Opioid peptides do not modulate atrial natriuretic peptide or aldosterone release under basal conditions in man

Borges, Flávio Notarnicola da Silva; Anderson, J. V.; Volta, C.; Perry, Les; Drury, Paul; Bloom, Stephen R.; Gm, Besser; Grossman, A.

doi:10.1677/joe.0.1160313

Cited by 6 publications

(3 citation statements)

References 20 publications

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“…While animal studies have clearly demonstrated opioid effects on ANF release, the published data from human subjects are controversial. Clinical investigations suggest that opioids have no influence on ANF release in human subjects under basal conditions (Kidd et al, 1987;Borges et al, 1988), although Ogutman et al (1990) found significant ANF release upon morphine administration. There is evidence of a f,-endorphin effect on ANF secretion.…”

Section: Renal Effects Of a U-opioid Agonist Discussionmentioning

confidence: 99%

Renal effects of TAPP, a highly selective μ‐opioid agonist

Gutkowska

Schiller

1996

British J Pharmacology

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The effect of i.v. administration of TAPP, a highly selective and exclusively peripherally‐acting μ‐opioid receptor agonist, on urine output, urinary sodium, potassium and cyclic GMP, and on plasma immunoreactive atrial natriuretic factor (IR‐ANF) levels was studied in conscious normally hydrated female rats (200–250 g). TAPP treatment produced a significant dose‐dependent increase of urine output and urinary sodium, potassium and cyclic GMP excretion during the first hour. The highest TAPP dose used (2.5 mg kg−1 body weight) elicited a 10 fold elevation of urine output from 0.23 ± 0.06 ml h−1 to 2.5 ± 0.3 ml h−1 (n = 18) accompanied by augmented sodium [from 17.0 ± 4.7 μEq h−1 to 79 ± 12.7 μEq h−1, n = 18 (P < 0.001)], potassium [from 9.5 ± 2.5 μEq h−1 to 39.4 ± 6.6 μEq h−1, n = 18 (P < 0.005)], and cyclic GMP excretion [from 191 ± 21 pmol h−1 to 1340 ± 322 pmol h−1, n = 18 (P < 0.001)]. Plasma IR‐ANF rose from 22 ± 4 pg ml−1 to 508 ± 22 pg ml−1 (n = 18) (P < 0.001) 5 min after administration of TAPP (2500 μg kg−1). TAPP lowered systemic blood pressure, also in a dose‐related manner, 1–5 min after injection. This decrease in blood pressure was transient and did not last more than 10 min. Pretreatment with the opioid antagonist naloxone (0.8 mg per rat) abolished the diuretic, natriuretic and kaliuretic effect of TAPP (250 μg kg−1): urine output dropped from 1.16 ± 0.15 ml h−1, n = 12, to the control value of 0.15 ± 0.06 ml h−1, n = 12 (P < 0.001), sodium excretion fell from 57.5 ± 11 μEq h−1, to 21.3 ± 8.5 μEq h−1, n = 12 (P < 0.001), and potassium excretion decreased from 45.4 ± 9.7 μEq h−1, n = 12, to 16.1 ± 7.0 μEq h−1, (P < 0.001). Pretreatment with anti‐ANF serum (0.4 ml) abolished the diuretic effect of TAPP: urine output diminished significantly from 1.93 ± 0.28 to 0.88 ± 0.29 ml h−1 (P < 0.01) (n = 6). The TAPP‐induced diuretic action, increased sodium/potassium excretion and elevated urinary cyclic GMP levels were also reversed by anti‐ANF antibodies. Since TAPP is totally unable to cross the blood‐brain barrier, the ensemble of these observations led to the conclusion that the diuretic, natriuretic, kaliuretic and hypotensive effects produced by this μ‐opioid agonist through interaction with peripheral μ‐opioid receptors occur via ANF release.

