Mechanosensory cilia as microcompartments. Primary cilia are mechanosensory compartments that house many sensory proteins. Activation of these compartments through the sensory machineries will generate a cascade of various proteins activation, which results in nitric oxide production. CaM, calmodulin; PKC, calcium-dependent protein kinase; eNOS, endothelial nitric oxide synthase. Figure was adapted from [22].

Mechanosensory cilia and nitric oxide production. The presence of cilia in vasculature plays an important role in the biochemical production of a potent vasodilator, nitric oxide (NO). The figure depicts the production of NO in an artery. Increases in blood pressure, which are translated to higher vascular shear stress, will be sensed by mechanosensory cilia. Bending or activation of the cilia involves mechanosensory polycystin-1 and polycystin-2 complex and a cascade of biochemical synthesis of NO. The cascade will further involve extracellular calcium influx (Ca²⁺), followed by activation of various calcium-dependent proteins, including calmodulin (CaM) and protein kinase C (PKC). Akt/PKB, CaM, and PKC are important downstream molecular components to activate endothelial nitric oxide synthase (eNOS). This figure is reproduced with permission [23].

RAAS regulation in polycystic kidney disease. Renal cysts are thought to compress and disrupt the vascular network in the kidney. The kidney would then become ischemic, which would induce renin release from the juxtaglomerular apparatus. The increase in renin secretion could accelerate the conversion of angiotensinogen to angiotensin I, which is converted by angiotensin-converting enzyme (ACE) to angiotensin II. Activation of angiotensin receptor (AT₁) would initiate cascades of physiological responses that would lead to hypertension.