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Chronic treatment with acetylcholinesterase inhibitors attenuates vascular dysfunction in spontaneously hypertensive rats.

BACKGROUND: Acetylcholinesterase inhibition prevents autonomic imbalance, reduces inflammation and attenuates the development of hypertension. Considering that vascular dysfunction is a crucial feature of arterial hypertension, we investigated the effects of chronic administration of acetylcholinesterase inhibitors - pyridostigmine or donepezil - on vascular reactivity of spontaneously hypertensive rats (SHR).

METHODS: Endothelium-dependent relaxant responses to acetylcholine and contractile responses induced by electric field stimulation (EFS) and alpha-adrenergic agonist were studied in mesenteric resistance arteries from SHR and Wistar Kyoto rats. SHR were treated for sixteen weeks with vehicle, pyridostigmine (1.5 mg/kg/day) or donepezil (1.4 mg/kg/day).

RESULTS: Pyridostigmine and donepezil decreased the vasoconstrictor responses to EFS, which were increased in vehicle-treated SHR. Acetylcholinesterase inhibition increased the modulatory effects of nitric oxide (NO) on SHR vascular reactivity, i.e., N(ω)-nitro-(L)-arginine methyl ester (L-NAME) increased EFS-induced contractions and reduced acetylcholine-induced relaxation, with more significant effects in pyridostigmine- and donepezil-treated SHR. The acetylcholinesterase inhibitors also decreased vascular reactive oxygen species levels.

CONCLUSIONS: This study demonstrates for the first time that long-term administration of acetylcholinesterase inhibitors, pyridostigmine or donepezil, attenuates vascular reactivity dysfunction in SHR by decreasing reactive oxygen species generation and increasing NO bioavailability; possibly via increased endothelial NO synthase activity, and inhibition of NADPH oxidase activity.

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