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)

The effect of substnace P (SP) on the uptake and release of radiolabelled dopamine (3H-DA), 5-hydroxytryptamine (3H-5-HT) and y-aminobutyric acid (3H-GABA) was studied in slices of rat substantia nigra and corpus triatum. SP, 10(-9) to 10(-5) m, failed to modify the uptakes of these compounds during incubations (10-90 min) with slices of either brain region. SP, 10(-6)M, had no apparent effect on the spontaneous output of any of these compounds in either substantia nigra or corpus striatum. In the corpus striatum, SP seemed to potentiate the potassium-stimulated outflow of 3H-DA and 3H-5-HT, but not 3H-GABA, while the realeases from substantia nigra were unaffected. Morphine (10(-3)M), but not met-enkephalin (5 X 10(-6)M), weakly antagonized K+- EVOKED RELEASE OF 3/-DA in the corpus striatum. These results are discussed with reference to the possible interaction of SP with transmitter mechanisms at presynaptic sites in the central nervous system.
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PMID:Investigation of possible interactions between substance P and transmitter mechanisms in the substantia nigra and corpus striatum of the rat. 2 66

The adenylate cyclase system present in a preparation enriched in plasma membranes derived from bovine adrenal cortex was investigated in considerable detail. This system is stimulated by adrenocorticotropic hormone (ACTH), by biologically active analogs of this hormone, and by fluoride ion. The preparation contains sodium-potassium- and magnesium-dependent ATPases that are markedly inhibited by 50 mM sodium fluoride. Incorporation of a pyruvate phosphokinase ATP generating system into the adenylate cyclase assay medium provided constant substrate levels. In the presence of the ATP generating system, the rate of cyclic AMP formation (basal, fluoride, and ACTH-activated) was proportional to enzyme concentration and was linear with time. Proportionality with respect to enzyme concentration as concerned the hormone-activated adenylate cyclase was achieved only when the ratio of hormone to enzyme protein was kept constant. The temperature optimum of the adenylate cyclase, basal or activated, was approximately 30 degrees. Michaelis-Menten kinetics were observed when the ratio of Mg2+ to ATP was approximately 6:1. Both calcium and ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid completely inhibited the adenylate cyclase system at concentrations of 5 and 0.5 mM, respectively. GTP was inhibitory at concentrations of 10-2 M but had little effect at lower concentrations. Freezing in liquid nitrogen and storage at -60 degrees exerted little effect on the fluoride-stimulated enzyme but lowered hormone stimulated activity. Preincubation in the presence of ACTH afforded a high degree of stabilization of the enzyme system while preincubation with a biologically inactive analog afforded no protection.
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PMID:Adenylate cyclase system of bovine adrenal plasma membranes. 16 47

Control of aldosterone responsiveness in terminal renal failure. Plasma aldosterone concentration in 30 hemodialysis patients correlated closely with renin concentration, renin activity or renin and potassium concentrations combined (r is greater than or equal to 0.62; P is less than 0.01), and increased consistently in response to upright posture or corticotropin administration. Aldosterone response to hemodialysis was variable. Significant correlations (r is greater than or equal to 0.65; P is less than 0.01) were demonstrated between postural plasma aldosterone and renin responses, between aldosterone responses to corticotropin and basal plasma aldosterone or renin and potassium values, between hemodialysis-induced changes in plasma aldosterone and those in potassium or renin; but not between various indexes of heparin treatment and aldosterone activity. Bilateral nephrectomy reduced basal plasma renin and aldosterone concentrations and aldosterone responsiveness in five preoperatively normoreninemic or hyperreninemic patients, but not in a hyporeninemic patient. These results demonstrate the complementary roles of circulating renin and potassium in the control of aldosterone release under basal and stimulatory conditions in patients with terminal renal failure. Administration of heparin in dosages used during long-term hemodialysis does not appear to significantly interfere with aldosterone control.
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PMID:Control of aldosterone responsiveness in terminal renal failure. 16 31

