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Figure 36-2. Schema of the sequence of events in heart failure. An increased load or myocardial abnormality leads to myocardial failure and
eventually to heart failure. This results in increased sympathetic activity, increased levels of renin-angiotensin-aldosterone, pulmonary and
peripheral congestion and edema and decreased cardiac output reserve. (Adapted from Schlant RC, Sonnenblick EH. Pathophysiology of
heart failure. In: Schlant RC, Alexander RW, eds. The Heart, 8th ed. New York, NY: McGraw-Hill, 1994; 525.)
Angiotensin II counters a decline in effective arterial blood II. Studies in dogs support the theory that the intrarenal action
volume by serving as a potent constrictor of veins and arteries, of angiotensin II increases sodium and water retention (Hall
and as a regulator of sodium-potassium homeostasis. Veno- and Brands, 1992). Angiotensin II also stimulates thirst, which
constriction facilitates the return of blood to the heart and facilitates expansion of blood and interstitial fluid volume.
increases cardiac preload. Arteriolar vasoconstriction helps Blood levels of aldosterone tend to parallel those of renin and
maintain systemic blood pressure. Angiotensin II also plays an angiotensin II (Riegger and Liebau, 1982). If effective blood
important role in maintaining blood pressure and volume by volume is restored, the stimulus for RAA secretion is with-
stimulating secretion of aldosterone from the adrenal cortex. drawn. However, if cardiovascular disease is severe, these hor-
Aldosterone promotes reabsorption of sodium and chloride, mones continue to stimulate the kidneys and tissue edema
and thus water, from the distal renal tubules and collecting ensues or worsens (Figures 36-2 and 36-3).
ducts. The effects of aldosterone on sodium excretion may be In addition to the RAA system, a locally active paracrine
less important than the direct intrarenal actions of angiotensin renin-angiotensin system may exist in a number of tissues, par-