Vasopressin, adrenocorticotropic hormone effects

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). 

Otfier fiormones accelerate tfie release of free fatty acids from adipose tissue and raise tfie plasma free fatty acid concentration by increasing the rate of lipolysis of the triacylglycerol stores (Figure 25—8). These include epinephrine, norepinephrine, glucagon, adrenocorticotropic hormone (ACTH), a- and P-melanocyte-stimulat-ing hormones (MSH), thyroid-stimulating hormone (TSH), growth hormone (GH), and vasopressin. Many of these activate the hormone-sensitive hpase. For an optimal effect, most of these lipolytic processes require the presence of glucocorticoids and thyroid hormones. These hormones act in a facilitatory or permissive capacity with respect to other lipolytic endocrine factors. 

The nonapeptide vasopressin (AVP) is synthesized in the paraventricular nucleus of the hypothalamus (PVN) and the nucleus supraopticus. Besides its role in fluid regulation, AVP is also a key modulator of the HPA system, where it potentiates the effects of CRH on adrenocorticotropic hormone (ACTH) release. Extrahypothalamic AVP-containing neurons are localized in the medial amygdala and the bed nucleus of the stria terminalis. AVP applied intracere-broventricularly or to the lateral septum has been shown to affect cognition, social behavior, and anxiety-like behavior in rodents (Insel et al. 2001). 

In addition to its central effects on blood pressure, Ang II acts on the central nervous system to stimulate drinking (dipsogenic effect) and increase the secretion of vasopressin and adrenocorticotropic hormone (ACTH). The physiologic significance of the effects of Ang II on drinking and pituitary hormone secretion is not known. 

Nicotine binds selectively to the nicotinic receptors that are present in the adrenal medulla, brain, autonomic ganglia, and neuromuscular junctions. It causes the release of several neurotransmitters and hormones such as acetylcholine, norepinephrine, dopamine, serotonin, arginine vasopressin, j3-endorphin, adrenocorticotropic hormone, and cortisol (187). This neuro-regulatory effect of nicotine is dose-dependent and occurs as plasma nicotine level rises when tobacco is smoked. The neurotransmitters released in the brain medi-... 

One of the best-known examples of this class is interferon (a glycoprotein), which has shown much promise as an antiviral agent and in the treatment of cancer (71). Numerous polymers (mostly polyelectrolytes) are effective in inducing the production of interferon in animals (72). Other well-known bioactive polypeptides are insulin, adrenocorticotropic hormone (ACTH), human growth hormone (HGH), prolactin, follicle stimulating hormone (FSH), and luteinizing hormone most of these have been synthesized, and some derivatives have been prepared (73). Some small bioactive polypeptides are the nonapeptides bradykinin, vasopressin, and oxytocin bioactive derivatives have been made for many of these also (74). 

Contrast the effects of desmopressin and vasopressin on circulating adrenocorticotropic hormone (ACTH) levels. 

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