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Section: Renal Effects Of a U-opioid Agonist Discussionmentioning

confidence: 99%

Renal effects of TAPP, a highly selective μ‐opioid agonist

Gutkowska

Schiller

1996

British J Pharmacology

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“…Guanyl-DAMME is a related analogue which has more recently become available, and which we have demonstrated to have a similar neuro-endocrine profile to DAMME itself (Borges, Anderson, Volta, Perry, Drury, Bloom, Besser and Grossman 1988). We confirm here that guanyl-DAMME stimulates the release of PRL, demonstrating that an endocrinologically effective dose of the compound was administered, but found no evidence of any effect on the adrenocortical response to a physiological dose of synthetic ACTH1-24 Our earlier data showing inhibition of Cortisol release following guanyl-DAMME, but no change in aldosterone (Borges et al 1988), thus appears to indicate an action which is wholly above the level of the adrenal.…”

Section: Discussionmentioning

confidence: 91%

Lack of Modulation of the Adrenocortical Response to ACTH by an Opioid Peptide

Howlett¹,

Grossman²,

Froud³

et al. 1991

Horm Metab Res

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Eight normal male subjects received 1 mg dexamethasone at 23.00 h and 0.5 mg on wakening followed by a physiological intravenous dose of synthetic ACTH1-24 250 ng, with and without the administration of a stable met-enkephalin analogue (guanyl-DAMME, 100 micrograms) 10 minutes prior to the ACTH. The opioid analogue caused no change in the peak, incremental, or incremental area under the curve responses of plasma cortisol to the ACTH. This study does not support a role for opioid peptides in the acute modulation of the adreno-cortical response to ACTH.

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“…This peptide has a very short biological half-life, so most of the studies on the effects of Met-enkephalin on adrenocortical function in vivo have used a long-acting analogue of the peptide, DALA. Experiments using DALA in vivo have shown a stimu¬ latory effect on aldosterone secretion when administered to rats either acutely or chronically (Robba et al 1986a), although the use of a different Met-enkephalin analogue ([D-Ala2-N-Phe4,Met(0)-ol-5]-enkephalin) did not alter aldosterone secretion in human subjects (Borges et al 1988). Some earlier studies reported that DALA has no effect on basal aldosterone production by rat zona glom¬ erulosa cells in vitro (Guaza & Borrell 1984), although another analogue (FK 33 824) stimulated aldosterone secretion by calf adrenal glomerulosa cells (Bevilacqua et al 1982).…”

Section: Zona Glomerulosa Cellsmentioning

confidence: 99%

Action of opioid peptides on the rat adrenal cortex: stimulation of steroid secretion through a specific μ opioid receptor

Kapas

Purbrick²,

Hinson³

1995

Journal of Endocrinology

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While there have been several studies on the actions of opioid peptides on adrenocortical steroidogenesis, the results of these studies have failed to resolve the question as to whether these peptides exert a direct action on the adrenal cortex. The present studies were designed to address this question directly, using collagenase-dispersed rat zona glomerulosa and zonae fasciculata/reticularis cells incubated in vitro. The results obtained clearly show that the opioid peptides tested (beta-endorphin, Leu-enkephalin, Met-enkephalin, and its long-acting analogue, DALA) all exerted a significant stimulatory effect on aldosterone secretion by zona glomerulosa cells and all, except Leu-enkephalin, stimulated corticosterone secretion by inner zone cells. The response was shown to be inhibited by naloxone. There did not appear to be a significant interaction between the effects of ACTH and the opioid peptides on adrenocortical cells. Studies using specific agonists for opioid receptor subtypes (DAMGO, DPDPE and U-50488H, specific for mu, delta and kappa receptors respectively) showed that the effect of opioid peptides on the zona glomerulosa appeared to be mediated exclusively by mu receptors while the response of inner zone cells was mediated by both mu and, to a lesser extent, kappa receptors. Finally, studies on the second messenger systems activated by the opioid peptides and the receptor agonists showed that these peptides act to increase labelling of inositol trisphosphate, and strongly suggest that, in the rat adrenal cortex, both mu and kappa opioid receptors are linked to the activation of phospholipase C.

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Opioid peptides do not modulate atrial natriuretic peptide or aldosterone release under basal conditions in man

Cited by 6 publications

References 20 publications

Renal effects of TAPP, a highly selective μ‐opioid agonist

Renal effects of TAPP, a highly selective μ‐opioid agonist

Lack of Modulation of the Adrenocortical Response to ACTH by an Opioid Peptide

Action of opioid peptides on the rat adrenal cortex: stimulation of steroid secretion through a specific μ opioid receptor

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