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The 5‐HT1A receptor and sympathetic neurotransmission to mesenteric blood vessels in salt‐sensitive hypertension

Salt‐sensitive hypertension is prevalent U.S. and elsewhere. Salt acts in the brain to activate sympathetic nerves which supply the heart and blood vessels. Increases in sympathetic nerve activity cause high blood pressure (hypertension). Serotonin modulates blood vessel tone in the mesentery, a major contributor to peripheral resistance and venous return. Previous studies showed that sympathetic α2‐adrenergic autoreceptor function is impaired leading to increased norepinephrine release and vasoconstriction in deoxycorticosterone acetate (DOCA)‐salt rats. We tested the hypothesis that there is also impaired function of 5‐HT1A receptors on sympathetic nerve terminals in the mesentery leading to increased vasoconstriction. We used computer assisted video microscopy to measure in vitro changes in mesenteric blood vessel diameter caused by transmural nerve stimulation in the presence of 8‐OH‐DPAT, a 5‐HT1A receptor agonist. In sham (normotensive) arteries and veins, 8‐OH‐DPAT produced a dose‐dependent inhibition of constriction. There was a significant rightward shift in response in DOCA‐salt arteries and veins (p<.05). These findings suggest that impaired 5‐HT1A receptor function in the mesentery may contribute to a loss in regulation of sympathetic activity. This may be a mechanism by which pathology is maintained in salt‐sensitive hypertension. (Supported by P01HL070687)