we exposed dispersed adrenocortical cells (90% glomerulosa/10% fasciculata) to decreased PO2 in vitro while simultaneously stimulating aldosterone secretion with angiotensin II, N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (dibutyryl cAMP) adrenocorticotropic hormone (ACTH)-(1-24), or progesterone. Decreasing buffer PO2 from approximately 150 to approximately 85 Torr significantly inhibited basal and angiotensin II, cAMP, progesterone, and ACTH-stimulated aldosterone secretion at all doses of secretagogue. Inhibition was largest for angiotensin II (55 +/- 9% inhibition at 1 microM) and cAMP (54 +/- 8% at 3 mM) and lowest for ACTH (24% at 100 nM) and basal aldosterone secretion (31 +/- 7%). This inhibition was reversed by returning the buffer PO2 to 150 Torr. Cortisol secretion was not significantly inhibited by decreased buffer PO2. We conclude that decreased buffer PO2 significantly inhibits aldosterone secretion in vitro, and this inhibition is reversible and specific. Hypoxia-induced inhibition of aldosterone secretion in vivo may be caused, at least in part, by a direct effect of low tissue PO2 within the adrenal cortex.
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PMID:Low oxygen selectively inhibits aldosterone secretion from bovine adrenocortical cells in vitro. 254 24

Potentiated adrenocorticotropin (ACTH) and cortisol responses occur after the second of two small hemorrhages (hems) spaced 24 h apart in the dog. To test whether increased responses of other hormones might be associated with this effect, we examined plasma renin activity (PRA), angiotensin II (ANG II), and vasopressin after paired 10% hem (H1 and H2) spaced 5 h apart in chronically prepared conscious dogs. Cortisol secretion increased after each hem, and the response to H2 was larger (P less than 0.05; H1 peak at 6.8 +/- 1.3 micrograms/min vs. H2 peak at 18.3 +/- 5.3 micrograms/min). ACTH did not change after H1 but increased after H2, and the H2 response was larger (P less than 0.01). Vasopressin increased after each hem, and the H2 response was larger (P less than 0.01). The time courses of ACTH and vasopressin responses were similar after H2 (significant increases by 8 min). PRA and ANG II increased by 4 min after each hem, and although the difference was small the early PRA and ANG II responses were greater after H2. Blood volume and hem volume did not differ between hems. Hemodynamic responses to the hems were not different. We conclude that, although the PRA and ANG II respond rapidly enough after hem to influence pituitary responses, the slightly greater responses of these factors to H2 are not responsible for greatly increased pituitary-adrenal responses to H2. On the other hand, the markedly potentiated vasopressin response to H2, which parallels that of ACTH, suggests that vasopressin may mediate the increased ACTH responses to H2.
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PMID:Potentiated cortisol response to paired hemorrhage: role of angiotensin and vasopressin. 254 52

We have reported that infusion of atrial natriuretic factor (ANF) inhibited the rise in plasma renin activity (PRA) in response to constriction of the abdominal aorta to cause a reduction in renal perfusion pressure (RPP). To evaluate the effect of ANF on neural control of renin release, acute thoracic inferior vena caval constriction (TIVCC) was performed in conscious dogs to reduce arterial pressure by 25% of control and stimulate PRA by a reflex increase in renal nerve activity and a reduction in RPP. Propranolol was used to block neural stimulation of renin release. TIVCC caused significant increases in PRA, plasma aldosterone, arginine vasopressin (AVP), and adrenocorticotropic hormone (ACTH) concentrations. The increase in PRA was significantly reduced by the infusion of either ANF at 20 ng.kg-1.min-1 or propranolol. The combined infusion of ANF and propranolol produced an additive and complete inhibition of the renin response to TIVCC; therefore the effect of ANF is independent of neural stimulation of renin release. ANF at 20 ng.kg-1.min-1 also inhibited increases in aldosterone, AVP, and ACTH, but ANF at 5 ng.kg-1.min-1 only affected the aldosterone response to TIVCC. Therefore ANF inhibits angiotensin II-stimulated aldosterone synthesis and/or secretion at very low doses and at higher doses attenuates reflex increases in AVP and ACTH caused by hypotension.
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PMID:Mechanism of inhibition of renin response to hypotension by atrial natriuretic factor. 254 56

