Vasopressin response

Kendler KS, Weitzman RE, Rubin RT (1978) Lack of arginine vasopressin response to central dopamine blockade in normal adults. J Cline Endocrinol Metab 47 204-207. 

Convertino, V.A., Keil, L.C. Greenleaf, J.E. (1983) Plasma volume, renin, and vasopressin responses to graded exercise after training. J. Appl. Physiol. Respirat. Environ. Exercise Physiol. 54, 508-514. 

Many studies have shown that AmB can induce a loss of concentrating ability of the kidney [18, 32, 33]. This abnormality is almost invariably present and occurs early (1-2 weeks) in the course of therapy. The impairment in concentrating ability probably reflects direct tubular toxicity since it occurs in the absence of a decrease in GFR, and is temporally unrelated to azotemia. Barbour et al. [34] reported a study of 3 patients whose inabihty to concentrate the urine was associated with a defect in free water reabsorption even under maximal stimuli, and concluded that a tubular functional abnormality was induced because of the failure of the vasopressin response in the medullary collecting tubule. 

RaffH, Kane C, Wood C. Arginine vasopressin responses to h3q)oxia and h3q)ercapnia in late-gestation fetal sheep. Am J Physiol 1991 260(6 Pt 2) R1077-R1081. 

Oxytocin and Vasopressin Receptors. The actions of oxytocin and vasopressin are mediated through their interactions with receptors. Different receptor types as well as different second messenger responses help explain their diverse activities in spite of the hormones stmctural similarities. Thus oxytocin has at least one separate receptor and vasopressin has been shown to have two principal receptor types, and V2. Subclasses of these receptors have been demonstrated, and species differences further compHcate experimental analysis. It is apparent that both oxytocin and receptors function through the GP/1 phosphoHpase C complex (75), while the V2 receptors activate cycHc AMP (76). 

Vasopressin (antidiuretic hormone [ADH]) secretion increases in response to decreased blood volume and/or reductions in effective blood volume via a decrease in inhibitory tone from both low-pressure and high-pressure baroreceptors to the hypothalamus. The neuronal pathways that mediate hemodynamic regulation of... 

Disorder characterized by an inability to concentrate urine in response to vasopressin due to mutations in the vasopressin V2 receptor gene or the AQP2 gene. 

ENaC activity is under the control of aldosterone and vasopressin that are secreted in response to stimuli... 

The release of NO from the endothelium is induced by various chemical substances, including acetylcholine polypeptides such as substance P, bradykinin, and arginine vasopressin histamine ATP/ADP a2-adrenoceptor agonists thrombin and Ca2+ iono-phores. NO formed in response to mechanical stimuli like shear stress or transmural pressure plays an important role in maintaining basal blood flow. Endothelial NO causes vasodilatation, decreased... 

Primary therapy is based on disease severity and type of hemorrhage.7 Most patients with mild to moderate disease and a minor bleeding episode can be treated with l-desamino-8-D-arginine vasopressin [desmopressin acetate (DDAVP)], a synthetic analog of the antidiuretic hormone vasopressin. DDAVP causes release of von Willebrand factor (vWF) and factor VIII from endogenous storage sites. This formulation increases plasma factor VIII levels by three- to fivefold within 30 minutes. The recommended dose is 0.3 mcg/kg intravenously (in 50 mL normal saline infused over 15 to 30 minutes) or subcutaneously or 300 meg intranasally via concentrated nasal spray every 12 hours. Peak effect with intranasal administration occurs 60 to 90 minutes after administration, which is somewhat later than with intravenous administration. Desmopressin infusion may be administered daily for up to 2 to 3 days. Tachyphylaxis, an attenuated response with repeated administration, may occur after several doses.8... 

Vasopressin is a peptide hormone produced by the hypothalamus and secreted by the posterior pituitary in response to stimulation. Normal stimuli for vasopressin release are hyperosmolarity and hypovolemia, with thresholds for secretion of greater than 280 mOsm/kg and greater than 20% plasma volume depletion. A number of other stimuli, such as pain, nausea, epinephrine, and numerous drugs, induce release of vasopressin. Vasopressin release is inhibited by volume expansion, ethanol, and norepinephrine. The physiological effect of vasopressin is to promote free water clearence by altering the permeability of the renal collecting duct to water. In addition, it has a direct vasoconstrictor effect. Consequently, vasopressin results in water retention and volume restoration. In patients with septic shock, vasopressin is appropriately secreted in response to hypovolemia and to elevated serum osmolarity (R14). 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Turnbull, A.V. and Rivier, C., Corticotropin-releasing factor, vasopressin and prostaglandins mediate, and nitric oxide restrains, the hypothalamo-pituitary-adrenal response to acute local inflammation in the rat, Endocrinology, 137,455, 1996. 

Taylor It is not prostaglandins because we can block the metabolism of arachidonate, and so prevent formation of prostaglandins and leukotrienes, but we still get activation of NCCE by vasopressin, indeed there is a modest potentiation of the response consistent with lesser degradation of the arachidonate. 

The effects of both oxytocin and vasopressin are particularly responsive to reproductive steroids (Tables 7 and 8). Oxytocin and vasopressin are best known as neurohypophyseal peptides, released by the posterior pituitary. However, both peptides also are released within the nervous system. Receptors for oxytocin and vasopressin are distributed in areas of the CNS that have been implicated in reproduction, emotion and autonomic functions. 

SIP induces hsp27 in AlO vascular smooth muscle cells and osteoblasts and amplifies inositol phosphates formation in response to vasopressin and prostaglandin F2c respectively (Kozawa et al, 1999a and b ... 

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