Relation of hypertension, lipids, and lipoproteins to atherosclerosis

Abstract

The evidence of work by many investigators lends further support to the concept that atherosclerosis is a multifaceted disease that may be accelerated by the presence of hypertension and hyperlipidemia. The results of experiments on rats suggest that hypertension alone or hyperlipidemia under certain selected conditions can induce atherogenesis. Genetic factors play an important role both in the laboratory rat and in the human being in establishing the serum lipoprotein pattern and lipid concentration. Genetic factors also may be important in determining blood pressure. Studies on the spontaneously hypertensive rat showing the importance of the genetic factor have been described in detail. Lipid and lipoprotein deposition in the arterial wall is accelerated by increased blood pressure, and if the plasma lipid and lipoprotein concentrations are also high, the process is further accelerated. Vascular permeability may be altered by the action of numerous hormones including renin, angiotensin, epinephrine, and norepinephrine, and thus may accelerate the passage of lipids into the arterial wall. Serum lipoprotein concentrations also may be greatly affected by hormonal actions, including that of growth hormone, insulin, various steroids, angiotensin, epinephrine, and norepinephrine, and by physical activity. Quality and quantity of diet, including minerals consumed (especially NaCl), also may play an important role. Neurological factors may affect not only lipid and lipoprotein levels, but also blood pressure. Evidence that is slowly accumulating suggests that atheromatous lesions may regress if the precipitating factors, including hypertension and hyperlipidemia, are controlled.