Interactions between the effects of endothelin-1, clonidine and yohimbine on electrically-induced contractions in rat vas deferens

Mutafova‐Yambolieva, Violeta N.; Petkov, O; Staneva-Stoytcheva, D; Lasova, L.

doi:10.1016/0306-3623(92)90123-2

Cited by 8 publications

(2 citation statements)

References 43 publications

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“…Besides their potent direct vasoconstrictor actions endothelin peptides may exert indirect control of vascular tone via modulation of sympathetic neurotransmission. Indeed, shortly after its identification, endothelin was shown to potentiate nerve‐induced contractions in a number of vascular and non‐vascular tissues (Hiley et al , 1989; Maggi et al , 1989; Tabuchi et al , 1989a; Wiklund et al , 1989; Mutafova‐Yambolieva et al , 1992). Furthermore, ET‐1 has been shown to reduce [ 3 H]‐noradrenaline ([ 3 H]‐NA) release in some sympathetically innervated tissues such as the rat mesenteric artery (Tabuchi et al , 1989b), guinea‐pig femoral artery, pulmonary artery and vas deferens (Wiklund et al , 1988; 1989; 1990).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory and facilitatory presynaptic effects of endothelin on sympathetic cotransmission in the rat isolated tail artery

Mutafova‐Yambolieva

Westfall

1998

British J Pharmacology

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1 The present study was undertaken to determine the modulatory eects of the endothelin peptides on the neurogenically-induced release of endogenous noradrenaline (NA) and the cotransmitter adenosine 5'-triphosphate (ATP) from the sympathetic nerves of endothelium-free segments of the rat isolated tail artery. The electrical ®eld stimulation (EFS, 8 Hz, 0.5 ms, 3 min) evoked over¯ow of NA and ATP, in the absence of endothelins, was 0.035+0.002 pmol mg 71 tissue and 0.026+0.002 pmol mg 71 tissue, respectively. 2 Endothelin-1 (ET-1; 1 ± 30 nM) signi®cantly reduced the EFS evoked over¯ow of both NA and ATP. The maximum inhibitory eect was produced by a peptide concentration of 10 nM, the amount of NA over¯ow being 0.020+0.002 pmol mg 71 and that of ATP over¯ow 0.015+0.001 pmol mg 71. Higher peptide concentrations (100 and 300 nM) reversed the EFS-evoked over¯ow of NA to control levels and that of ATP to above control levels. The inhibitory eect of ET-1 (10 nM) was resistant to the selective ET A receptor antagonist cyclo-D-Trp-D-Asp(ONa)-Pro-D-Val-Leu (BQ-123) but was prevented by ET B receptor desensitization with sarafotoxin S6c (StxS6c) or by ET B receptor blockade with N, cis-2,6-dimethylpiperidinocarbonyl-L-gmethylleucyl-D-1-methoxycarbonyltryptophanyl-D-norleucine (BQ-788). 3 StxS6c, upon acute application, exerted a dual eect on transmitter release. At concentrations of 0.001 ± 0.3 nM the peptide signi®cantly reduced the EFS-evoked NA over¯ow, whereas at concentrations of 1 ± 10 nM it caused a signi®cant increase in the evoked over¯ow of both ATP and NA. Both the maximum inhibitory eect of StxS6c at a concentration of 0.003 nM (approximately 85% reduction of NA over¯ow and 40% of ATP over¯ow) and the maximum facilitatory eect of the peptide at a concentration of 3 nM (approximately 400% increase of ATP over¯ow and 200% of NA over¯ow) were completely antagonized by either BQ-788 or by StxS6c-induced ET B receptor desensitization. 4 ET-3 (10 ± 100 nM) did not aect the EFS evoked over¯ow of either ATP or NA, but at a concentration of 300 nM signi®cantly potentiated the release of both transmitters (0.118+ 0.02 pmol mg 71 tissue ATP over¯ow and 0.077+0.004 pmol mg 71 NA over¯ow). This eect was prevented either by BQ-123 or by BQ-788. 5 In summary, the endothelin peptides exerted both facilitatory and inhibitory eects on the neurogenically-induced release of the sympathetic cotransmitters ATP and NA in the rat tail artery. Both transmitters were modulated in parallel indicating that the endothelins do not dierentially modulate the release of NA and ATP in this tissue.

