Anterior pituitary, effect

In humans, the hypothalamic-derived protein and the hormone noncovalent complexes are packaged in neurosecretory granules, then migrate along axons at a rate of 1 4 mm/h until they reach the posterior pituitary where they are stored prior to release into the bloodstream by exocytosis (67). Considerable evidence suggests that posterior pituitary hormones function as neurotransmitters (68) vasopressin acts on the anterior pituitary to release adrenocorticotropic hormone [9002-60-2] (ACTH) (69) as well as on traditional target tissues such as kidneys. Both hormones promote other important central nervous system (CNS) effects (9,70). 

In contrast to the posterior pituitary lobe, the anterior pituitary lobe is under the control of several releasing and inhibiting hormones secreted from the hypothalamus via a portal vein system. The anterior pituitary lobe, in turn, synthesizes and secretes six major hormones. Figure 43-1 summarizes the physiologic mediators and effects of each of these hormones. 

Located in close proximity to the primary capillary plexus in the hypothalamus are specialized neurosecretory cells. In fact, the axons of these cells terminate on the capillaries. The neurosecretory cells synthesize two types of hormones releasing hormones and inhibiting hormones (see Table 10.2). Each of these hormones helps to regulate the release of a particular hormone from the adenohypophysis. For example, thyrotropin-releasing hormone produced by the neurosecretory cells of the hypothalamus stimulates secretion of thyrotropin from the thyrotrope cells of the adenohypophysis. The hypo-thalamic-releasing hormone is picked up by the primary capillary plexus travels through the hypothalamic-hypophyseal portal veins to the anterior pituitary leaves the blood by way of the secondary capillary plexus and exerts its effect on the appropriate cells of the adenohypophysis. The hypophyseal hormone, in this case, thyrotropin, is then picked up by the secondary capillary plexus, removed from the pituitary by the venous blood, and delivered to its target tissue. 

The acute CNS effects of MDMA administration are mediated by the release of monoamine transmitters, with the subsequent activation of presynaptic and postsynaptic receptor sites.40 As specific examples in rats, MDMA suppresses 5-HT cell firing, evokes neuroendocrine secretion, and stimulates locomotor activity. MDMA-induced suppression of 5-HT cell firing in the dorsal and median raphe involves activation of presynaptic 5-HT1A autoreceptors by endogenous 5-HT.4142 Neuroendocrine effects of MDMA include secretion of prolactin from the anterior pituitary and corticosterone from the adrenal glands 43 Evidence supports the notion that these MDMA-induced hormonal effects are mediated via postsynaptic 5-HT2 receptors in the hypothalamus, which are activated by released 5-HT. MDMA elicits a unique profile of locomotor effects characterized by forward locomotion and elements of the 5-HT behavioral syndrome such as flattened body posture, Straub tail, and forepaw treading.44 6 The complex motor effects of MDMA are dependent on monoamine release followed by activation of multiple postsynaptic 5-HT and DA receptor subtypes in the brain,47 but the precise role of specific receptor subtypes is still under investigation. 

Hormones have a profound effect on carbohydrate metabolism. Great interest has been aroused by reports of hormonal control of hexokinase activity by specific proteins in animal tissues.99- 100 Hexokinase action is the rate-limiting step in the uptake of D-glucose by muscle. Hexokinase is inhibited in diabetic muscle, but the inhibition can be partially reversed by insulin. A protein fraction from the anterior pituitary gland will inhibit the hexokinase of extracts of brain and muscle, and the effect of this... 

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