Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

Three series of experiments were performed in conscious dogs to test the possibility that the stimulation of adrenocorticotropin (ACTH) release by angiotensin II (ANG II) is mediated by arginine vasopressin (AVP). In the first protocol, the effect of ANG II on ACTH release was studied in dogs in which endogenous AVP levels had been increased by water deprivation. Water deprivation for 24 h increased plasma AVP concentration from 3.0 +/- 0.5 to 7.7 +/- 0.5 pg/ml (P less than 0.01) and increased the AVP response to the highest dose of ANG II (20 ng X kg-1 X min-1). Despite these changes, water deprivation failed to increase the ACTH response to ANG II. Next, the contribution of endogenous AVP to the stimulation of ACTH release by ANG II was examined using the V1-receptor antagonist, d(CH2)5Tyr[Met]-AVP (10 micrograms/kg iv). The ACTH response to ANG II in the presence of the AVP antagonist (66.4 +/- 3.1 to 100.1 +/- 15.9 pg/ml) was not significantly less than that in its absence (53.0 +/- 4.8 to 72.2 +/- 11.1 pg/ml). Finally, ANG II and AVP were infused in combination to determine whether there is a synergism between these two peptides in the release of ACTH. In one protocol, AVP and ANG II were infused separately and in combination. The ACTH response to ANG II and AVP in combination (48.7 +/- 6.5 to 61.5 +/- 8.5 pg/ml) was not enhanced compared with the responses to ANG II (59.8 +/- 7.3 to 71.0 +/- 10.1 pg/ml) or AVP (48.8 +/- 5.7 to 55.6 +/- 6.5 pg/ml) alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of vasopressin in stimulation of ACTH secretion by angiotensin II in conscious dogs. 301 91

These experiments were designed to test for an interaction between angiotensin II (ANG II) and stress in the control of plasma adrenocorticotropin hormone (ACTH), corticosteroids, and aldosterone. The stimulus to ACTH used in this study was insulin-induced hypoglycemia, a stimulus that does not increase plasma ANG II concentrations. Five trained dogs with exteriorized carotid arteries were studied. Each dog was infused with ANG II intravenously (10 ng X kg-1 X min-1) or into the carotid artery (1 ng X kg-1 X min-1) or with saline (iv) for 80 min. Twenty minutes after the start of the infusion, insulin (0.10 U/kg iv) was injected. Intravenous infusion of ANG II increased mean arterial pressure (MAP) and plasma aldosterone concentrations but did not increase ACTH or corticosteroid responses to hypoglycemia. Intracarotid infusion of ANG II did not increase MAP and also failed to increase ACTH and corticosteroid responses to hypoglycemia. Since ANG II infusions did not increase basal corticosteroids, the failure of ANG II to stimulate ACTH is not a result of steroid negative feedback. Thus it appears that increased plasma ANG II concentrations do not increase ACTH responses to hypoglycemic stress.
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PMID:Angiotensin II does not alter ACTH responses to hypoglycemia in conscious dogs. 303 Jan 43

We studied the effects of cyclosporin A on the renin-aldosterone axis in Sprague-Dawley rats. Two weeks of intragastric administration of cyclosporin A (5 mg/kg/day or or 20 mg/kg/day) resulted in large increases in plasma renin concentration (23 +/- 5, 70 +/- 12, and 79 +/- 11 ng/ml/hr in control rats and rats receiving 5 mg and 20 mg of cyclosporin A, respectively), with no parallel increments in plasma aldosterone. In vitro angiotensin II (ANG II)-stimulated aldosterone secretion by zona glomerulosa cells obtained from cyclosporin A-treated rats was also reduced (4.8 +/- 0.5, 1.5 +/- 0.2, and 0.2 +/- 0.2 ng/10(5) cells in control rats and rats receiving 5 mg and 20 mg of cyclosporin A, respectively). In contrast, in vitro aldosterone response to graded increments of potassium (3.7-10.7 mmol/L) or adrenocorticotropic hormone (ACTH) (10(-11)-10(-8) M) was preserved in cyclosporin A-treated rats. When added in vitro to zona glomerulosa cells from untreated rats, cyclosporin A also attenuated ANG II-stimulated aldosterone secretion, but did not affect potassium or ACTH-mediated aldosterone production. Thus, cyclosporin A-induced hyperreninemic hypoaldosteronism in the rat depends on opposing renal and adrenal effects, with a direct or feedback stimulation of renin secretion and a specific blockade of ANG II-mediated aldosterone production.
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PMID:Cyclosporin A-induced hyperreninemic hypoaldosteronism. A model of adrenal resistance to angiotensin II. 329 44

