Figure 5.

A model for a mechanistic explanation of chronic dietary salt loading increases the blood pressure in prenatal hypoxia rats. Although functional number of Cav1.2 channel expression in mesenteric arterial myocytes from salt‐loading and prenatal hypoxia offspring (HHS) was reduced, the depolarization of resting membrane potential (E_m) and decreased of transient hyperpolarizations (THs) in HHS cells led to down‐regulated inhibition of Cav1.2 channels, resulting in increasing of resting vascular tone, leading to hypertension in salt‐loading offspring with prenatal hypoxia. BK, large‐conductance calcium‐activated K⁺; Cav1.2, L‐type voltage‐gated Ca²⁺; I_Kv, voltage‐gated K⁺ channel current; K_V, voltage‐gated K⁺.