Relaxations to NO in venous smooth muscle involve intracellular processes similar to those in arterial smooth muscle, specifically activation of soluble guanylate cyclase and potassium channels.
No direct clinical implications from animal data; leaves open conservation of NO signaling mechanisms in human veins.
Experiments were designed to examine mechanisms of relaxations to nitric oxide (NO) in venous smooth muscle. Rings of canine femoral veins without endothelium were suspended for measurement of isometric force in organ chambers. Concentration-response curves to NO and 8-Br-cyclic guanosine monophosphate (cGMP) were obtained in veins contracted with KCl (60 mM) or prostaglandin F2alpha (PGF2alpha; 2x10(-6) M) in the absence and presence of inhibitors of soluble or particulate guanylate cyclase or K+ channel antagonists. In rings contracted with PGF2alpha, relaxations to NO were reduced significantly by inhibition of soluble but not particulate guanylate cyclase. Relaxations to NO were reduced in rings contracted with KCI. Tetraethylammonium (10(-2) M) and glibenclamide (10(-7) M) + charybdotoxin (10(-7) M) significantly reduced relaxations to NO in rings contracted with PGF2alpha. Relaxations to 8-Br-cGMP were decreased significantly only by charybdotoxin. These results suggest that relaxations to NO in canine femoral veins involve at least two intracellular processes: activation of soluble guanylate cyclase and activation of adenosine triphosphate (ATP)-sensitive and large-conductance, Ca+2-activated K+ channels. The large-conductance, Ca+2-activated K+ channels seem to be activated by cGMP-dependent mechanisms. Therefore relaxations to NO in venous smooth muscle involve intracellular processes similar to those in arterial smooth muscle.
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Bracamonte et al. (1999) studied this question.