Carotid vascular control of ACTH secretion in lambs.
To test the hypothesis that changes in carotid vascular pressure influence ovine ACTH and corticosteroid secretion, we subjected 6- to 7-wk-old conscious lambs to bilateral carotid occlusion with or without prior vagosympathetic blockade. Reversible vagosympathetic blockade, produced by injection of 2% lidocaine onto the vagosympathetic trunks, inhibited the reflex changes in heart rate after intravenous injection of phenylephrine or during carotid occlusion. Vagosympathetic blockade by itself did not alter arterial pressure or heart rate but did increase circulating levels of ACTH and corticosteroids. This suggests that afferent fibers in the vagosympathetic trunks tonically inhibit the secretion of ACTH. Bilateral carotid occlusion did not change plasma ACTH or corticosteroid concentrations. Bilateral carotid occlusion plus prior vagosympathetic blockade stimulated increases in plasma ACTH and corticosteroid concentrations that were larger than responses to vagosympathetic blockade alone. The results demonstrate that changes in carotid vascular pressure influence ovine ACTH and corticosteroid secretion only during vagosympathetic blockade and therefore suggest that carotid vascular mechanoreceptors interact with other mechanoreceptors having vagosympathetic afferent fibers.
D000305:Adrenal Cortex Hormones / Q000097:blood; D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries / Q000502:physiology*; D005263:Femoral Artery / Q000502:physiology; D007700:Kinetics; D008012:Lidocaine / Q000494:pharmacology; D012756:Sheep; D014630:Vagus Nerve / Q000502:physiology
D000305:Adrenal Cortex Hormones; D000324:Adrenocorticotropic Hormone; D008012:Lidocaine