Cardiovascular responses evoked by acetylcholine in prelimbic cortex is mediated by nitric oxide – guanylate cyclase mechanism in rats

Abstract

The stimulation of PL with acetylcholine (ACh) caused depressor response mediated by muscarinic receptors. Studies in literature demonstrated that stimulation of muscarinic receptors induced cyclic GMP formation mediated by nitric oxide. Hence, the objective of this study was to investigate if cardiovascular response caused by muscarinic receptors stimulation is mediated by nitric oxide and cyclic GMP formation. Male Wistar rats (240–280g) were used and guide cannulae were implanted in the PL for drug injection. The cardiovascular responses evoked by ACh (30nmol/200nL) microinjected into the PL were measured before and 15 min after PL treatment with, J 104129 fumarate ‐ M3 antagonist (6nmol/200nL), pirenzepine ‐ M1 antagonist (6nmol/200nL), N‐Propyl ‐ inhibitor of neuronal nitric oxide synthase (nNOS) (0,04nmol/200nL), carboxy‐PTIO ‐ scavenger NO (1nmol/200nL) or ODQ ‐ guanylate cyclase inhibitor (1nmol/200nL). A polyethylene catheter was implanted in the femoral artery for MAP and HR records. The statistical test utilized was two‐way ANOVA. The pre‐treatment with pirenzepine did not blockade the decrease of the MAP (F1,220=6.526; P=0.0113) and increase of the HR (F1,220=0.2313; P=0.6310), while J 104129 fumarate (MAP: F1,220=200.7; P<0.0001; HR: F1,220=170.1; P<0.0001), N‐Propyl (MAP: F1,264=79.04; P<0.0001; HR: F1,264=257.4; P<0.0001), C‐PTIO (MAP: F1,176=115.4; P<0.0001; HR: F1,176=255.7; P<0.0001) or ODQ (MAP: F1,220=165.7; P<0.0001; HR: F1,220=161.3; P<0.0001) blocked depressor and tachycardic responses caused by ACh microinjection into the PL. This results demonstrated that the cardiovascular responses caused by ACh in PL are mediated by local nitric oxide – guanylate cyclase mechanism. Financial Support: CAPES and FAEPA.