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Endothelin‐1 potentiates the beta‐adrenergic relaxation of rat coronary arteries
Author(s) -
GarciaVillalon Angel Luis,
Amezquita Yesika Maria,
Monge Luis,
Fernandez Nuria,
Sanchez Ana,
Salcedo Adeli,
Dieguez Godofredo
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1396-b
It is known that endothelin‐1 at subthreshold concentrations potentiates the coronary vasoconstriction to alpha‐adrenoceptor stimulation. The objective of this study was to test whether endothelin‐1 modulates the beta‐adrenergic coronary vasodilation. To this, segments, 2 mm long from rat coronary arteries were prepared for isometric tension recording in an organ bath, and precontracted with U46619 (10 −7 M). The relaxation to a single concentration of isoproterenol (3x10 −8 M) or to field electrical stimulation (4 Hz, 0.1 ms, 1 seg, supramaximal voltaje) was recorded before and after treatment during 15 min with endothelin‐1 (3x10 −10 M and 10 −9 M). Isoproterenol produced relaxation (25±4 %), and this relaxation was higher after treatment with endothelin‐1 3x10 −10 M (32±4 %, P<0.01) and at 10 −9 M (42±7%, P<0.01). Field electrical stimulation produced relaxation (41±6%) which was reduced with tetrodotoxin and was not modified significantly by endotelin‐1 at 3x10 −10 M at (41±5 %) or at 10 −9 M (38±6 %). Therefore, endothelin‐1 potentiates the relaxation of coronary arteries to beta‐adrenergic stimulation but not to electrical stimulation. (This study was supported, in part, by MEyC, BFU2004‐04054)

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