A 61 year old woman presented with profound hyponatremia and markedly low serum osmolality. Urine osmolality was greater than the serum osmolality, an abnormality that was corrected by water restriction, suggesting inappropriate ADH secretion. Although there were no physical signs of Cushing's syndrome, her serum potassium level was low and markedly elevated levels of plasma and urine corticosteroids were not altered by the administration of large amounts of dexamethasone, suggesting the ectopic ACTH-MSH syndrome. Plasma levels of immunoreactive ACTH and beta-MSH were elevated. At autopsy, a metastastic oat cell carcinoma of the lung, not detected antemortem by chest roentgenograms and bronchoscopy, was found. Immunoreactive ADH, ACTH and beta-MSH were detected in the primary tumor and in metastases to the liver. beta-MSH was also detected in the spleen, in which metastases were observed. This is the first documented case of the simultaneous production of ADH, ACTH and beta-MSH by neoplastic tissue associated with clinical manifestations of the syndrome of inappropriate ADH secretion and the ectopic ACTH-MSH syndrome.
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PMID:Ectopic production of antidiuretic hormone (adh), adrenocorticotrophic hormone (ACTH) and beta-melanocyte stimulating hormone (beta-MSH) by an oat cell carcinoma of the lung. 18 5

Adrenal steroid secretion rates and the renin-angiotensin-aldosterone (RAA) system were studied in the normothermic marmot. Adrenal secretion by the anesthetized, laparotomized marmot was (mean +/- SEM); aldosterone 1.2 +/- 0.3 ng/min, deoxycorticosterone 16.7 +/- 11.5 ng/min, corticosterone 15.2 +/- 7.8 ng/min, and cortisol 554 +/- 108 ng/min. Four forcings were investigated that affect feedback control at different sites: adrenocorticotropic hormone (ACTH) and angiotensin II (AII) infusion, sodium (Na) depletion, and Na loading. Plasma aldosterone, cortisol, Na, and potassium (K) concentrations as well as plasma renin activity (PRA) hematocrit (Hct), and in some studies, blood pressure were measured. ACTH infusion increased the plasma concentrations of aldosterone and cortisol. AII infusion increased aldosterone concentration, blood pressure, and Hct. Na depletion increased aldosterone, Hct, and PRA; plasma Na and K were decreased. Aldosterone concentration, Hct, and PRA decreased after salt loading. Normothermic, salt-depleted marmots demonstrated a pronounced fall in blood pressure following infusion of the AII analog, 1-sarcosine-8-alanine AII. The average plasma values for aldosterone, PRA, and cortisol found in 44 control animals were: aldosterone 3.8 +/- 0.3 ng/100 ml, PRA 1.9 +/- 0.2 ng AI-ml-1-h-1, and cortisol 54 +/- 4 ng/ml. It was concluded that normothermic marmots have a RAA system comparable to other mammalian species.
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PMID:Renin-angiotensin-aldosterone system of the normothermic marmot. 19 79

Rat adrenal glomerulosa and fasciculata-reticularis cell sensitivity to comparable molar doses of angiotensin II (AII) (2.4 X 10(-12) to 2.4 X 10(-4) M) and ACTH (alpha-1-24-adrenocorticotropin) (3.5 X 10(-13) to 3.5 X 10(-8) M) as well as small increments in potassium (K+) (3.7 to 13 meq/liter) was investigated. Glomerulose cells responded to physiological levels of AII (2.4 X 10(-10) M) and alpha-1-24-ACTH (3.5 X 10(-12) M), whereas an increment of as little 0.3 meq/liter in medium K+ also significantly increased aldosterone production. Of the three stimuli, alpha-1-24-ACTH caused the greatest aldosterone rise (11 times control). Fasciculata-reticularis cells responded only to alpha-1-24-ACTH. Whereas the threshold sensitivity was no lower than with glomerulosa cells, the maximum response was significantly greater (63 times control). These findings are consistent with findings documented in vivo in man, suggesting that the control of aldosterone secretion is similar in these two species.
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PMID:Rat adrenal cell sensitivity to angiotensin II, alpha-1-24-ACTH, and potassium: a comparative study. 20 Jan 47

Effect of methionine-, leucine-enkephalin (met-, leu-enkephalin) and substance P on the transmission in mouse vas deferens was studied. Both met- and leu-enkephalin inhibited electrically induced contraction of vas deferens at 10(-8)-10(7) M, met-enkephalin being 1.4 times more active than leu-enkephalin. Nalorphine (10(-6) M) antagonized these effects. Substance P (10(-9)-10(-7) M) had no effect on the contraction. Met- and leu-enkephalin (10(-7)-10(-5) M) decreased the high potassium induced [3H]-norepinephrine release from vas deferens, while substance P (10(-6) M) significantly increased it. Nalorphine (10(-5) M) reversed the inhibitory effect of met-enkephalin. These results indicate that these peptides modify the transmission of sympathetic nerve in mouse vas deferens.
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PMID:Effect of enkephalin and substance P on sympathetic nerve transmission in mouse vas deferens. 20 50

