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Pazit Pianka, Yoram Oron, Moshe Lazar, Orna Geyer; Nonadrenergic, Noncholinergic Relaxation of Bovine Iris Sphincter: Role of Endogenous Nitric Oxide. Invest. Ophthalmol. Vis. Sci. 2000;41(3):880-886.
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purpose. To investigate the role of endogenously generated nitric oxide (NO) in
the relaxation of bovine iris sphincter.
methods. Isolated bovine sphincters were mounted on an isometric tension
apparatus. Contraction–relaxation response was elicited by electrical
field stimulation (ES; 12 Hz, 50-msec duration, 70–80 V). Relaxation
was arbitrarily defined as maximal decrease of tension below
prestimulation baseline after cessation of ES. We also determined the
tissue levels of cyclic guanosine monophosphate (cGMP) by
results. ES produced a biphasic response: contraction followed by relaxation.
After cessation of ES, the muscle relaxed to below the initial baseline
tension. Tetrodotoxin (TTX) abolished most of the contraction and all
the relaxation response. Atropine blocked most of the contraction
component, leaving the relaxation component unchanged. Prazosin and
bupranolol (α1-adrenergic and β-adrenergic antagonists,
respectively) also did not affect the relaxation component of the
response. Neither substance P nor its antagonist
(trifluoromethyl)-benzyl ester; ATTB) inhibited or mimicked the
response. The nitric oxide synthase (NOS) inhibitors
Nω-nitro-l-arginine methyl ester
(l-NAME), N ω-nitro-l-arginine
(l-NNA), and aminoguanidine dose-dependently inhibited the
relaxation response by 50% to 70%. The free radical scavenger
(carboxy-PTIO) and the guanylyl cyclase inhibitor methylene blue also
abrogated 70% and 45% of the relaxation response, respectively. ES
caused an increase in muscle cGMP from 2.3 ± 0.3 to 3.9 ±
0.5 picomoles per muscle. l-NNA or l-NAME
significantly decreased the tissue cGMP content (to 1.2 ± 0.1
picomoles per muscle) and prevented the increase caused by ES.
conclusions. The relaxation component of the iris sphincter response to ES is a
distinct nonadrenergic, noncholinergic, ES-induced event. Most of the
relaxation is mediated by the endogenously generated NO-guanylyl
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