Effect of nitric oxide compounds on monkey ciliary muscle in vitro

The effects of various nitric oxide compounds and their inhibitors on monkey ciliary muscle contraction in vitro were investigated in both the longitudinal and circular vectors. The responses to nitric oxide compounds in carbachol precontracted ciliary muscle consisted of an initial relaxation often followed by recovery to near carbachol precontracted levels while the compound was still present. Sodium nitroprusside produced the greatest relaxation responses (nearly 100% relaxation in both vectors at 10−3 M). The highest concentrations of isosorbide dinitrate (10−4 M) and l-arginine (10−3 M) produced relaxation responses of approximately 50% in both vectors. 8-Bromo cyclic GMP produced the smallest relaxation responses (25–35%). Nitric oxide synthase inhibition enhanced carbachol contraction up to 20% in the longitudinal but not the circular vector. Phosphodiesterase inhibition did not further enhance the relaxation response to l-arginine. Guanylate cyclase inhibition partially attenuated the relaxation response to sodium nitroprusside. Nitric oxide generating compounds were effective in relaxing precontracted monkey ciliary muscle in vitro. Endogenous production of nitric oxide is likely involved in the regulation of the contractile response in monkey ciliary muscle. Nitric oxide generating compounds may have potential value in therapeutic areas where modulation of ciliary muscle tension is desirable.

► Nitric oxide compounds relax monkey ciliary muscle contracted with carbachol.
► Sodium nitroprusside nearly completely relaxed the carbachol contracted muscle.
► Guanylate cyclase inhibition partially attenuated the relaxation response.
► Nitric oxide synthase inhibition enhanced the carbachol contraction response.