Although other investigators have suggested that reductions in either Na or chloride concentration stimulate aldosterone secretion, we previously found that small reductions in NaCl (3-7 mM) that enhanced angiotensin II-(ANG II) and [K]- but not adrenocorticotropic hormone (ACTH)-stimulated aldosterone secretion are due to a change in osmolality. In the present study, aldosterone secretion by an isolated perfused canine adrenal gland was stimulated by low doses of ANG II or ACTH or by small increases in perfusate [K], and during this stimulation, replacing 25 mM NaCl with an isosmotic amount of mannitol enhanced aldosterone secretion induced by each of the above secretagogues. Choline chloride significantly enhanced ANG II-stimulated aldosterone secretion when used in place of 25 mM NaCl, but sodium methylsulfate did not. Large isosmotic reductions in [NaCl] failed to alter ACTH-stimulated cortisol secretion or the conversion of either exogenous corticosterone or 11-deoxycorticosterone to aldosterone. Thus, reductions in Na, but not in chloride concentration, specifically enhance the ability of the adrenal glomerulosa to secrete aldosterone in response to ANG II, K, and ACTH by an action on some site in the steroidogenic cascade that is sensitive to ANG II, potassium, and ACTH.
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PMID:Dissociation of osmotic and ionic modulation of aldosterone secretion. 334 86

We studied the effect of chronic carotid body denervation on renin (plasma renin activity, PRA), adrenocorticotropin (ACTH), blood pressure, and hematocrit responses to acute normocapnic (arterial CO2 partial pressure, PaCO2, 35 Torr) and hypercapnic (PaCO2, 65 Torr) hypoxia (arterial O2 partial pressure, PaO2, 31 Torr) in five anesthetized, artificially ventilated dogs. Animals were studied at least 3 days before and again at least 10 days after carotid body denervation (bilateral carotid sinus nerve resection). Increases in PRA during hypercapnic normoxia [21.8 +/- 6.4 ng angiotensin I (ANG I) X ml-1 X 3 h-1] and normocapnic hypoxia (13.3 +/- 4.2 ng ANG I X ml-1 X 3 h-1) were not attenuated by carotid body denervation. Increases in ACTH during normocapnic hypoxia (117 +/- 34 pg/ml) were attenuated but not eliminated by carotid body denervation; the increase in ACTH during hypercapnic hypoxia (295 +/- 93 pg/ml) was not attenuated by carotid body denervation. Both the blood pressure and hematocrit responses to normocapnic and hypercapnic hypoxia were attenuated by carotid body denervation. We concluded that 1) the renin response to hypercapnia and hypoxia is not a carotid chemoreflex, 2) the ACTH response to hypoxia is partially a carotid chemoreflex, and 3) blood pressure and hematocrit responses to hypoxia are primarily carotid chemoreflexes.
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PMID:Renin and ACTH responses to hypercapnia and hypoxia after chronic carotid chemodenervation. 608 93

Angiotensin II (ANG II) acts on the brain to elevate blood pressure (BP), stimulate drinking, increase the secretion of vasopressin and corticotropin (ACTH), and inhibit the secretion of renin. The present studies were designed to evaluate the possible physiological significance of these effects. The experiments were performed in conscious dogs with small catheters chronically implanted in both carotid and both vertebral arteries. ANG II was infused into both carotid or both vertebral arteries in doses of 0.1, 0.33, 1.0, and 2.5 ng.kg-1.min-1. Intravertebral ANG II produced dose-related increases in BP that were generally accompanied by increases in heart rate. Intracarotid angiotensin also increased BP but did not change heart rate. Intracarotid ANG II stimulated drinking and, at the highest dose only, increased the secretion of vasopressin, ACTH, and corticosteroids. Intravertebral and intracarotid ANG II suppressed plasma renin activity (PRA). In a parallel series of experiments, the effects of intravenous ANG II, in doses of 2, 5, 10, and 20 ng.kg-1.min-1, were studied. These infusions produced dose-related increases in BP and water intake and suppressed PRA. Only the highest dose of ANG II increased vasopressin or corticosteroid secretion. Analysis of these results in terms of calculated or measured changes in plasma ANG II concentration indicate that the central cardiovascular and dipsogenic actions of angiotensin, as well as the suppression of PRA, can be elicited by concentrations of the peptide that are within the physiological range. On the other hand high, probably supraphysiological, levels of ANG II are required to increase vasopressin or ACTH secretion.
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PMID:Analysis of the actions of angiotensin on the central nervous system of conscious dogs. 628 22

