Blood pressure normally follows a circadian pattern: it rises during the day and falls by roughly 10–20% during sleep, a dip known as nocturnal dipping. This dip gives the vasculature and heart a period of reduced load. Sleep restriction disrupts it in two ways. First, the sympathetic nervous system remains active when it should be withdrawing, keeping heart rate and peripheral vascular resistance elevated through the night. Second, the cortisol rhythm is flattened and shifted, so the normal late-night cortisol trough is shallower. Together these keep blood pressure higher during the hours it should be lowest.
Repeated night after night, the elevated nocturnal load does not simply disappear in the morning. Sustained sympathetic tone and higher vascular resistance promote structural changes in the arterial wall, including increased stiffness and hypertrophy of the left ventricle, which in turn sustain higher baseline blood pressure. This is the pathway from acute nightly elevation to chronic hypertension.
Two changes from the previous chapter feed into the same pathway. Reduced insulin sensitivity and the resulting compensatory hyperinsulinemia promote sodium retention and sympathetic activation, both of which raise blood pressure. Chronic low-grade inflammation, marked by elevated CRP and IL-6, damages the vascular endothelium and accelerates atherosclerosis. The three pathways — sympathetic, metabolic, and inflammatory — converge on the same outcome: sustained hypertension and accelerated vascular disease.