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• W2911505211 abstract "Introduction: Apelin is a peptide found in fat cells, endothelial cells and CNS neurons. Apelin levels are increased in conditions linked to cardiovascular disease (e.g. obesity, diabetes). Apelin inhibits NO-induced relaxation of cerebral arteries (CA) but its effect on relaxation to EDHF, which often compensates for impaired NO responses in diseased arteries, is unknown. Methods and Results: Immunoblot analysis identified apelin receptor expression in human and rat CA. In isolated rat CA, A23187 (10 -9 – 10 -6 M) caused endothelium-dependent relaxation that was unaffected by inhibitors of eNOS (nitro-l-arginine (3 x 10 -5 M), guanylyl cyclase (ODQ (10 -5 M), cyclooxygenase (indomethacin (10 -5 M) and the H 2 O 2 -scavenger, PEG-catalase (500 U/ml) (n=6). A23187-induced relaxation was attenuated by MS-PPOH (10 -5 M), a selective inhibitor of cyp450-catalyzed synthesis of epoxyeicosatrienoic acids (EETs) (pD 2 =6.86 ± 0.3 vs 5.90 ± 0.1, without and with MS-PPOH; n=6; p<0.05), and abolished by 14,15-EE(Z)E (10 -5 M), a selective EET-receptor antagonist (n=7; p<0.05). Apelin (10 -7 M) inhibited A23187-induced relaxation (pD 2 =7.08 ± 0.2 vs 6.44 ± 0.1, without and with apelin; n=7; p<0.05) as well as relaxation to 11,12-EET, 14,15-EET and NS1619 (BK Ca channel opener), but had no effect on relaxation evoked by levcromakalim (K ATP channel opener). In whole cell patch clamp studies (10mv steps from -60mv to +80mv, 200ms duration) in CA smooth muscle cells, 11,12-EET (10 -5 M), 14,15-EET (10 -5 M), and NS1619 (10 -5 M) each caused an approximately 2-fold increase in BK Ca peak current density (at +80 mV; n=6; p<0.05), which was completely abrogated in the presence of apelin (10 -7 M). The effects of apelin on EET-induced relaxation and activation of BK Ca currents were mimicked by iberiotoxin (10 -7 M) (selective BK Ca channel blocker) and abolished by F13A (10 -7 M), an apelin receptor antagonist. Conclusion: Apelin regulates CA vascular tone by inhibiting endothelium-dependent relaxation evoked by an EDHF-like mediator (possibly an EET) through a mechanism involving activation of apelin receptors and inhibition of BK Ca channels in CA smooth muscle cells. These effects could increase the risk of cerebrovascular dysfunction under conditions where apelin levels are elevated." @default.
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• W2911505211 date "2019-02-01" @default.
• W2911505211 modified "2023-10-18" @default.
• W2911505211 title "Abstract WP543: Apelin Impairs Endothelium-Derived Hyperpolarizing Factor (EDHF)-Induced Relaxation of Cerebral Arteries by Inhibiting Activation of Large Conductance, Calcium-Activated K (BK Ca ) Channels in Vascular Smooth Muscle" @default.
• W2911505211 doi "https://doi.org/10.1161/str.50.suppl_1.wp543" @default.
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