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)

In a double-blind crossover study of 10 normal healthy subjects, we examined the effects of slow-release nifedipine (nifedipine-SR, 10 mg b.i.d) administration on exercise capacity, hormone levels during exercise, and quality of life (QOL) after a 2-week treatment. Two exercise tests, a progressive exercise test and a constant work-rate exercise test, were performed. Maximal oxygen uptake (VO2max) and blood lactate concentration were measured during the progressive exercise test and the exercise intensity corresponding to half lactate threshold (LT), LT, and 4 mmol/l of lactate concentration was determined. Subjects underwent 20 minutes of constant work-rate exercise at each work load, and blood lactate, plasma epinephrine, plasma norepinephrine, plasma renin activity, plasma aldosterone, atrial natriuretic peptide, plasma beta-endorphin, and met-enkephalin were measured. Taking nifedipine-SR had no effect on the responses of blood pressure, heart rate, VO2max, maximal work load, and LT compared to taking placebo. Blood lactate, plasma catecholamine, plasma renin activity, aldosterone, atrial natriuretic peptide, and beta-endorphin levels increased during exercise, and there was no difference between nifedipine-SR and placebo. Met-enkephalin did not increase with either treatment. In the QOL questionnaires, no differences were noted between the two treatments. These findings suggest nifedipine-SR to be a potentially useful drug in view of the lack of effect on exercise capacity, hormone release, and QOL.
Cardiovasc Drugs Ther 1992 Feb
PMID:Administration of slow-release nifedipine does not affect lactate threshold, hormone release during exercise, and quality of life in normal subjects. 157 99

Calcium plays an important role in endocrine reactions such as hormone biosynthesis, release, secretion, and action on target organs. The aim of this study was to evaluate the effects of a new long-lasting calcium-channel blocker, lacidipine, on basal and stimulated anterior pituitary hormone secretion. In a single-blind crossover study comparing lacidipine 4 mg p.o. once daily with placebo, variations in plasma levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), thyroid-stimulating hormone (TSH), and adrenocorticotropic hormone (ACTH) were evaluated in 10 hypertensive patients. Basal or stimulated anterior pituitary hormone secretion was similar after lacidipine and placebo. Lacidipine treatment significantly reduced blood pressure. It can thus be concluded that lacidipine is an effective calcium antagonist that has no effect on pituitary function.
J Cardiovasc Pharmacol 1991
PMID:Effect of lacidipine on pituitary function in essential hypertension. 172 47

To elucidate the mechanism of clonidine's effect on hormone release, serum growth hormone (GH), luteinizing hormone (LH), cortisol, and plasma beta-endorphin concentrations were determined after clonidine, naloxone, or the combined therapy of clonidine plus naloxone in six healthy women investigated in the luteal phase of their menstrual cycles. The clonidine injection increased GH levels. Naloxone (0.05, 0.1, and 0.2 mg/kg) decreased serum GH concentrations. Naloxone also increased serum LH, whereas clonidine decreased LH levels. Only the maximal dose of naloxone significantly increased serum cortisol concentrations. Clonidine had opposite effects on cortisol levels. These results demonstrate that combined therapy with clonidine plus naloxone leads to inhibition of the response of GH, LH, and cortisol to clonidine injection.
Cardiovasc Drugs Ther 1990 Aug
PMID:The effect of clonidine on hormone release mediated through activation of opiate receptors. 196 78

Pressor (VLPA) and depressor (VLDA) areas of the ventrolateral medulla were identified by microinjections of L-glutamate in urethane-anesthetized rats. Cardiovascular effects of opiate agonists microinjected into the same sites were then studied. Agents used to stimulate mu, delta, sigma, kappa, and beta-endorphin (epsilon) receptors were morphiceptin, D-Ala2-D-Leu5-enkephalin, N-allyl-normetazocine, dynorphin, and beta-endorphin, respectively. Opiate receptor stimulation in VLPA decreased blood pressure (BP) and heart rate (HR), while in VLDA it increased BP and HR. Thus, it is the site of injection rather than the type of opiate receptor that determines cardiovascular responses. Naloxone, an opiate antagonist, reversed and prevented these responses. Abolition of cardiovascular responses by spinal transection at the C1 level indicated that the sympathetic nervous system mediated these responses. The following mechanism is proposed for these actions of opiates: Cell bodies in VLPA, but not in VLDA, project to the intermediolateral cell column of the spinal cord. Opiates inhibit VLPA and lower BP and HR by decreasing sympathetic outflow. Opiate-induced inhibition of VLDA, which has an inhibitory effect on VLPA, results in an increase in BP and HR.
J Cardiovasc Pharmacol
PMID:Cardiovascular responses to medullary microinjections of opiate agonists in urethane-anesthetized rats. 242 96

