Role of the Baroreceptor Reflexes and Vasoactive Polypeptides in the Corticotropin Release Evoked by Hypotension

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Abstract
The factors involved in the mediation of ACTH release in the cat in response to hypotension have been investigated. Reduction of mean arterial pressure from control levels of over 100 mm Hg to a hypotensive level of 35 mm Hg by bleeding from the femoral artery resulted in a mean increment in plasma ACTH concentration of 4.5 [plus or minus] 0.82 (5) mU ACTH/100 ml. After adrenalectomy of 2 hr. duration, the increment evoked by hypotension was increased to 26.7 [plus or minus] 5.59 (3) mU/100 ml plasma. Hypophysectomy of 20 min. duration eliminated the change in plasma ACTH concentration evoked by hypotension. Occlusion of the common carotid arteries evoked an increment in plasma ACTH concentration. Prior vagosympathectomy increased the increment induced by carotid occlusion and decreased the increment in response to hypotension. Carotid-aortic denervation resulted in a 50% decrease in the ACTH increment evoked by hypotension. The residual hypotensively elicited ACTH increment persisted after C1 cord section in carotid-aortic denervated cats and also after midbrain transection. Bilateral superior cervical and nodose ganglion-ectomy tended to diminish the increment evoked by hypotension in carotid-aortic denervated cats. Nephrectomy alone did not result in a change in the ACTH increment evoked by hypotension, but nephrectomy reduced the response of carotid-aortic denervated cats and abolished the response of carotid-aortic denervated, ganglionectomized cats. In view of this evidence, it is suggested that ACTH release during hypotension is dependent upon the integrity of the carotid-aortic receptors, the kidneys and the autonomic innervation of the head. It is believed that neural paths from the carotid-aortic receptors ascend in the brain stem to the hypothalamus where ACTH release is activated. This viewpoint is supported by the ACTH release observed after electrical stimulation of several sites in the hypothalamus. Support for a contribution from the renin-angiotensin system was obtained when it was found that infusion of angiotensin into the carotid-aortic denervated, ganglionectomized, nephrectomized preparation, which is unresponsive to hemorrhage, elicited an increment in plasma ACTH concentration. That the autonomic nervous system may also be involved in the mediation of ACTH release during hypotension is supported by evidence that bradykinin, a substance which has been shown to stimulate the superior cervical ganglia, evokes ACTH release when infused into the carotid vascular bed. On the other hand, electrical stimulation of the distal ends of the sectioned cervical sympathetic nerves has not been successful in evoking ACTH release. This evidence suggests that the cervical sympathetic innervation of the head performs a role in sustaining the responsiveness of the pituitary gland rather than in initiating ACTH release.