Diurnal Rhythm of Beta Endorphin in Normotensive and Hypertensive Patients : The Effect of Clonidine1

Farsang, Csaba; Vajda, L; Kapocsi, J.; Malisák, Z.; Alföldi, Sándor; Varga, K; Juhász, I; Kunos, George

doi:10.1210/jcem-56-4-865

Cited by 44 publications

(9 citation statements)

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“…The observation that the alpha-2-adrenoceptor agonist clonidine had no inhibitory action on cortisol secretion in human subjects under similar conditions [25] is compatible with this interpreta tion. Small reduction of cortisol secretion [8,29) and lack of effect on beta-endorphin concentrations [19] have also been re ported following administration of clonidine in man.…”

Section: Discussionmentioning

confidence: 99%

The Role of Alpha-2-Adrenoceptors in the Control of ACTH Secretion; Interaction with the Opioid System

Al-Damluji

Bouloux²,

White³

et al. 1990

Neuroendocrinology

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This study examined the effects of an alpha-2-adrenoceptor antagonist on the secretion of ACTH basally and in response to the opioid antagonist naloxone, which is known to stimulate ACTH secretion by an adrenergic mechanism. Eight normal men were given, in double-blind, random order, intravenous infusions of normal saline (placebo), idazoxan (alpha-2-adrenoceptor antagonist), naloxone and the combination of idazoxan and naloxone. Naloxone increased plasma ACTH and cortisol concentrations in comparison to placebo. Idazoxan significantly enhanced the ACTH and cortisol responses to naloxone but had no effect on plasma ACTH or cortisol concentrations when given alone. These findings suggest that during some conditions of increased ACTH secretion, inhibitory alpha-2-adrenoceptors are activated and that these receptors limit the ACTH response. This provides an explanation for some of the apparent contradictions in interpreting the data from previous studies on the effects of catecholamines on the secretion of ACTH.

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Section: Discussionmentioning

confidence: 99%

The Role of Alpha-2-Adrenoceptors in the Control of ACTH Secretion; Interaction with the Opioid System

Al-Damluji

Bouloux²,

White³

et al. 1990

Neuroendocrinology

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“…In humans, the evidence is less compelling. Several studies have noted that hypertensives have higher levels of betaendorphins in the peripheral circulation (e.g., Farsang, Vajda, Kapocsi, Malisak, Alfoldi, Varga, Juhasz & Kunos, 1983;Guasti, Cattaneo, Daneri, Bianchi, Gaudio, Bonora Regazzi, Grandi, Bertolini, Restelli & Venco, 1996;Hughes, Ringer, Francom, Caswell, DeLoof & Spillers, 1991;McNeilly & Zeichner, 1989;Sheps et al, 1992). It has been proposed that a relative opioid insensitivity of paraventricular hypothalamic corticotrophin-releasing factor neurons may account for the phenomenon of hypertensive hypoalgesia in humans (see France & Ditto, 1996;France, 1999).…”

Section: Introductionmentioning

confidence: 99%

Effects of naltrexone on electrocutaneous pain in patients with hypertension compared to normotensive individuals

Ring

Al’Absi

Edwards

et al. 2008

Biological Psychology

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An opioid mechanism may help explain hypertensive hypoalgesia. A double-blind placebocontrolled design compared the effects of opioid blockade (naltrexone) and placebo on electrocutaneous pain threshold, pain tolerance, and retrospective McGill Pain Questionnaire ratings in 35 unmedicated patients with essential hypertension and 28 normotensive individuals. The hypertensives experienced less pain than normotensives during the assessment of their pain tolerance; however, this manifestation of hypertensive hypoalgesia was not moderated by naltrexone. These findings fail to support the hypothesis that essential hypertension is characterised by relative opioid insensitivity.

