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)

To determine the effect of hypothermic pulsatile and nonpulsatile cardiopulmonary bypass (CPB) with hemodilution on adrenocortical function we measured plasma levels of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin in two groups of patients. Group I, comprising 11 patients had routine CPB (nonpulsatile), and Group II, comprising 12 patients, had pulsatile flow during CPB (pulsatile). Both groups demonstrated comparable increases in cortisol, ACTH, and aldosterone with operation. Levels for all three hormones appeared to decline during CPB and then rose again in the post-CPB period. There were no significant differences between groups. Plasma renin activity gradually declined in a comparable manner in both groups. In the post-CPB period, renin activity was slightly higher in the nonpulsatile group (1.7 +/- 0.5 versus 0.8 +/- 0.2 ng/ml/hr, p less than 0.05). Correction for the effect of hemodilution demonstrated no decrease in cortisol and a slight increase in ACTH in both groups during CPB. Significant increases occurred in both groups during CPB in urinary Na+ excretion rate and urinary Na+/K+ ratio, more so for the nonpulsatile group. There was no correlation between urinary Na+/K+ ratios and either plasma cortisol or aldosterone levels. Thus routine CPB demonstrates no evidence of adrenocortical hypofunction and the addition of pulsatile flow produces little improvement.
J Thorac Cardiovasc Surg 1983 Jan
PMID:Adrenocortical hormone levels during cardiopulmonary bypass with and without pulsatile flow. 629 18

To identify factors that regulate the levels of immunoreactive digitalis-like substances (irEDLS) in body fluids, two studies were carried out. Plasma and urine levels of irEDLS were measured in uremic and normal subjects. Extracted material was fractionated (12 fractions) and assayed by digoxin radioimmunoassay. In four fractions, higher levels of irEDLS were found in uremic than in normal plasma. Urine from healthy subjects contained very high levels of irEDLS, but in urine collected from uremic patients irEDLS levels were similar to those in plasma. In another study, eight healthy subjects were given dexamethasone 1 mg orally and tetracosactide [an adrenocorticotropic hormone (ACTH) analogue] 0.25 mg i.v., on separate occasions. Dexamethasone suppressed the plasma and urine levels of cortisol and irEDLS. ACTH increased the levels of cortisol in plasma and urine, and of irEDLS in plasma. Taken together, these results support the hypothesis that irEDLS are of adrenal origin. However, decreased renal clearance, rather than increased production or release, may be the main cause of increased plasma levels of irEDLS in uremia.
J Cardiovasc Pharmacol 1993
PMID:Immunoreactive endogenous digoxin-like substances: plasma levels are dependent on the hypothalamic-pituitary-adrenal axis for release and on kidney function for elimination. 750 14

Proopiomelanocortin (POMC) is a protein that contains the amino acid sequences of numerous peptide hormones, including the melanocyte-stimulating hormones (MSH). MSH peptides of alpha, beta, and gamma primary structure are present in plasma, and all exhibit natriuretic activity. Intravenous infusion of alpha or beta-MSH leads to a time- and dose-dependent natriuresis, whereas gamma-MSH is reported to be natriuretic at low doses but antinatriuretic at high doses. The natriuretic activity of MSH peptides occurs without change in arterial pressure or renal hemodynamics, suggesting a possible direct tubular inhibition of sodium reabsorption. Intravenously infused gamma-MSH is associated with an increase in the plasma concentration of atrial natriuretic peptide. In addition, gamma-MSH also has a direct intrarenal natriuretic action that is dependent on the renal nerves. In rats, gamma-MSH-related peptides are involved in the reflex control of sodium excretion in situations such as the natriuresis that occurs (a) from the remaining kidney after acute unilateral nephrectomy, (b) from the contralateral kidney shortly after unilateral ureteral pressure elevation, and (c) after unilateral carotid artery traction. POMC-derived peptides (including MSH) are modulated in response to salt loading, and alterations in POMC metabolism and plasma peptide concentrations have been observed in genetically hypertensive rats and during the development of adrenal regeneration hypertension. In addition, plasma gamma-MSH levels are elevated in patients with severe congestive heart failure, and in primary hyperaldosteronism. These observations suggest a possible involvement of MSH-related peptides in sodium homeostasis as well as in certain forms of hypertension.
J Cardiovasc Pharmacol 1993
PMID:Natriuretic properties of melanocyte-stimulating hormones. 750 15

