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Effects of the reversible acetylcholinesterase inhibitor pyridostigmine on vascular reactivity of spontaneously hypertensive rats (SHR)
Author(s) -
Lataro Renata Maria,
Silva Marcondes A. B.,
Tostes Rita C. A.,
Salgado Helio Cesar
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1119.4
Subject(s) - sodium nitroprusside , atropine , phenylephrine , pyridostigmine , contraction (grammar) , acetylcholine , chemistry , vasodilation , nitric oxide , endocrinology , medicine , pyridostigmine bromide , endothelium , mesenteric arteries , acetylcholinesterase , electrical impedance myography , stimulation , spontaneously hypertensive rat , pharmacology , blood pressure , biochemistry , artery , myasthenia gravis , enzyme
We investigated the chronic (16 weeks) effect of pyridostigmine (PYR; 1.5 mg/kg/day) on mesenteric vascular reactivity of SHR. Responses to phenylephrine (Phe), sodium nitroprusside (SNP) and acetylcholine (Ach) were determined with and without endothelium and in the presence of vehicle or L‐NAME plus indomethacin. Electrical stimulation (EE)‐induced contractions were determined in the presence of vehicle, atropine or atropine plus L‐NAME. Ach‐induced relaxation was similar between groups. However, Ach‐induced vasodilation, in the presence of L‐NAME plus indomethacin, was augmented in SHR as compared to WKY and SHR+PYR. No differences in Phe‐induced contraction or SNP‐induced relaxation were observed among groups. EE‐induced contractions, in the presence of atropine, were significantly augmented in endothelium‐intact SHR, but not in SHR+PYR. L‐NAME augmented EE‐induced contractions in WKY and SHR+PYR, but not in SHR. No differences in EE‐induced contraction were observed under atropine plus L‐NAME. In conclusion, PYR improves vascular dysfunction in SHR, which is associated with decreased bioavailability of nitric oxide and is compensated by other endothelium‐derived factors. Financial support:FAPESP.