In the guinea-pig carotid arteries, nitroarginine elevated the resting tension (greater than 3 x 10(-6) M) and enhanced the noradrenaline (NA)- and high-potassium (high-K, 29.6 mM) induced contractions (greater than 10(-7) M), in a concentration-dependent manner, with no significant change in the resting membrane potential and depolarizations elicited by NA or high-K. ACh (10(-6) M) relaxed the muscles precontracted with NA or high-K by 96 or 46% of the contraction, respectively. In the presence of nitroarginine (10(-5) M) for 1-3 h, the ACh-induced relaxation was reduced to 40 or 0% of the NA- or high-K-contractions, respectively. In tissues contracted with NA and exposed to nitroarginine, the ACh-induced relaxation changed from a sustained to a transient form. ACh relaxed the muscles to a similar extent, at any given level of tension, as elevated by different concentrations of NA to 1-3 times the level produced by 10(-6) M NA, either in the presence or absence of nitroarginine. ACh (greater than 10(-8) M) produced a transient hyperpolarization of the membrane, in an endothelium-dependent manner, and the responses were blocked by atropine (10(-6) M) or high-K solution, but not by NA or nitroarginine. We propose that 1) endothelium-derived hyperpolarizing factor (EDHF) is produced by pathways independent of the biosynthesis of endothelium-derived relaxing factor (EDRF), 2) the sustained release of EDRF maintains the muscle tone at a low level, and 3) the endothelium-dependent relaxation is produced by both EDRF and EDHF, and they elicit sustained and transient relaxations, respectively.
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Suzuki et al. (1992) studied this question.