Renin release is followed by conversion of hepatic angiotensinogen to angiotensin I which is subsequently converted to angiotensinogen II by the enzyme angiotensin converting enzyme (ACE). ACE is found in high concentrations in the pulmonary circulation, systemic vasculature and kidney. Angiotensinogen in turn carries out two important independent actions to bring the hemostasis back to normal: the direct vasoconstrictve effect to improve the blood pressure and stimulation of adrenal cortex to secrete aldosterone which results in sodium retention and potassium excretion. Aldosterone also responds to adrenocorticotrpic hormone (ACTH) and potassium excess for its release. The aldosterone action for sodium resorption by the distal convoluted involves the mineralocorticoid receptor (MR); the induction of the basolateral sodium-potassium ATPase pump and the apical sodium channel (Stewart pp1-10) (Weber 2001).
Congestive cardiac failure is the condition when heart is unable to carry out its normal function of pumping blood to supply oxygen and nutrients to different parts of the body including vital organs, in other words there is an insufficient cardiac out to meet the demand of the body. Human body, initially, responses to this pathology by the expansion of the intravascular volume. The renin-angiotensin-aldosterone system comes into action to bring back the perfusion pressure and then maintain it.
Renin stimulation increases the level of angiotensinogen II in the blood, which in turn increases the peripheral resistance to improve blood pressure and thus perfusion of the tissue. Secondly, it also stimulates the adrenal cortex to secrete aldosterone. Some other major stimuli, like angiotensinogen act to increase the secretion of aldosterone, which include: elevated potassium levels in exchange for sodium excretion and plasma corticotrophin level which increases in the congestive cardiac failure on long term basis. These two stimuli are very strong and eventually result in high levels of aldosterone in the circulation (Weber 2001) (Peterson 2002).
Another factor which keeps aldosterone in very high concentration in the circulation is its decreased degradation in the liver because of reduced perfusion of liver in congestive cardiac failure. This reduction causes many fold increase in aldosterone level. So increase in angiotensinogen II due to overactivity of the renin-angiotensin-aldosterone system results in the resorption of sodium from the proximal nephron and aldosterone release increases the resorption from the distal nephron. This also results in decreased serum level of potassium and magnesium.
As body respond to the congestive cardiac failure on long-term basis so these changes in the renin-angiotensin-aldosterone system may result in remodeling of various tissues in the body (Weber 2001).
There are some morphological changes which occur as a result of the remodeling of various tissues. In response to increased aldosterone secretions, Na+ /K+-ATPase activity increases to maintain the osmolarity between extracellular and intracellular compartments. Some morphologic changes also occur resulting in perivascular, atrial and ventricular fibrosis. Thus may be due to increase in