Table 3.

Pathogenesis of hypertension in PKD.

Theories	Descriptions
Inherent cardiovascular dysfunction (Figure 2)	(i) Ciliopathy (ii) Endothelial dysfunction (iii) Nitric oxide synthase dysfunction (iv) Increased sympathetic nerve activity
Secondary to renal cystic formation (Figure 3)	(i) Compression of renal vasculature releases renin (ii) Renin converts angiotensinogen to angiotensin (iii) Activation of angiotensin receptor will induce:
	(1) Vasoconstriction
	(2) Sensitivity to catecholamines
	(3) Salt retention, and so forth.