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Section: Introductionmentioning

confidence: 99%

Inhibitory and facilitatory presynaptic effects of endothelin on sympathetic cotransmission in the rat isolated tail artery

Mutafova‐Yambolieva

Westfall

1998

British J Pharmacology

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“…The involvement of ET, imidazoline and/or adrenergic receptors in the enhancement of morphine and oxycodone analgesia has not been studied. An interaction between clonidine and ET-1 in the cardiovascular effects involving the sympathetic nervous system has also been reported [23,[36][37][38] . ET-1 has also been found to potentiate hypotension produced by clonidine [39] .…”

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confidence: 99%

Determination of Adrenergic and Imidazoline Receptor Involvement in Augmentation of Morphine and Oxycodone Analgesia by Clonidine and BMS182874

Gulati

Bhalla²,

Matwyshyn³

et al. 2008

Pharmacology

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Background: Numerous agents have been demonstrated to potentiate morphine analgesia, including clonidine (α₂-adrenergic and I₁-imidazoline receptor agonist) and BMS182874 (endothelin-A, ET_A, receptor antagonist). ET has been shown to affect pharmacological actions of clonidine. The present study was conducted to determine whether α₂-adrenergic and/or I₁-imidazoline receptors are involved in the augmentation of morphine and oxycodone analgesia by clonidine and BMS182874. Methods: Analgesic tail flick latencies were measured in rats at various time intervals, and were converted to AUC₀→_{360 min}. Results: It was found that clonidine produced mild analgesia, while BMS182874 did not have any analgesic effect. Clonidine (p = 0.015) and BMS182874 (p = 0.009) enhanced the analgesic action of morphine and oxycodone. Clonidine- or BMS182874-induced increases in the analgesic effect of morphine were not inhibited by idazoxan (I₁-imidazoline receptor antagonist), while increases in the analgesic effect of oxycodone were blocked by idazoxan. Yohimbine (α₂-adrenergic receptor antagonist) blocked the clonidine-induced potentiation of analgesic effect of morphine (p = 0.036) and oxycodone (p = 0.0167), while yohimbine did not affect BMS182874-induced potentiation of the analgesic effect of morphine or oxycodone. Conclusions: This is the first report showing that clonidine and BMS182874 augment oxycodone analgesia. Results suggest that α₂-adrenergic receptors are involved in clonidine-induced, but not in the BMS182874-induced, potentiation of the analgesic effects of morphine or oxycodone, and that I₁-imidazoline receptors are involved in the potentiation of oxycodone analgesia, but not morphine analgesia, by clonidine and BMS182874.

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Effects and mechanisms of action of endothelins on non-vascular smooth muscle of the respiratory, gastrointestinal and urogenital tracts

Rae

Calixto

D’Orléans-Juste

1995

Regulatory Peptides

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Interactions between the effects of endothelin-1, clonidine and yohimbine on electrically-induced contractions in rat vas deferens

Cited by 8 publications

References 43 publications

Inhibitory and facilitatory presynaptic effects of endothelin on sympathetic cotransmission in the rat isolated tail artery

Inhibitory and facilitatory presynaptic effects of endothelin on sympathetic cotransmission in the rat isolated tail artery

Determination of Adrenergic and Imidazoline Receptor Involvement in Augmentation of Morphine and Oxycodone Analgesia by Clonidine and BMS182874

Effects and mechanisms of action of endothelins on non-vascular smooth muscle of the respiratory, gastrointestinal and urogenital tracts

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