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RAT AORTIC ENDOTHELIUM ANTAGONIZES NITROPRUSSIDE‐INDUCED RELAXATION BY RELEASE OF THE PEPTIDE ENDOTHELIN
Author(s) -
Macdonald P. S.,
Kudo K.,
Dubbin P. N.,
Dusting G. J.
Publication year - 1989
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1989.tb01547.x
Subject(s) - sodium nitroprusside , thromboxane a2 , phenylephrine , endothelin 1 , vasodilation , endocrinology , thromboxane , medicine , endothelin receptor , chemistry , endothelium , vasoconstriction , agonist , pharmacology , nitric oxide , platelet , receptor , blood pressure
SUMMARY 1. The effects of porcine endothelin were examined in rat thoracic aortic rings. 2. Endothelin was a potent contractile agonist (EC 50 4.0 ± 0.6 nmol/L). 3. Endothelin (1 nmol/L) did not affect contractile responses to cumulative concentrations of the thromboxane analogue, U46619. 4. In the presence of U46619, but not phenylephrine, endothelin (1 nmol/L) and endothelium abrogated the vasodilator response to cumulative concentrations of sodium nitroprusside. 5. The inhibitory effect of endothelin on vasodilator responses to nitroprusside in the presence of U46619 was abolished by nifedipine (0.1 μmol/L) but unaffected by indomethacin (3 μmol/L) or haemoglobin (10 μmol/L). 6. These data suggest that endothelin generated by native endothelium exerts a physiological antagonism of sodium nitroprusside in the presence of thromboxane.