Monitoring vascular sclerosis in hypertension: a new window of opportunity.

The pressure with which circulating blood is contained in the arterial circulation is related to a number of factors. Prominent among these is the structure of resistance vessels, or arterioles, and conduit vessels, or arteries. For a normal intravascular volume and cardiac output, pathological distortions in arteriolar structure are accompanied by intravascular pressures greater than the expected norm. Such abnormalities include endothelial cell hyperplasia; intimal hyalinization; vascular smooth muscle cell hypertrophy and/or hyperplasia; and increased vessel wall collagen, including its adventitia, here referred to as a perivascular fibrosis. Subsequent to such arteriolar remodeling and rise in arterial pressure are iterations in conduit vessel structure. This includes medial thickening and increased concentrations of collagen and elastin in arteries and the aorta. Arteriolosclerosis and arteriosclerosis, a thickening and hardening of arterioles and arteries, respectively, of systemic organs, such as kidney, heart, brain, and eyes, account for and sustain arterial hypertension. Such arteriolar and arterial remodeling is associated with increased risk of adverse cardiovascular events, including myocardial infarction, heart failure, and stroke. Effective monitoring of arteriolosclerosis and arteriosclerosis would have important clinical applications. An example addresses vascular remodeling in response to pharmacological intervention that offers potential as either a cardioprotective or cardioreparative strategy.