After intracerebroventricular (i.c.v.) administration of ACTH-(4-10) or gamma 2-MSH in doses of < or = 1,500 pmol, no changes were observed in mean arterial pressure (MAP) of conscious and urethane-anesthetized rats. When gamma 2-MSH was administered intracisternally (i.c.), a significant increase in MAP of approximately 15 mm Hg was observed after the two highest doses used (500 and 1,500 pmol) in conscious rats and also, though less pronounced, in urethane-anesthetized rats. Although the pressor effect of gamma 2-MSH after intravenous (i.v.) administration to conscious rats was maximal within 25 s and MAP had returned to preinjection values < or = 60 s, the pressor response after i.c. administration was slower in onset (maximal effect after 1-2 min) and of longer duration (return to preadministration values after 5 min). ACTH-(4-10) had a slight pressor effect after i.c. administration in doses of 1,500 and 2,500 pmol in conscious rats, but had no effect in urethane-anesthetized rats. These results indicate that sustained leakage of the peptides after i.c. administration, but not after i.c.v. administration, to the periphery is the causal factor of a modest pressor response. These results do not support the suggestion that the central nervous system (CNS) is the principal target of gamma-MSH-like peptides with respect to their pressor effect.
J Cardiovasc Pharmacol 1993 Jun
PMID:Effect of ACTH-(4-10) and gamma 2-MSH on blood pressure after intracerebroventricular and intracisternal administration. 768 15

We sought to enhance the sensitivity of selective bilateral blood sampling to determine adrenocorticotropin (ACTH) and prolactin levels in the inferior petrosal sinus (IPS) by administering two stimulatory agents--corticotropin-releasing factor (CRF) and thyrotropin-releasing hormone (TRH). We then determined the ACTH and prolactin levels in the IPS of 10 patients with Cushing's disease. After peripheral administration of both CRF and TRH, ACTH levels were significantly higher on the tumor side in all patients. The prolactin level was significantly higher on the tumor side when CRF or TRH was used to stimulate pituitary secretion. Postsurgical immunohistochemistry studies revealed production of both ACTH and prolactin in tumor cells, explaining the abnormal secretion pattern of the pituitary adenoma. The use of CRF and TRH may therefore improve the reliability of selective blood sampling and tests from the IPS in those cases of Cushing's disease for which noninvasive methods have otherwise failed to clarify the diagnosis.
Cardiovasc Intervent Radiol
PMID:Selective bilateral blood sampling from the inferior petrosal sinus in Cushing's disease: effects of corticotropin-releasing factor and thyrotropin-releasing hormone on pituitary secretion. 826 24

Adrenocorticotropic hormone (ACTH; 5 microg/kg/ day) infused into 10 pregnant ewes (gestation age, 127-139 days) for 72 h caused an increase in arterial pressure within 1-2 h (p < 0.05), which was sustained for the rest of the experiment. Cardiac output was increased at 24 h (p < 0.05). Total peripheral resistance did not change. There were no changes in four pregnant ewes infused with 0.15 M saline at the same rate for 72 h. In ACTH-treated pregnant ewes, a relation between arterial pressure and plasma renin activity observed in nontreated pregnant ewes (r = 0.71; p = 0.0005) was no longer evident. Compared with nonsurgical pregnant ewes, total angiotensin II (Ang II)-receptor density in the uterine artery was decreased in ewes that had previously had surgery (p = 0.015) and further reduced in ACTH-treated ewes (p < 0.0005). This was due to a reduction in the AT2-receptor density, which was inversely related to plasma cortisol levels (r = 0.73; p < 0.03). AT1-receptor density and the affinities of the AT1 and AT2 receptors were unchanged. The correlation between plasma cortisol and AT2-receptor density in uterine blood vessels may partly explain why these receptors are downregulated after surgery.
J Cardiovasc Pharmacol 1999 Dec
PMID:Effects of ACTH-induced hypertension in the pregnant ewe. 1059 25

