Sympathetic Nerves and Endothelium Influence the Vasoconstrictor Effect of Low Concentrations of Ouabain in Pressurized Small Arteries

Abstract

Here, we tested the involvement of arterial endothelium and peri‐vascular sympathetic nerve terminals (NT) in ouabain‐induced vasoconstriction. Segments of rat arteries were pressurized and exposed to ouabain (10−11M–10−7M). Endothelium removal enhanced ouabain‐induced (10−9M) vasoconstriction as much as 2‐fold. A component of the ouabain‐induced vasoconstriction is due to enhanced spontaneous release of norepinephrine (NE) from NT's in the arterial wall. The α1‐adrenoceptor blocker, prazosin (10−6M) decreased ouabain induced vasoconstrictions by as much as 50%. The electrically evoked release of NE from sympathetic NT was not affected by ouabain (< 10−7M). However, neither the ouabain induced contraction nor the NE release (measured directly by carbon fiber amperometry) was increased by sympathetic nerve activity (SNA). However, following brief bursts of SNA, vasoconstrictor responses to ouabain were transiently increased (1.75‐fold). In arteries lacking endothelium and exposed to prazosin, ouabain (>10−11M) caused vasoconstriction, indicating a direct effect on arterial smooth muscle. Conclusions: Endothelium opposes ouabain induced vasoconstriction, which is caused by both enhanced spontaneous NE release and direct effects on smooth muscle. Ouabain does not enhance SNA mediated contractions, but SNA enhances ouabain‐induced contraction.NIH grants R01‐HL073094 & P01‐HL078870