Renal and humoral pathophysiological actions of angiotensin II in congestive heart failure

Abstract

The renin-angiotensin-aldosterone axis is an integral component linking the renal-humoral system to the cardiovascular system. It is involved in the normal control of blood pressure and intravascular volume. Its activity is also enhanced in pathologic states, namely congestive heart failure, in which stimulation of the axis leads to further deleterious effects on the heart. The well-established dogma that the renin-angiotensin-aldosterone system (RAAS) is a linear cascade is evolving into a vision of this system as a more complex process. It is now known that angiotensin has several subtypes. Each subtype is a ligand at several receptor subtypes and these interactions are not mutually exclusive. The aim of this review is to discuss the different angiotensin subtypes, their receptor interactions and their pathophysiological roles in humoral and renal functions in congestive heart failure. In addition, we will also review the different therapeutic approaches that interrupt the RAAS and the evidence that supports their utility in congestive heart failure (CHF).

Neurohumoral Activation in Heart Failure

“…During its persistence in the tissues, angiotensin II raises blood pressure by two mechanisms that include vasoconstriction with an attendant rise in peripheral resistance and venous return and a concomitant diminution in the renal excretion of sodium and water, raising extracellular fluid volume, either directly and/or via the stimulation of aldosterone secretion from the adrenal glands [46]. In HF, the formation of angiotensin II is deleterious, leading to the production of fibrosis in the heart and kidneys [47]. Angiotensin II also worsens neurohormonal activation, as it instigates the release of norepinephrine and also the production of aldosterone in the adrenal cortex.…”