Changes

===Vascular Hormal Effects===

===Vascular Hormal Effects===

'''Angiotensin II''' is a potent vasoconstrictor  which causes an increase in mean arterial pressure), and the direct stimulation of sodium retention in the proximal convoluted tubule of the kidney via the increased synthesis and release of aldosterone. '''Aldosterone''' stimulates reabsorption of sodium and chloride, and the secretion of potassium and protons. Initially, the effects are advantageous by protecting perfusion to essential vascular beds and expanding the circulation fluid volume, and therefore increasing contractility by the Starling mechanism. As systemic vascular resistance increases, however, there is increased myocardial work and increased myocardial oxygen demand. Expanded circulatory volume ultimately results in congestion of vascular beds once the Starling mechanism is overwhelmed in the failing heart. Angiotensin II and aldosterone also effect genetic expression, which may lead to a progression of the myocardial dysfunction present. They therefore play a role in the progression of hypertrophy and fibrosis.

'''Angiotensin II''' is a potent vasoconstrictor  which causes an increase in mean arterial pressure), and the direct stimulation of sodium retention in the proximal convoluted tubule of the kidney via the increased synthesis and release of aldosterone. '''Aldosterone''' stimulates reabsorption of sodium and chloride, and the secretion of potassium and protons. Initially, the effects are advantageous by protecting perfusion to essential vascular beds and expanding the circulation fluid volume, and therefore increasing contractility by the [[Heart_Failure_-_Pathophysiology#Introduction|Starling mechanism]]. As systemic vascular resistance increases, however, there is increased myocardial work and increased myocardial oxygen demand. Expanded circulatory volume ultimately results in congestion of vascular beds once the Starling mechanism is overwhelmed in the failing heart. Angiotensin II and aldosterone also effect genetic expression, which may lead to a progression of the myocardial dysfunction present. They therefore play a role in the progression of hypertrophy and fibrosis.

==Kidney and Fluid Balance Mechanisms==

==Kidney and Fluid Balance Mechanisms==