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“…As (4)(5)(6)(7)(8)(9) pmolI1) or in those without ascites (4-7 (4-6) pmolI1) (Figure). In the patients with renal failure, it was increased approximately 2-5 fold (12-4 (7-23) pmolIl, p<0OOO1) compared with the value in disease control subjects (4-9 (4-7) pmol/1) and healthy control subjects (4-9 (4-6) pmolI1) and correlated significantly (r=0-531, p<0OO5) with their high plasma concentration of creatinine (1045 (794-1117) iimol/ 1).…”

Section: Subjectsmentioning

confidence: 88%

Plasma beta endorphin in cirrhosis and renal failure.

Thornton

Losowsky

1991

Gut

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Whether the plasma concentration of ,B endorphin was increased in hepatic cirrhosis like that of smalier opioid peptides methionine enkephalin and leucine enkephalin was determined. Its concentration in chronic renal failure was also measured. Plasma , endorphin was not significantly raised in cirrhotic patients with or without ascites (medians 5.2 pmol/l and 4.7 pmol/l respectively) compared with disease control subjects (4.9 pmoVll) and healthy control subjects (4.9 pmol/l). In contrast, the peptide was increased 2.5 fold (p<0.001) in chronic renal failure (12.4 pmol/V) and was found in many of these patients' urine. The data are compatible with the hypothesis that the liver may play an important role in the elimination of opioid peptides of octapeptide size or less but not the larger peptides such as P endorphin.The plasma concentrations of the pentapeptides methionine enkephalin'2 and leucine enkephalin3 are increased in patients with liver disease. These findings are consistent with the hypothesis that the liver may play a major role in the elimination of blood borne opioid peptides of octapeptide size or less.' We investigated whether the plasma concentration of a much larger opioid peptide, P endorphin, is increased in patients with hepatic cirrhosis or chronic renal failure, or both. Methods SUBJECTSThe following groups of subjects were studied: (1) Fifteen patients with hepatic cirrhosis which was decompensated as judged by the presence of ascites. As assessed by Pugh's modification of Child's classification,4 six of these patients were grade C and nine grade B.(2) Fifteen patients with hepatic cirrhosis without ascites. All these patients were Pugh's grade A. (3) Fifteen patients with chronic renal failure, eight of whom were having haemodialysis and four peritoneal dialysis. (4) Fifteen disease controls who were hospital inpatients with a wide variety of illnesses (three congestive cardiac failure, three acute exacerbations of asthma, three acute on chronic pancreatitis, two untreated coeliac disease, two insulin dependent diabetes mellitus, one chronic intestinal pseudo-obstruction, and one pneumococcal pneumonia complicating bronchial carcinoma). (5) Fifteen healthy control subjects. As haemorrhage is a stimulus to (3 endorphin secretion,5 only subjects who had not bled within the previous 10 days and were haemodynamically stable were studied. SAMPLE COLLECTIONVenepuncture was performed with the subjects at rest -a heparinised cannula having been inserted 20 minutes earlier. Because of the diurnal variation in plasma ( endorphin6 all blood and urine samples were taken between 9 and 11 am. Venous blood and urine samples for ( endorphin measurement were collected into chilled containers, the bottles for the former being primed with ethylenediamine tetra-acetic acid. The samples were transferred immediately to a precooled centrifuge at 4°C, spun at 3000 rpm, and stored at -70°C. Blood was also obtained for measurement of plasma creatinine, bilirubin, and alanine aminotransferase by routine l...

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Diurnal Rhythm of Beta Endorphin in Normotensive and Hypertensive Patients : The Effect of Clonidine1

Cited by 44 publications

References 0 publications

The Role of Alpha-2-Adrenoceptors in the Control of ACTH Secretion; Interaction with the Opioid System

The Role of Alpha-2-Adrenoceptors in the Control of ACTH Secretion; Interaction with the Opioid System

Effects of naltrexone on electrocutaneous pain in patients with hypertension compared to normotensive individuals

Plasma beta endorphin in cirrhosis and renal failure.

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