Rat adrenal glomerulosa cells labelled for 18 h with [3H]inositol responded to angiotensin II with a dose-dependent stimulation of the accumulation of inositol monophosphate, inositol bisphosphate and inositol trisphosphate. Addition of adrenocorticotropic hormone (ACTH) (10(-7)M) reduced the maximum responses without altering the EC50 values for angiotensin II. Thus, ACTH acted as a non-competitive inhibitor with respect to angiotensin II. No inhibition was observed in cells labelled for 2 h with [3H]inositol. Detailed examination of the inhibition showed that ACTH(1-24) was the most potent inhibitor, with ACTH(1-39) being 10-fold less potent. A mixture of alpha-melanocyte-stimulating hormone (alpha-MSH) (ACTH(1-13] and corticotropin-like intermediate lobe peptide (ACTH(18-39] was similarly inactive. ACTH(5-24) did not produce detectable inhibition. In terms of specificity, the receptor mediating ACTH inhibition of phosphatidylinositol turnover was similar to the receptor which mediated stimulation of aldosterone synthesis. Inhibition by ACTH was additive with inhibition produced by dibutyryl cAMP demonstrating that it was not mediated by rises in intracellular cAMP. ACTH inhibition also was additive with inhibition by the calcium channel blocker, nifedipine. These results demonstrate an interaction between ACTH receptors and angiotensin II receptors in adrenal glomerulosa cells at the level of their receptor-second messenger pathways.
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PMID:Adrenocorticotropic hormone inhibits angiotensin II-stimulated inositol phosphate accumulation in rat adrenal glomerulosa cells. 254 42

The responses of human adrenocortical cells to stimulation by ACTH(1-24), desacetyl-alpha-MSH, alpha-MSH and angiotensin II amide have been compared. Both desacetyl-alpha-MSH, thought to be the major form of the peptide in the human pituitary and in circulating plasma, and alpha-MSH caused a significant stimulation of aldosterone, corticosterone and cortisol secretion. Significant stimulation of the production of these steroids was obtained with desacetyl-alpha-MSH at a concentration of 1 nmol/l, while the response to alpha-MSH was considerably less sensitive, with a minimum effective concentration of 0.1 mumol/l. These values compared with minimum effective concentrations of 1 pmol/l for ACTH and 0.1 mumol/l for angiotensin II amide. Although cell types were not separated, it is possible to conclude that none of the peptides showed any specificity for the zona glomerulosa, and in each case the same minimum effective concentration of peptide was required for both aldosterone and cortisol secretion. Yields of steroid obtained under conditions of maximal stimulation by ACTH(1-24), alpha-MSH and desacetyl-alpha-MSH were at least three to five times the basal output of aldosterone, four to eight times that for corticosterone and more than seven to sixteen times that for cortisol. Angiotensin II amide was a relatively poor stimulant with maximal stimulation only 1.5 x basal. In these experiments the minimum effective concentration for desacetyl-alpha-MSH (1 nmol/l) was close to the circulating concentration of desacetyl-alpha-MSH (0.3 nmol/l) in man, and it is thus possible that this peptide may have a physiological role in the control of adrenocortical function.
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PMID:Actions of desacetyl-alpha-melanocyte-stimulating hormone on human adrenocortical cells. 254 12

