Vasorelaxant action of the total alkaloid fraction obtained from Solanum paludosum Moric. (Solanaceae) involves NO/cGMP/PKG pathway and potassium channels.
Λέξεις-κλειδιά
Αφηρημένη
BACKGROUND
Solanum paludosum Moric. (jurubeba-roxa) is commonly used to treat hypertension as a substitute for Solanum paniculatum L. (jurubeba verdadeira). The total ethanolic extract from the root bark of Solanum paludosum have been found to cause hypotension in rats.
OBJECTIVE
To investigate the mechanism by which the total alkaloid fraction obtained from the root bark of Solanum paludosum (FAT-SP) acts as a vasorelaxant agent on rat thoracic aorta.
METHODS
Rings of rat aorta were suspended in organ bath containing Krebs solution at 37°C, bubbled with carbogen mixture (95% O(2) and 5% CO(2)) under a resting tension of 1 g. Isometric contractions were measured using a force transducer coupled to an amplifier and a microcomputer.
RESULTS
FAT-SP has been found cause relaxation of the aortic rings pre-contracted with phenylephrine (Phe) in a concentration-dependent manner, in the presence and absence of endothelium. This effect was more potent on the endothelium-intact aorta. In the presence of endothelium, neither indomethacin (non-selective cyclooxygenase inhibitor) nor atropine (non-selective muscarinic receptor antagonist), produced significant changes on the relaxation response. On the other hand, in the presence of calmidazolium (a calmodulin inhibitor), N-nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhibitor), hydroxocobalamin (HDX) (scavenger of free-radical nitric oxide), 1-H-[1,2,4]-oxadiazolo-[4,3a]-quinoxalin-1-one (ODQ, selective blocker of soluble guanylate cyclase), Rp-8-bromo-β-phenyl-1,N(2)-ethenoguanosine 3':5'-cyclic monophosphorothioate sodium salt hydrate (Rp-8-Br-PET-cGMPS, competitive inhibitor of cGMP-dependent protein kinase G) or TEA(+) (tetraethylammonium, nonselective potassium channel blocker), the vasorelaxant effect was significantly reduced, suggesting the involvement of NO/sCG/PKG pathway and potassium channel opening in vasorelaxant action of the FAT-SP.
CONCLUSIONS
The mechanism of vasorelaxant activity of the FAT-SP on rat aorta involves both NO/sCG/PKG pathway and potassium channels.
