Ancylostoma wrote:
actually the reason is simple. decrease contractility causes a decrease in blood pressure. This lead to compensation, your carotid sinus receptors recognize the decrease in blood pressure and decrease parasypathetic outflow and increase sympathetic outflow. this lead to the release of renin. The compensation via sypathetice is actually counterproductive in heart failure. Sypathetic outflow causes increase pvr in the arterioles, increasing pressure in arteries, increasing afterload, then it causes venoconstiction causing increase preload, on top of it it causes renin secretion leading to a further increase of preload. this makes the failing heart do more work. This is also the reason that ace inhibitors are the drug of choice(besides prolonging survival). Ace inhibitors cause a decrease in preload by decreasing fluid retention (aldosterone) and the cause vasodilation by increasing bradykinin. If you didnt know, another function of angiotensin converting enzyme is to break down bradykinin, by blocking that action this increases bradykinin leading to the vasodilation. Increased bradykinin is also the reason we get a dry cough and angioedema as side effects. Hope that explains it all. Good luck