ADH’s original name, vasopressin, was derived from the observation that large nonphysiologic doses increase blood pressure by promoting the contraction of smooth muscle in small arteries and arterioles. However, the physiologic levels of ADH have only minimal effects on blood pressure. ADH is the main hormone involved in regulation of water homeostasis and osmolarity of body fuids. The primary physiologic effect of ADH on the kidney is the insertion of water channels (aquaporins) into cells of the distal convoluted tubules and collecting ducts, which increases the permeability for water. Insertion of aquaporin-2 (AQP-2) into the apical domain and aquaporin-3 (AQP-3) into the basolateral domain of these cells is responsible for rapid resorption of water across the tubule epithelium.
ADH acts through its specific V2 receptor on the basolateral domain of cells lining the distal convoluted tubules and collecting ducts; mutation of this receptor is responsible for nephrogenic diabetes insipidus (Folder 21.3).
Plasma osmolality and blood volume are monitored by specialized receptors of the cardiovascular system (e.g., carotid bodies and juxtaglomerular apparatus). An increase