Review
Copyright ©The Author(s) 2015.
World J Nephrol. Nov 6, 2015; 4(5): 500-510
Published online Nov 6, 2015. doi: 10.5527/wjn.v4.i5.500
Figure 2
Figure 2 Pathophysiologic mechanisms of hypertension in chronic kidney disease. A: Volume overload is associated with increase in cardiac output (CO) which ultimately leads to hypertension; B: Increase in total peripheral resistance (TPR) due to systemic vasoconstriction leads to hypertension; C: Arterial tunica media calcification causing vascular stiffening and failure of vasodilatation and vasoconstriction are illustrated. Chronic hyperparathyroidism promotes vascular wall mineralization or calcification leading to vascular stiffening and increase in TPR with consequent hypertension. Blood pressure = CO × TPR. RAAS: Renin-angiotensin-aldosterone system; ANG II: Angiotensin II; ET-1: Endothelin 1; PTH: Parathyroid hormone.