BACKGROUND: Atorvastatin calcium (Lipitor) is a new 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor. The present study was conducted to examine the effect of pronounced cholesterol lowering on adrenal function in patients with severe hypercholesterolemia. METHODS AND RESULTS: Adrenal function was examined under basal conditions and following adrenal corticotropin hormone stimulation in 40 patients (36 with heterogeneous familial and 4 with polygenic hypercholesterolemia). The study was part of a larger study comparing the efficacy and safety of atorvastatin, colestipol, atorvastatin + colestipol, and simvastatin + colestipol treatment over a 1-year period. Maximum doses of all agents were studied: 80 mg atorvastatin once daily, 40 mg simvastatin once daily, and 20 g/day colestipol. At the end of the 1-year treatment period, reductions in low-density lipoprotein cholesterol were 57%, 54%, and 49% for the atorvastatin, colestipol + atorvastatin, and colestipol + simvastatin groups, respectively. No clinically significant changes in basal serum cortisol levels were seen in any treatment group during the 1-year treatment period. Mean serum cortisol concentrations and area under the curve for cortisol concentration versus time data following adrenal corticotropin hormone stimulation were not clinically different during treatment compared with values obtained at baseline for any of the treatment groups. CONCLUSIONS: Treatment with maximum doses of atorvastatin for 1-year did not have any adverse effects on adrenal function under basal conditions or during maximum stimulation. Similarly, colestipol therapy alone and in combination with either atorvastatin or simvastatin did not appear to affect adrenal function.
J Cardiovasc Pharmacol Ther 1997 Oct
PMID:Atorvastatin, a New HMG-CoA Reductase Inhibitor, Does Not Affect Glucocorticoid Hormones in Patients With Hypercholesterolemia. 1068 65

A novel subtype of corticotropin-releasing hormone (CRH) receptor, designated type-2 CRH receptor (CRHR-2), has been cloned by a number of laboratories, and its mRNA has been found to be distributed not only in the brain but in peripheral tissues such as heart and skeletal muscle. To date, however, the regulation of CRHR-2 mRNA is poorly understood. Therefore, we examined the effect of glucocorticoid treatment, adrenalectomy, and systemic administration of urocortin, a possible endogenous ligand for CRHR-2, on heart CRHR-2 mRNA levels in male Wistar rats, using in situ hybridization histochemistry. CRHR-2 mRNA in the heart was significantly decreased 9 h after systemic administration of urocortin (5 microg/kg b.w.). Systemic administration of corticosterone (CORT; 10 mg/rat/day for 12 days) or CORT pellet (200 mg) implant for 7 and 14 days also decreased CRHR-2 mRNA in the heart, whereas it was unchanged 7 days after adrenalectomy. Thus, similar regulation of CRHR-2 mRNA in the rat heart by its ligand and glucocorticoids was observed. The precise mechanism of the regulation of CRHR-2 mRNA in the heart and the physiologic significance of cardiac CRHR-2 remains to be elucidated.
J Cardiovasc Pharmacol 2000 Oct
PMID:Regulation of type-2 corticotropin-releasing hormone receptor mRNA in rat heart by glucocorticoids and urocortin. 1102 51

Recent studies have suggested an involvement of the endogenous opioid system in blood pressure control. The purpose of the present study was to determine the role of beta-endorphin in the regulation of sympathetic nervous activity in the central nervous system of hypertension. The effects of beta-endorphin on the electrically evoked release of [3H]norepinephrine (NE) were investigated in superfused slices of rat medulla oblongata. Beta-endorphin inhibited the stimulation-evoked NE release in a dose-dependent manner in rat medulla oblongata. In the medulla oblongata of spontaneously hypertensive rats (SHR), the inhibitory effect of beta-endorphin on the stimulation-evoked NE release was significantly smaller than in the medulla oblongata of Wistar-Kyoto rats. These results showed that beta-endorphin might reduce NE release in rat medulla oblongata. Furthermore, the lesser inhibitory effect of beta-endorphin on NE release in SHR might suggest that the opioid peptide could be involved in the regulation of central sympathetic nervous activity in hypertension.
J Cardiovasc Pharmacol 2000
PMID:Effects of beta-endorphin on norepinephrine release in hypertension. 1120 24

Since its discovery 2 decades ago, potent effects of corticotropin-releasing hormone (CRH) on the heart and vasculature have been consistently observed. The recent discoveries of novel CRH-related peptides residing in the heart and a distinct cardiac CRH receptor (CRH-R2), have renewed interest in the role of the CRH family on cardiovascular function. This review highlights the emerging view of a peripheral, cardiac CRH system and its potential relevance in mediating the adaptive response of the heart to stress.
Trends Cardiovasc Med 2002 May
PMID:Corticotropin-releasing hormone-related peptides and receptors: emergent regulators of cardiovascular adaptations to stress. 1206 58


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