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Nitroprusside enhances isoprenaline-induced increases in cAMP in rat aortic smooth muscle

https://doi.org/10.1016/0014-2999(90)94182-WGet rights and content

Abstract

Low concentrations of sodium nitroprusside (SNP) and of isoprenaline acted synergistically to inhibit the phenylephrine-induced contraction of rat aortic smooth muscle. In experiments with these concentrations, SNP enhanced the increases in smooth muscle cAMP caused by isoprenaline by 4- to 5-fold, whereas the SNP-induced increases in tissue cGMP were unaffected by isoprenaline. We conclude that cAMP is likely to mediate the synergistic inhibition of the contraction of rat aortic smooth muscle by these compounds.

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    Indeed, by inhibiting cAMP hydrolysis by a cGMP-inhibited cAMP PDE, Phosphodiesterase 3A (PDE3A), or by promoting cAMP hydrolysis by a cGMP-stimulated PDE, phosphodiesterase 2A (PDE2A), cGMP-elevating agents could act to augment, or antagonize, actions of cAMP-elevating agents, respectively [15–18]. Similar PDE2A- and PDE3A-mediated crosstalk also operates in rat and bovine arterial smooth muscle cells (ASMC) [19–23]. How cells can allow compartmentation of cyclic nucleotide signalling, with its resultant selectivity, while simultaneously allowing crosstalk between these two systems, is the focus of the studies described here.

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