The effect of exogenous and locally generated angiotensin II (ANG II) on the release of beta-endorphin (beta-END) from anterior pituitary cell cultures of rats was studied. Angiotensin I (ANG I) and ANG II stimulated the release of beta-END, the ANG I effects being inhibited by addition of the converting enzyme inhibitor captopril. Renin and angiotensinogen had no effect when given separately, but their combination increased beta-END release. Thus ANG II causes the release of beta-END, but the putative pituitary renin system cannot be stimulated by exogenous renin or angiotensinogen; converting enzyme, however, acts locally to produce biologically active ANG II from ANG I.
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PMID:Angiotensin stimulates beta-endorphin release from anterior pituitary gland cell cultures of rats. 632 83

We studied the effect of surgery on hemorrhage-induced facilitation in the pituitary-adrenal system using repeated hemorrhage in chronically prepared dogs. Animals underwent splenectomy and adrenal venous and femoral arterial catheterization. Two (day 2) or five (day 5) days later, animals were anesthetized with pentobarbital, respired, and subjected to two periods of hypovolemia (20% hemorrhage with reinfusion of shed blood at 30 min; H1 and H2) separated by 90 min. Arterial and adrenal venous blood was sampled, and adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), angiotensin II (ANG II), cortisol, and cortisol secretion were measured. On day 2, cortisol secretion increased similarly after H1 and H2, despite a smaller response of ACTH to H2. On day 5, neither ACTH nor cortisol secretion changed after H1, but both increased significantly after H2. The adrenal sensitivity to ACTH increased after H2 on day 2 and was similar after H2 on both days. AVP and ANG II increased similarly after H1 and H2 on each day but had larger responses on day 2. These results suggest 1) either surgery or initial hemorrhage can lead to enhanced pituitary-adrenal responses to subsequent hemorrhage, 2) this effect may have both central and adrenal components, 3) negative feedback may inhibit enhanced responses of ACTH in this model, 4) changes in adrenal sensitivity to ACTH may not depend on an initial pituitary-adrenal response and may not be blocked by increased circulating corticosteroids, and 5) differences in circulating AVP or ANG II do not account for facilitation in pituitary-adrenal responses.
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PMID:Effect of surgery on the pituitary-adrenal response to repeated hemorrhage. 802 54

This study was performed to test the hypothesis that smaller reflex increases in vasopressin, cortisol, adrenocorticotropic hormone (ACTH), and angiotensin II (ANG II) concentrations are produced by hemorrhage in pregnant compared with nonpregnant conscious dogs. Equivalent hemorrhages (1% of the initial blood volume per minute) produced larger decreases in arterial pressure [P < 0.01; 107 +/- 6 to 73 +/- 10 mmHg (pregnant); 109 +/- 6 to 90 +/- 5 mmHg (nonpregnant)] but produced similar increases in plasma vasopressin concentration in the pregnant animals. As a result, the slope of the arterial pressure-to-vasopressin relationship was reduced (P < 0.05). During pregnancy, smaller increases in plasma cortisol concentration and heart rate were also produced for a given decrease in arterial pressure, but the relationship between pressure and ACTH was not significantly affected. In contrast, higher levels of plasma renin activity and plasma ANG II concentration were achieved in the pregnant dogs. In general, the relationships between plasma hormone levels and either left or right atrial pressure were not significantly altered. These results indicate that reflex increases in heart rate, vasopressin, and cortisol concentration are attenuated in pregnant dogs and that this attenuation may contribute to the inability of pregnant animals to achieve normal cardiovascular homeostasis during hemorrhage.
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PMID:Hemorrhage decreases arterial pressure sooner in pregnant compared with nonpregnant dogs: role of baroreflex. 818 41

The relative abilities of the hypothalamic peptides corticotropin-releasing factor (CRF), arginine vasopressin (AVP), oxytocin (OT), and angiotensin II (ANG II) to stimulate adrenocorticotropic hormone (ACTH) secretion from cultured sheep anterior pituitary cells were studied. Incubation of cells with CRF, AVP, and OT, but not ANG II, was associated with increased ACTH secretion. CRF and AVP were equally effective in stimulating ACTH release at 0.1 nM, but larger doses of each resulted in distinctly different ACTH secretory patterns. The minimally effective dose of OT was 10 nM; greater doses of this peptide resulted in ACTH secretory responses similar to those measured after addition of AVP. Cotreatment with ANG II did not affect the ACTH-secretory response to CRF, AVP, or OT. These data confirm that AVP is a potent stimulus for ACTH secretion from sheep anterior pituitary in vitro and also show that CRF is effective in low concentrations in releasing ACTH. In contrast, the data do not support a regulatory role for ANG II in stimulating ACTH release directly from sheep corticotroph cells.
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PMID:Hypothalamic peptide regulation of ACTH secretion from sheep pituitary. 823 55


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