Reduction of Effective Arterial Volume In many forms of edema, the effective arterial blood volume, a parameter that represents the filling of the arterial tree, is reduced. Underfilling of the arterial tree may be caused by a reduction of cardiac output and/or systemic vascular resistance. As a consequence of underfilling, a series of physiologic responses designed to restore the effective arterial volume to normal are set into motion. A key element of these responses is the retention of salt and, therefore, of water, ultimately leading to edema. Renal Factors and the Renin-Angiotensin-Aldosterone (RAA) System (See also Chap. 336) In the final. | Chapter 036. Edema Part 2 Reduction of Effective Arterial Volume In many forms of edema the effective arterial blood volume a parameter that represents the filling of the arterial tree is reduced. Underfilling of the arterial tree may be caused by a reduction of cardiac output and or systemic vascular resistance. As a consequence of underfilling a series of physiologic responses designed to restore the effective arterial volume to normal are set into motion. A key element of these responses is the retention of salt and therefore of water ultimately leading to edema. Renal Factors and the Renin-Angiotensin-Aldosterone RAA System See also Chap. 336 In the final analysis renal retention of Na is central to the development of generalized edema. The diminished renal blood flow characteristic of states in which the effective arterial blood volume is reduced is translated by the renal juxtaglomerular cells specialized myoepithelial cells surrounding the afferent arteriole into a signal for increased renin release Chap. 336 . Renin is an enzyme with a molecular mass of about 40 000 Da that acts on its substrate angiotensinogen an a2-globulin synthesized by the liver to release angiotensin I a decapeptide which is broken down to angiotensin II AII an octapeptide. AII has generalized vasoconstrictor properties it is especially active on the efferent arterioles. This efferent arteriolar constriction reduces the hydrostatic pressure in the peritubular capillaries while the increased filtration fraction raises the colloid osmotic pressure in these vessels thereby enhancing salt and water reabsorption in the proximal tubule as well as in the ascending limb of the loop of Henle. The RAA system has long been recognized as a hormonal system however it also operates locally. Intrarenally produced AII contributes to glomerular efferent arteriolar constriction and this tubuloglomerular feedback causes salt and water retention. These renal effects of AII are mediated by activation of .
