D-myo-inositol 1,2,6-trisphosphate blocks neuropeptide Y-induced facilitation of noradrenaline-evoked vasoconstriction of the mesenteric bed.
Eur J Pharmacol
; 240(1): 93-7, 1993 Aug 10.
Article
in En
| MEDLINE
| ID: mdl-8405129
ABSTRACT
Perfusion of the rat mesenteric bed with 0.1 or 10 nM neuropeptide Y potentiated the noradrenaline-induced increase in mesenteric pressure; the peptide did not modify basal perfusion pressure. While perfusion with 0.1 nM neuropeptide Y significantly increased the maximal noradrenaline-evoked vasoconstriction without modifying its EC50, 10 nM neuropeptide Y potentiated the maximal noradrenaline effect and significantly shifted its concentration-response curve to the left. Perfusion with 1-10 microM D-myo-inositol 1,2,6-trisphosphate (alpha-trinositol) reduced, in a concentration-dependent fashion, the neuropeptide Y-induced potentiation of the noradrenaline-evoked vasoconstriction without altering the potency or maximal response evoked by the catecholamine alone. Perfusion with 0.1 nM neuropeptide Y plus 1 microM alpha-trinositol completely abolished the neuropeptide Y-induced facilitation of the noradrenaline effect. alpha-Trinositol 1 microM in the presence of 10 nM neuropeptide Y caused a nonparallel rightward shift of the noradrenaline concentration-response curve as compared to that obtained in the presence of 10 nM neuropeptide Y alone. The alpha-trinositol blockade of the facilitatory action of neuropeptide Y was reversible.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Vasoconstriction
/
Neuropeptide Y
/
Norepinephrine
/
Inositol Phosphates
Limits:
Animals
Language:
En
Journal:
Eur J Pharmacol
Year:
1993
Type:
Article