Abstract
Norepinephrine (NE) is released from sympathetic nerves supplying arteries and veins. We studied differences in NE release mechanisms in vitro in mesenteric arteries (MA) from normotensive (sham) and DOCA‐salt hypertensive rats using amperometry with a microelectrode. NE oxidation currents were larger in DOCA‐salt MA compared to sham MA. Idazoxan (1 µM, blocks α2 adrenergic receptors, α2ARs) increased NE current in sham but not DOCA‐salt MA indicating impaired function of α2ARs in DOCA‐salt rats. α2ARs on sympathetic nerve terminals couple to inhibition of NE release via pertussis toxin inhibited G‐proteins. After 2h incubation in pertussis toxin (2 µg/ml), NE currents increased in sham MA but not DOCA‐salt MA indicating that pertussis toxin sensitive G‐proteins were inactive in DOCA‐salt MA. O2− levels are elevated in MA of DOCA‐salt rats. Therefore, we treated DOCA‐salt rats with the NADPH oxidase inhibitor, apocynin (1.5 mM) in the drinking water for 4 weeks. NE currents were similar in sham MA and apocynin‐treated DOCA‐salt MA and α2AR function was restored in MA from apocynin‐treated DOCA‐salt rats. We conclude that α2AR receptor function is impaired in sympathetic nerves supplying MA in DOCA‐salt rats. This effect is mediated by O2− induced inhibition of PTX sensitive G‐proteins linking α2ARs to NE release. These data support a new mechanism for the beneficial effect of antioxidant treatment in hypertension.
Published Version
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