In adrenal glomerulosa cells, angiotensin II (AII) rapidly stimulates the formation of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and causes marked long-term changes in the levels of highly phosphorylated inositols. Glomerulosa cells prelabeled with [3H]inositol for 48 h and exposed to AII for 10 min showed prominent increases in inositol 1,3,4,5-tetrakisphosphate (Ins-1,3,4,5-P4) and smaller increases in two additional tetrakisphosphates, Ins-1,3,4,6-P4 and another (Ins-3,4,5,6-P4) eluting in the position of Ins-3,4,5,6-P4 and its stereoisomer, Ins-1,4,5,6-P4, on anion exchange liquid chromatography. A concomitant decrease in InsP5 indicates that an increase in Ins-1,4,5,6-P4, the breakdown product of InsP5, is probably responsible for the initial rise in Ins-3,4,5,6-P4 during 10 min stimulation by AII. During prolonged stimulation by AII, Ins-1,3,4,5-P4 began to decline from its high, stimulated level after the first hour but the level of Ins-1,3,4,6-P4 remained elevated for several hours. There were also progressive increases in the levels of Ins-3,4,5,6-P4 and InsP5 during stimulation for up to 16 h with AII. Treatment of adrenal cells for 16 h with the cyclic AMP-mediated secretagogue, adrenocorticotropic hormone (ACTH), slightly increased basal levels of Ins-1,3,4,6-P4, Ins-3,4,5,6-P4, and InsP5, and enhanced the subsequent AII-stimulated increases in the two additional tetrakisphosphate isomers but not of inositol trisphosphates or Ins-1,3,4,5-P4. This change in the pattern of the higher inositol phosphate response to AII was manifested within 2 h after exposure to ACTH, and was mimicked by treatment with 8-bromo cyclic AMP or forskolin. Treatment with 50 microM cycloheximide abolished the ACTH-induced increases in inositol polyphosphate responses during AII stimulation, but had no effect on the responses of untreated cells to AII. The conversion of [3H]Ins-1,3,4-P3 to [3H]Ins-1,3,4,6-P4, a reaction linking the receptor-mediated InsP3 response to higher inositol phosphates, was enhanced in permeabilized cells that were pretreated for 16 h with either ACTH or AII. These results demonstrate that the reactions by which Ins-1,3,4,6-P4 and Ins-3,4,5,6-P4 are formed and converted to InsP5 are influenced by agonist-stimulated regulatory processes that include both calcium-dependent and cyclic AMP-dependent mechanisms of target cell activation. They also reveal changes consistent with agonist-induced conversion of InsP5 to its dephosphorylated metabolite, Ins-1,4,5,6-P4, during short-term stimulation by AII.
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PMID:Agonist-induced regulation of inositol tetrakisphosphate isomers and inositol pentakisphosphate in adrenal glomerulosa cells. 254 68

Aldosterone is a major regulator of fluid and electrolyte balance after hemorrhage and is released from the adrenal cortex by the action of adrenocorticotropin (ACTH) and angiotensin II (AII). Past work has shown that the hemorrhage-induced release of ACTH and cortisol is potentiated by prior hemorrhage. We therefore studied the response of adrenal aldosterone secretion to repeated hemorrhage and its control by ACTH and AII. Six awake dogs with chronic lumboadrenal vein catheters were bled 10% of measured blood volume (H1) with reinfusion at 30 minutes. The hemorrhage was repeated 5 hours later (H2). Adrenal presentation rates for AII (AII-PR) and ACTH (ACTH-PR) were calculated for each sample. Control hormonal and hemodynamic parameters before each hemorrhage were not different; hemodynamic responses to H1 and H2 did not differ. Aldosterone secretion increased significantly after each hemorrhage. The increase in aldosterone secretion after H1 was associated with an early increase in AII-PR and late increase in ACTH-PR. Aldosterone secretion following H2 was greater than that following H1 and was associated with early and larger responses of AII-PR and ACTH-PR. Aldosterone secretion following H1 correlated with the AII-PR (r = 0.75; p less than 0.001), but not with the ACTH-PR. In contrast, aldosterone secretion following H2 correlated with both the AII-PR (r = 0.54; p less than 0.01) and ACTH-PR (r = 0.71; p less than 0.001) and multiple regression analysis showed a highly significant relation with both AII and ACTH (r = 0.81; p less than 0.001). The data suggest that aldosterone secretion after initial small hemorrhage occurs as a result of increased AII, whereas both AII and ACTH may contribute to the larger aldosterone secretory response to H2. Since major trauma commonly involves at least two insults separated in time (e.g., injury followed by surgery), potentiated responses of aldosterone and other pituitary-adrenal hormones (ACTH, vasopressin, and cortisol) may have important implications for the control of fluid and electrolyte balance and metabolism in injured patients.
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PMID:Aldosterone secretion following non-hypotensive hemorrhage is potentiated by prior blood loss. 254 67

