The inferior hypophyseal artery arises most frequently from the meningohypophyseal trunk (see Fig. 2-12F, G) or directly from the medial surface of the posterior ascending segment of the cavernous carotid artery (see Fig. 2-12H–J, N). It passes medially across the cavernous sinus to reach the lateral surface of the posterior lobe and capsule of pituitary gland. The artery divides into superior and inferior branches that anastomose with their mates of the opposite side, forming an arterial circle anterior to the dorsum sellae (see Fig. 2-12H). The inferior branch of this arterial circle, along with the more anteriorly located capsular arteries, may supply the dura on the sellar floor. The capsular arteries usually arise directly from the medial surface of the horizontal cavernous carotid (see Fig. 2-12N), but may also be branches of the inferior hypophyseal artery.The dura of the posterior clinoid and cavernous sinus can also be supplied by the inferior hypophyseal branch, through the medial clival artery, which can also arise directly from the cavernous carotid.
Luschka, in 1860 first identified the inferior hypophyseal artery in man. This artery is the adult remnant of the primitive maxillary artery. In the lateral angiogram, the inferior hypophyseal artery is superimposed on the carotid siphon and is therefore impossible to identify even after subtraction studies.
IHA is a branch of the meningohypophyseal trunk (and occasionally a direct branch of the cavernous ICA) that courses within the cavernous sinus from lateral to medial and from posterior to anterior on its way to the dura that covers the posterior lobe of the pituitary gland; it is a constant artery but it is often hypoplastic on one side.
The superior hypophyseal arteries (from the ICA or the posterior communicating artery) supply the hypothalamus and infundibular stalk and anastomose with branches of the inferior hypophyseal artery (from the ICA). A unique aspect of this arterial distribution is the hypophyseal portal system, whose primary plexus derives from small arterioles and capillaries that then send branches into the anterior pituitary gland. This plexus allows neurons producing hypothalamic releasing factors and inhibitory factors to secrete these factors into the hypophyseal portal system, which delivers a very high concentration directly into the secondary plexus in the anterior pituitary. Thus, anterior pituitary cells are bathed in releasing and inhibitory factors in very high concentrations. This private vascular communication channel allows the hypothalamus to exert fine control, both directly and through feedback, over the secretion of anterior pituitary hormones.
The primary hypophyseal portal system coalesces into long hypophyseal portal veins that give rise to a secondary hypophyseal plexus. This arrangement allows the secretion of releasing and inhibitory factors from nerve endings, whose cell bodies are located in the hypothalamus and other structures, into a private vascular portal system, to be delivered to the pituicytes in the anterior pituitary gland in extraordinarily high concentrations. The ultimate CNS control of the releasing and inhibitory factors profoundly influences neuroendocrine secretion and its downstream effects both target endocrine organs and the entire body. For example, corticotrophin releasing hormone or factor induces the release of adrenocorticotropic hormone from the anterior pituitary, which is released into the systemic circulation and activates the adrenal cortex to release cortisol and other steroid hormones. This hypothalamo-pituitary-adrenal system helps to regulate glucose metabolism, insulin secretion, immune responses, adipose distribution, and a host of other vital functions. The corticotrophin releasing hormone neurons are under extensive regulatory control by neural inputs, hormonal feedback, and inflammatory mediators; these neurons help to orchestrate stress reactivity for the organism as a whole.
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