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Vasopressin receptor blood concentrations

ADH, a nonapeptide, released from the posterior pituitary gland promotes re-absorption of water in the kidney. This response is mediated by vasopressin receptors of the V2 subtype. ADH enhances the permeability of collecting duct epithelium for water (but not for electrolytes). As a result, water is drawn from urine into the hyperosmolar inter-stitium of the medulla. Nicotine augments (p. 110) and ethanol decreases ADH release. At concentrations above those required for antidiuresis, ADH stimulates smooth musculature, including that of blood vessels ( vasopressin ). The latter response is mediated by receptors of the Vi subtype. Blood pressure rises coronary vasoconstriction can precipitate angina pectoris. Lypres-sin (8-L-lysine vasopressin) acts like ADH. Other derivatives may display only one of the two actions. [Pg.164]

Desmopressin has little vasoconstrictor effect but has potent antidiuretic action, through renal vasopressin V2 receptors, and at high doses hemostatic properties, by increasing concentrations of factor VIII and von Willebrand factor in the blood. [Pg.521]

Other mediators have also been related to CsA-in-duced functional nephrotoxicity. Increased plasma level of adenosine due to reduced uptake by red blood cells was observed in CsA-treated renal transplant recipients [183]. In the same way, rats receiving CsA showed increased concentration of adenosine in renal artery paralleled by a decrease in mRNA expression for Aj and A2a renal adenosine receptors [184]. Experimental use of selective Aj adenosine receptors antagonists or theophylline resulted in contradictory results with some authors finding renal hemodynamic and functional protection whereas other did not [38, 185-187]. Moderate increases in plasma vasopressin were observed in CsA-treated renal transplant recipients [188] and CsA enhanced vasopressin-induced rise in intracellular calcium in cultured glomerular mesangial... [Pg.409]

RENAL ACTIONS OF VASOPRESSIN Several actions of vasopressin in the kidney involve both Vj and receptors. Vj receptors mediate contraction of mesangial cells in the glomerulus and vascular smooth muscle cells in the vasa recta and efferent arteriole. Indeed, Vj-receptor-mediated reduction of inner medullary blood flow contributes to the maximum concentrating capacity of the kidney (Figure 29-4). Vj receptors also stimulate prostaglandin synthesis by... [Pg.503]


See other pages where Vasopressin receptor blood concentrations is mentioned: [Pg.682]    [Pg.168]    [Pg.94]    [Pg.289]    [Pg.363]    [Pg.514]    [Pg.243]    [Pg.185]    [Pg.339]    [Pg.115]    [Pg.623]    [Pg.289]    [Pg.933]    [Pg.175]    [Pg.404]    [Pg.271]    [Pg.54]    [Pg.117]    [Pg.395]   
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