The effects of angiotensin II (A-II) and corticotropin (ACTH) on insulin-like growth factor-I (IGF-I) receptors of bovine adrenocortical cells were investigated. Pretreatment of cells for 48 h with ACTH or A-II induced in a dose-dependent manner an increase in [125I]IGF-I binding (ED50 congruent to 10(-11)M, Vmax = 10(-10) M with ACTH; ED50 congruent to 3.10(-9) M, Vmax = 10(-7) M with A-II). This resulted from an increase in the number of binding sites without modification of the binding affinity. Pretreatment with 8-Bromo-cAMP (10(-3) M), a phorbol ester (PMA 10(-7) M) + ionophore A23187 (10(-7) M) produced a positive regulation of IGF-I receptors. Glucocorticoids did not mediate the effect of A-II and ACTH on IGF-I receptors. Since previous studies have shown that IGF-I increased ACTH and A-II receptors the present data indicate the existence of a reciprocal positive trophic effect between IGF-I and the two hormones on the regulation of their specific membrane-bound receptors.
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PMID:Regulation of IGF-I receptors by corticotropin and angiotensin-II in cultured bovine adrenocortical cells. 254 91

Examination of the cardiovascular effects produced by peripheral administration of peptide sequences derived from adrenocorticotropic hormone (ACTH) led to the discovery of the pressor, cardioaccelerator, and natriuretic actions of intravenous (iv) ACTH-(4-10). Based on pharmacological studies in rats with alpha- and beta-adrenergic receptor antagonists, the cardiovascular effects of this peptide appeared to be mediated by the release of catecholamines. A peptide sequence analogous to ACTH-(4-10), gamma-melanocyte-stimulating hormone (gamma-MSH), possesses greater than 100-fold more cardiovascular activity and 1,000-fold more natriuretic activity than ACTH-(4-10). The pressor effect of iv gamma-MSH peptides appears to be dependent on the maintenance of preganglionic sympathetic drive, with no significant contribution of circulating vasopressin or angiotensin II. However, the presence of central vasopressinergic, and perhaps angiotensinergic, pathways appears to be crucial for expression of the full pressor effect of circulating gamma-MSH. Further evidence for the potential importance of the central nervous system (CNS) in these cardiovascular effects was obtained from central lesion experiments and a comparison of intracarotid vs. intrajugular infusions. Structure-activity studies suggested that the cardiovascular effects of ACTH-(4-10) or gamma-MSH are dependent on an Arg-hydrophobic amino acid sequence, located at or near their COOH-terminal. A similar requirement for biological activity is found in molluscan cardioexcitatory peptides, and the molluscan peptides have cardiovascular effects in rats, which resemble ACTH-(4-10) or gamma-MSH. This suggests that peptides of the gamma-MSH family are the pharmacological analogues, and perhaps the physiological homologues, of a cardioexcitatory family of peptides found in molluscs and birds. Elevated circulating levels of peptides derived from the NH2-terminal of pro-opiomelanocortin (POMC) have been found in psychological stress, cardiovascular distress, and hemorrhage. Increases in central sympathetic drive are common to all of these states. gamma-MSH peptides have been localized to POMC neurons in the arcuate nucleus and nucleus commissuralis of the rat. Projections from the latter nucleus innervate hindbrain vasomotor centers. Intraventricular administration of gamma-MSH produces prolonged elevation of mean arterial pressure. gamma-MSH peptides may provide a link between humoral and neurogenic mechanisms in cardiovascular regulation and could potentially be important neurotransmitters for central control of the cardiovascular system.
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PMID:ACTH-(4-10) through gamma-MSH: evidence for a new class of central autonomic nervous system-regulating peptides. 255 43


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