Key result
Addition of nitric oxide synthesis inhibitors to rabbit cavernous smooth muscle strips significantly increased tension and almost completely abolished the relaxing effects of acetylcholine.
Cholinergically induced endothelial formation of nitric oxide plays a crucial role in mediating the relaxation of cavernous smooth muscle.
Should not change erectile dysfunction management; leaves open translation of nitric oxide mechanisms from rabbit models.
Externally applied acetylcholine (ACh) in human corpus cavernosum has been shown to cause endothelium-dependent smooth muscle relaxation. Changes in isometric tension in rabbit cavernous smooth muscle strips mounted in organ bath chambers were monitored in the presence of blocking agents. Nitric oxide (NO) is known as an endothelium-derived relaxation factor (EDRF). Addition of specific inhibitors of nitric oxide synthesis, such as L-n-monomethyl arginine (L-NMMA) at 5 x 10(-4) mol/l.. or L-n-nitro arginine (L-NOARG) at 2 x 10(-4) mol/l. to strips precontracted with phenylephrine (PE) at 3.16 x 10(-6) mol/l. led to significant increases in tension. In the presence of L-NMMA or L-NOARG, relaxing effects of ACh at 10(-8)-3.16 x 10(-5) mol/l. mediated by muscarinic receptors were almost completely abolished. These data indicate that rabbit cavernous smooth muscle is under the control of basal NO release. They constitute strong evidence that cholinergically induced endothelial formation of NO plays a crucial role in relaxing cavernous smooth muscle.
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Knispel et al. (1991) studied this question. Nitric oxide synthesis inhibitors (L-NMMA or L-NOARG) was evaluated on Changes in isometric tension and relaxing effects of acetylcholine. Addition of nitric oxide synthesis inhibitors to rabbit cavernous smooth muscle strips significantly increased tension and almost completely abolished the relaxing effects of acetylcholine.
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