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Chapter 036. Edema (Part 3)

Endothelin This potent peptide vasoconstrictor is released by endothelial cells; its concentration is elevated in heart failure and contributes to renal vasoconstriction, Na+ retention, and edema in heart failure. Natriuretic Peptides Atrial distention and/or a Na+ load cause release into the circulation of atrial natriuretic peptide (ANP), a polypeptide; a high-molecular-weight precursor of ANP is stored in secretory granules within atrial myocytes. Release of ANP causes (1) excretion of sodium and water by augmenting glomerular filtration rate, inhibiting sodium reabsorption in the proximal tubule, and inhibiting release of renin and aldosterone; and (2) arteriolar and venous dilation by antagonizing the vasoconstrictor actions. | Chapter 036. Edema Part 3 Endothelin This potent peptide vasoconstrictor is released by endothelial cells its concentration is elevated in heart failure and contributes to renal vasoconstriction Na retention and edema in heart failure. Natriuretic Peptides Atrial distention and or a Na load cause release into the circulation of atrial natriuretic peptide ANP a polypeptide a high-molecular-weight precursor of ANP is stored in secretory granules within atrial myocytes. Release of ANP causes 1 excretion of sodium and water by augmenting glomerular filtration rate inhibiting sodium reabsorption in the proximal tubule and inhibiting release of renin and aldosterone and 2 arteriolar and venous dilation by antagonizing the vasoconstrictor actions of AII AVP and sympathetic stimulation. Thus ANP has the capacity to oppose Na retention and arterial pressure elevation in hypervolemic states. The closely related brain natriuretic peptide BNP is stored primarily in ventricular myocardium and is released when ventricular diastolic pressure rises. Its actions are similar to those of ANP. Circulating levels of ANP and BNP are elevated in congestive heart failure and in cirrhosis with ascites but obviously not sufficiently to prevent edema formation. In addition in edematous states there is abnormal resistance to the actions of natriuretic peptides. Clinical Causes of Edema Obstruction of Venous and Lymphatic Drainage of a Limb In this condition the hydrostatic pressure in the capillary bed upstream proximal to the obstruction increases so that an abnormal quantity of fluid is transferred from the vascular to the interstitial space. Since the alternative route i.e. the lymphatic channels may also be obstructed or maximally filled an increased volume of interstitial fluid in the limb develops i.e. there is trapping of fluid in the extremity. Tissue tension rises in the affected limb until it counterbalances the primary alterations in the Starling forces at which time no further .