Article date: February 2007
By: J Overend, W Martin in Volume 150, Issue 4, pages 488-493
Background and purpose:
We have previously demonstrated that L‐NMMA (NG‐monomethyl‐L‐arginine) selectively inhibits vasodilatation produced by endothelium‐derived nitric oxide but not nitrergic nerves in the bovine penile artery. The present study investigated whether L‐NMMA had a similar selective action in the bovine ciliary artery. We also investigated whether two recently introduced inhibitors of neuronal nitric oxide synthase (nNOS), AAAN (N‐(4S)‐4‐amino‐5‐[aminoethyl]aminopentyl‐N′‐nitroguanidine) and L‐NPA (NG‐propyl‐L‐arginine), produced selective blockade of vasodilatation induced by nitrergic nerves but not endothelium‐derived nitric oxide.
Experimental approach:
Rings of bovine ciliary artery were suspended in a wire myograph for tension recording. Neurogenic (nitrergic) vasodilatation was elicited by electrical field stimulation, and endothelium‐dependent, nitric oxide‐mediated dilatation was evoked using bradykinin.
Key results:
L‐NMMA inhibited vasodilatation induced by endothelium‐derived nitric oxide but not the nitrergic nerves. In fact, L‐NMMA, acted like L‐arginine in protecting nitrergic vasodilatation against inhibition by L‐NAME (NG‐nitro‐L‐arginine methyl ester). AAAN had no effect on vasodilatation induced by either nitrergic nerves or endothelium‐derived nitric oxide, but L‐NPA inhibited both with equal potency.
Conclusions and implications:
In the bovine ciliary artery, L‐NMMA acts as a selective inhibitor of the vasodilatation induced via endothelial NOS, without affecting that operating via nNOS. Furthermore, the putative nNOS inhibitors, AAAN and L‐NPA failed to produce the expected selective inhibition of nitrergic vasodilatation in this artery.
DOI: 10.1038/sj.bjp.0707113
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