Autoregulation of nitric oxide‐soluble guanylate cyclase‐cyclic GMP signalling in mouse thoracic aorta

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Abstract
The sensitivity of the soluble guanylate cyclase (sGC)‐cyclic guanosine‐3′,5′‐monophosphate (cyclic GMP) system to nitric oxide (NO) was investigated in mouse aorta from wild type (WT) and NO synthase (NOS) knockout (KO) animals. The NO donor, spermine‐NONOate (SPER‐NO) was more potent in aortas from eNOS KO mice compared to WT (pEC50 7.30±0.06 and 6.56±0.04, respectively; n=6; P50 4.38±0.04 and 4.40±0.05, respectively; n=5; P>0.05). Zaprinast (10−5 M) a phosphodiesterase type V (PDE V) inhibitor, had no effect on the response to SPER‐NO in vessels from eNOS WT or KO mice. The NOS inhibitor NG‐nitro‐L‐arginine methyl ester (L‐NAME; 3×10−4 M) increased the potency of SPER‐NO in aortas from WT mice (pEC50 6.64±0.02 and 7.37±0.02 in the absence and presence of L‐NAME, respectively; n=4; PBritish Journal of Pharmacology (1999) 128, 1082–1088; doi:10.1038/sj.bjp.0702874

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