Opioid peptides are thought to be involved in blood pressure regulation, possibly via an interaction with the sympathetic nervous system (CNS). To further elucidate this hypothesis the plasma concentrations of beta-endorphin, leucine-enkephalin and noradrenaline were determined overnight (9 p.m. to 8 a.m.) in young patients with mild essential hypertension and then compared to normotensive controls. The mean concentrations of beta-endorphin during the early night (9 p.m. to 2 a.m.) and leucine-enkephalin were lower (p less than 0.05, p less than 0.01, respectively) than in the normotensive subjects, but the noradrenaline concentration was higher. After 14 days of treatment with clonidine, which decreases sympathetic activity via a central action, beta-endorphin, leucine-enkephalin, and noradrenaline concentrations did not differ between both groups. It is concluded that the lower plasma concentrations of beta-endorphin and leucine-enkephalin in the hypertensive group could reflect reduced opioidergic activity in the CNS and in the peripheral sympathetic neurons and also could be involved in the increased sympathetic activity of these patients. Besides via sympathetic inhibition, clonidine also may reduce the increased blood pressure further by normalizing central beta-endorphin release.
J Cardiovasc Pharmacol 1987
PMID:Normalization of blood pressure and plasma concentrations of beta-endorphin and leucine-enkephalin in patients with primary hypertension after treatment with clonidine. 245 69

The purpose of this study was to evaluate the effect of clonidine--an alpha 2-adrenergic agonist--and naloxone--an opiate antagonist--on pituitary hormone release. The study involved 43 women: 20 menopausal women, 9 untreated women with ACTH-dependent Cushing's disease, and 14 healthy women. Serum GH, ACTH, LH, FSH, TSH, cortisol, and plasma beta-endorphin concentrations were measured with RIA methods. A significant increase in GH and a significant decrease in ACTH and in cortisol was observed after clonidine injection in healthy women. Clonidine caused a significant decrease in LH concentration in the luteal phase of the menstrual cycle. However, naloxone induced the opposite effect on pituitary hormone release. In Cushing's disease, ACTH significantly decreased in response to clonidine. In postmenopausal women with hypertension a decrease in blood pressure, a marked decrease in the number of hot flashes, as well as a diminution in amplitude and frequency of LH pulsatility was found. Conclusions are as follows: (1) Clonidine may be useful in the treatment of hypertensive menopausal women; and (2) a diminution in ACTH, beta-endorphin, and cortisol release in response to clonidine was observed in Cushing's disease.
J Cardiovasc Pharmacol 1987
PMID:The effect of clonidine on pituitary hormone secretion in physiological and pathological states. 245 86

We investigated the possibility that angiotensin II (ANGII) augments the sensitivity of the pituitary to corticotropin releasing factor (CRF) by comparing, in patients with essential hypertension, the responses of plasma adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin activity to a bolus injection of either 0.5 or 1.0 microgram/kg of synthetic ovine CRF in control conditions and after chronic treatment with the converting enzyme inhibitor captopril to block the formation of ANGII; the effects of CRF were examined up to 4 h after its administration. In control studies, we found that the two doses of CRF induced similar increments in ACTH and cortisol, the levels of which remained elevated throughout the studies; these changes were associated with increments in plasma aldosterone that were dose dependent, less pronounced, and of shorter duration and with a slight decrease in plasma renin activity. Captopril treatment increased basal plasma renin activity and lowered plasma aldosterone while leaving basal ACTH and cortisol unchanged. During converting enzyme inhibition, the responses of ACTH and cortisol to CRF were similar to those observed in control studies, whereas the changes in plasma aldosterone and plasma renin activity were, respectively, smaller and greater. From these results, it appears that during ANGII blockade the sensitivity of ACTH to CRF stimulation is unaffected, whereas that of the adrenals to ACTH is selectively reduced at the level of the zona glomerulosa.
J Cardiovasc Pharmacol 1987
PMID:Effects of angiotensin II blockade on the responses of the pituitary-adrenal axis to corticotropin-releasing factor in humans. 248 58

