In this study the isolated rabbit renal artery segments contracted
with 0.1 μM phenylephrine and in the presence of nitric oxide synthase
inhibitor, N-nitro-L- arginine methyl ester (L-NAME), carbachol
produced endothelium-dependent relaxations.
In the present work, the mechanism underlying this (L- NAME)
resistant relaxation was studied. The relaxation was not affected by cyclooxygenase
inhibitor indomethacin.
In arteries contracted with 30mM K+ L-NAME resistant relaxation
induced by carbachol was absent.
The Na + -K+ ATPase inhibitor ouabain reduced this relaxation in a
concentration dependent manner.
In le free media, addition of K+ (5mM) produced significant
relaxation of phenylephrine-induced contraction. This relaxations was
endothelium-independent and ouabain-sensitive.Neither le channel blocker Tetraethylammonium (TEA) nor the
cytochrome p 450 inhibitor miconazole produce any significantly change
the maximal response of renal artery to carbachol.
In conclusion, in rabbit isolated renal artery, carbachol produced a
non-Nitric oxide, non prostacyline 12 dependent relaxation. This
relaxation might be mediated by an endothelium-derived hyperpolarizing
factor (EDHF). This factor does not appear to be a cytochrome P450
metabolite. The inhibition by ouabain of these relaxations suggests the
possible involvement of Na+ - K+ ATPase activation in EDHF responses
although other mechanisms cannot be ruled out. |