The interaction of beta-endorphin with opiate receptors was studied by using the radioiodinated, metabolically stable D-Ala2 derivative of human beta-endorphin. This analog binds specifically to rat brain membrane preparations with an apparent Kd of about 2.5 x 10-9 M. The ability of various enkephalin analogs, as well as opiate agonists and antagonists, to inhibit the binding of beta-endorphin clearly demonstrates that this peptide can bind to opiate receptors. However, the effects of various cations on the binding of 125I-[D-Ala2]beta-endorphin are markedly different from those found for enkephalin binding. Sodium ion at physiological concentrations decreases substantially the binding of enkephalins but only slightly decreases endorphin binding, whereas manganese enhances enkephalin binding but has no effect on endorphin binding. Moreover, potassium (100 mM) decreases the binding of beta-endorphin but does not affect enkephalin binding. These results suggest that beta-endorphin and enkephalin bind differently to the same receptor or bind to different receptors with overlapping specificity.
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PMID:Interaction of iodinated human [D-Ala2]beta-endorphin with opitate receptors. 21 69

The role of cyclic AMP in the regulation of aldosterone production by adrenocorticotropic hormone (ACTH), angiotensin II (A II), potassium, and serotonin was examined in collagenase-dispersed adrenal glomerulosa cells. The ability of 8-bromo cyclic AMP and choleragen to stimulate maximum aldosterone production indicated that cyclic AMP could act as second messenger for certain of the aldosterone-stimulating factors. The actions of ACTH and choleragen on aldosterone and cyclic AMP production were correlated in dog and rat cells, and a similar relation was seen during stimulation of rat cells by serotonin. In contrast, A II and potassium did not cause changes in cyclic AMP formation while stimulating aldosterone production. Intracellular and receptor-bound cyclic AMP were increased 3-fold by 10(-7) M ACTH but not by A II. Addition of a phosphodiesterase inhibitor increased the magnitude of the cyclic AMP response to ACTH but did not change the lack of stimulation by A II or potassium. In dog cells, the effects of A II and potassium on aldosterone production were partially additive to those of ACTH, choleragen, and 8-bromo cyclic AMP. In contrast, no additivity was observed between A II and potassium, or between combinations of the cyclic AMP-dependent stimuli. These results indicate that the actions of ACTH on aldosterone secretion are mediated by cyclic AMP formation, whereas A II and potassium stimulate aldosterone production through an independent mechanism. The lack of additivity between steroid responses to A II and potassium suggests that these factors could share a common mode of action on steroidogenesis in zona glomerulosa cells.
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PMID:The role of cyclic AMP in aldosterone production by isolated zona glomerulosa cells. 22 59

The plasma concentration of hydrocortisone was determined in mares given either cosyntropin (100 IU, given IV) or corticotropin (200 IU, given IM). Plasma hydrocortisone concentrations of the mares treated with cosyntropin increased by 46%, 57% and 80% at 30, 60, and 120 minutes, respectively, when compared with base-line values; these values returned to base line at 240 minutes. In mares treated with corticotropin, mean plasma hydrocortisone concentrations increased by 42%, 143%, 101% and 155% at 30, 60, 120, and 240 minutes, respectively, when compared with base-line values. Differences in total leukocyte count, total eosinophil count, and plasma concentrations of electrolytes (calcium, sodium, magnesium, potassium) of cosyntropin- and corticotropin-treated mares, and these values in control animals were not significant. Results of the present study indicated that the horse responds to small dosages of cosyntropin (IV) in a prompt and reproducible manner as determined by plasma hydrocortisone values. Response to corticotropin was slow and less consistent. Thus, administration of cosyntropin to the horse, according to test results with paired samples collected (before administration and again at 2 hours after injection), was found to be a prompt and meaningful test of adrenal gland function.
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PMID:Adrenal gland function in the horse: effects of cosyntropin (synthetic) and corticotropin (natural) stimulation. 22 37


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