Various opioids were used to investigate the role they might play in the cardiovascular responses to fatiguing isometric contractions. Changes in blood pressure were measured in cats anaesthetised with alpha-chloralose. Fatiguing isometric contractions of the hind limb muscles (ergoreceptor activation) were generated using a microprocessor controlled stimulator (50 Hz, 0.2 ms, 200-800 mV). Baroreceptor inactivation was elicited by carotid artery occlusion. Muscle contraction caused an increase in mean arterial pressure of 51 (SEM 12) mm Hg and carotid occlusion an increase of 56(9) mm Hg above resting levels in control conditions. Injection of dynorphin (0.5-5.0 micrograms.5 microliters-1) into the cerebral aqueduct just rostral to the 4th ventricle eliminated the pressor response to muscular contraction (mean arterial pressure at rest, 80-118 mm Hg: on fatigue, 72-129 mm Hg) but did not affect the pressor response to carotid occlusion in the same cats. Similarly, injections of met-enkephalin (1-100 micrograms.5 microliters-1) or beta-endorphin (10-100 micrograms.5 microliters-1) eliminated the ergoreceptor induced changes in mean arterial pressure during isometric contractions but had no effect on the changes caused by carotid occlusion. Pressor responses to nerve crush were not eliminated. These results support the suggestion that a catecholaminergic-opioidergic pathway in part mediates the cardiovascular responses to ergoreceptor afferent but probably not baroreceptor afferent input.
Cardiovasc Res 1989 Mar
PMID:Effects of opiates during baroreceptor and ergoreceptor induced changes in blood pressure. 257 74

Postoperative pain relief and stress hormones were examined during the use of continuous epidural infusion of morphine at a rate of 0.1 mg/hr in 30 patients (Group B) after coronary artery bypass grafting. This was compared to our routine method of postoperative analgesia of intravenous morphine 2 mg/2 hr and as needed in another 30 patients (Group A). Continuous epidural morphine infusion required occasional supplementation with intravenous morphine and achieved effective analgesia in 80% of the patients. Pain relief was adequate in 50% of the patients in Group A. The mean dose of morphine used in Group B during the first 3 postoperative days was 5 mg per patient per day and was significantly lower than that used in Group A (mean 18 mg per patient per day). Serum morphine was undetectable (below 2.5 ng/ml) in Group B and was significantly lower than that in Group A (17 ng/ml). Epidural analgesia was associated with adequate postoperative pulmonary and cardiovascular functions; nausea and vomiting occurred in two patients. Levels of postoperative stress, serum cortisol, and beta-endorphin were significantly lower in Group B than in Group A. This study shows that continuous epidural infusion of morphine at a rate of 0.1 mg/hr provides selective and effective pain relief and reduces postoperative stress after cardiac operations. This method of analgesia was also associated with minimal side effects and provides an alternate approach for treatment of pain after cardiac operations.
J Thorac Cardiovasc Surg 1987 Jun
PMID:Continuous epidural infusion of morphine for pain relief after cardiac operations. 295 42

This study deals with the effects of beta-endorphin on blood pressure, heart rate, and respiratory frequency in anesthetized and conscious rats after both peripheral and central administration. Intravenous injection of beta-endorphin (40 and 160 micrograms/kg) in urethane-anesthetized rats resulted in a prolonged decrease in blood pressure, which, after the higher dose, was accompanied by bradycardia. In the pentobarbitone-anesthetized animals the same doses of beta-endorphin caused a small rise in blood pressure without affecting heart rate. No effect on respiratory frequency was observed. In urethane-anesthetized rats with hemorrhagic shock intravenous naloxone elicited a small pressor effect. Intracerebroventricular injection (i.c.v.) of beta-endorphin (40 micrograms/rat) in urethane-anesthetized rats resulted in severe respiratory depression and death. With lower doses there was a decrease in all parameters studied without ensuing death. Respiratory depression was even more pronounced in pentobarbitone-anesthetized rats, occurring with much lower doses of the peptide than in the urethane-anesthetized animals. beta-endorphin in the dose of 0.6 micrograms/rat still reduced respiratory frequency as well as heart rate without affecting blood pressure. Naloxone pretreatment antagonized the respiratory depression and death, while the decrease in heart rate was diminished. In conscious rats 10 microgram/rat, i.c.v., of beta-endorphin resulted in a decrease in heart rate and blood pressure without affecting respiratory frequency. It is concluded that beta-endorphin, or related opioid peptides, may be involved in cardiovascular and respiratory regulation. The effects of beta-endorphin, however, are markedly modified by the anesthetic agent used.
J Cardiovasc Pharmacol
PMID:Cardiovascular and respiratory effects of beta-endorphin in anesthetized and conscious rats. 618 78


1 2 3 Next >>