4x

10x

20x

40x

40x

4x 10x

20x 40x

40x

4x

10x 20x

40x 40x

20x 40x

10x 40x

20x

40x

4x 10x

4x 10x

20x 40x

10x 20x

4x 10x

40x 40x

4x 4x

20x 20x

4x 10x

40x

4x 10x

20x 40x

4x 10x

10x 20x

40x 40x

4x

10x 40x

40x 10x

4x 20x

40x

Interactions between ANP and the renin-angiotensin-aldosterone system. Hypotension or hypovolemiatriggers release of renin from the afferent arteriole, causing the formation of angiotensin II, whichstimulates release of aldosterone from the adrenalcortex. Angiotensin II and aldosterone cause vasoconstriction and sodium retention, ultimatelyresulting in reexpansion of the intravascular volume; this causes atrial distention, which triggers release of ANP. ANP inhibits: release of renin, renin's action on angiotensinogen to form angiotensin II, angiotensin-induced vasoconstriction, stimulation of aldosteronesecretion by angiotensin II, and the actions of aldosterone on the collecting duct. Thus, the actionsof ANP promote vasodilation and sodium excretion.

Miller RD. Miller's Anesthesia. 7th ed. Churchill Livingstone, 2009 [online]Availlable at: http://www.mdconsult.com/das/book/body/170934075-7/0/2053/0.html

The cardiorenal axis, demonstrating production and release of ANP and BNP from the heart, and CNP from the endothelium, with cardiorenal protective actions. Thiscontrasts with the RAAS of renal and adrenal origin, whichhas deleterious actions in the regulation of intravascularvolume and myocardial structure and function. ANP, atrialnatriuretic peptide; BNP, brain natriuretic peptide; CNP, C-type natriuretic peptide.

Mann DL. Heart Failure: A Companion to Braunwald's Heart Disease, 1st ed. Saunders, 2009 [online].Availlable at: http://www.mdconsult.com/das/book/body/170934075-7/0/1280/0.html

4x

20x

40x