Abstract
Summary
In vagotomized dogs, there was no increase in plasma ADH concentration following (A) common carotid occlusion if the carotid sinuses had been denervated, or (B) occlusion of external and internal carotid arteries above the bifurcation. Hence the release of ADH in vagotomized dogs during common carotid occlusion was a reflex phenomenon due to the alteration in the state of excitation of receptors in the carotid sinus area and the ensuing changes in afferent impulses traveling in the sinus nerves. In vagotomized dogs, occlusion of common carotid arteries above and below the thyrocarotid junction caused similar increases in plasma ADH, indicating that the nerves of the thyrocarotid junction do not play a significant role in such ADH release.
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