Many peripheral hormone systems are controlled by the hypothalamus and pituitary. The hypothalamus is sited at the base of the brain around the third ventricle and above the pituitary stalk, which leads down to the pituitary itself, carrying the hyophyseal-pituitary portal blood supply.
The important anatomical relationships of the hypothalamus and pituitary include the optic chiasm just above the pituitary fossa; any expanding lesion from the pituitary or hypothalamus can thus produce visual field defects by pressure on the chiasm. The pituitary is itself encased in a bony box; any lateral, anterior or posterior expansion must cause bony erosion. Upward expansion of the gland through the diaphragma sellae is termed ‘suprasellar extension’. The normal fossa is of very variable size but a true lateral X-ray should show a welldefined outline with a single floor. The commonest cause of apparent abnormality is a poorly aligned film.
Embryologically, the anterior pituitary is formed from Rathke’s pouch (endodermal) which meets an outpouching of the third ventricular floor to become the posterior pituitary.
This contains many vital centres for such functions as appetite, thirst, thermal regulation and sleep/waking. It acts as an integrator of many neural and endocrine inputs to control the release of releasing factors. Amongst other important influences it plays a role in the circadian rhythm, menstrual cyclicity, stress, exercise and mood. From the hypothalamus the portal system runs down the stalk through which releasing factors are transported to the pituitary.
Releasing or inhibitory hormones produced in the hypothalamus travel down the portal system and stimulate or inhibit specific cells within the pituitary. These cells then stimulate or inhibit the synthesis and release of trophic hormones, which in turn stimulate the peripheral glands. This pattern is illustrated. Many hormones are under dual control of stimulatory and inhibitory hypothalamic factors. For example: GROWTH HORMO E RELEASE is stimulated by growth hormone releasing hormone (GHRH) but inhibited by somatostatin (growth hormone release inhibitory hormone, GHRIH).
TSH RELEASE is stimulated by TRH but partially inhibited by somatostatin.
SOME HORMONES have a dual stimulatory control, e.g. corticotrophin releasing factor (CRF) and vasopressin are endogenous stimulators of ACTH release. Uniquely, prolactin is under predominant inhibitory dopaminergic control with some stimulatory TRH control.
This, in contrast, acts merely as a storage organ. Antidiuretic hormone (ADH, vasopressin) and oxytocin, both nonapeptides, are synthesized in the supraoptic and paraventricular nuclei in the anterior hypothalamus. They are then transported along a single axon and stored in the posterior pituitary. This means that damage to the stalk or pituitary alone does not prevent synthesis and release of ADH and oxytocin. ADH; oxytocin produces milk ejection and uterine myometrial contraction.
Synthetic hypothalamic hormones and their antagonists are now available for testing of endocrine function and for treatment.
Endorphins and the ACTH families of peptides Some but not all of the endorphins (ENDogenous mORPHINe) are derived from part of the ACTH precursor molecular (Fig. 16.7). This scheme demonstrates some of the complex processing of pituitary peptides including the role of a ‘prohorrnone’, proopiomelanocortin, from which the major hormone, ACTH, is split. Pigmentation in humans is due to ACTH and l3-lipotrophin, not from a- and l3-melanocyte stimulating hormone (MSH) which are not found in humans.
The endorphins have opioid activity and are thought to be mediators of stress-induced analgesia. They have also been found within the gut but their physiological role remains uncertain. The hypothalamus also contains large amounts of other neuropeptides such as natriuretic factor, bombesin and vasoactive intestinal peptide (VIP) that can also alter pituitary hormone secretion.