Hypertension and atherosclerosis. Cause and effect, or two effects with one unknown cause?
Hypertension is associated with an increased risk of clinical cardiovascular complications due to atherosclerosis. However, attempts to reduce that risk with antihypertensive treatment have not always been successful. Therefore, it may be significant to discuss antihypertensive treatment in view of the cellular pathogenesis of atherosclerosis. Endothelial and smooth muscle cells are found in both normal and atherosclerotic arterial tissue, but cellular characteristics appear to be affected during atherogenesis. Lymphocytes and monocytes are found primarily in the atherosclerotic lesion and may be of critical importance for both cell proliferation and lipid accumulation. In the present review, processes involved in the regulation of functional properties of the various cell populations in the atherosclerotic lesions are discussed. The significance of the smooth muscle population as a quantitatively dominating cell constituent in both the atherosclerotic lesion and in the resistance vessels of hypertensives is emphasized. Two different mechanisms possibly involved in the increase of size of the smooth muscle population are discussed. Proliferation of a stem cell population or of differentiated medial smooth muscle cells might be involved. In addition, generalized, possibly genetically determined changes in cellular reactivity to adrenergic stimuli and growth factors may be implicated. If so, hypertension and atherosclerosis might perhaps be regarded as two independent expressions of the same cellular defect. This would have implications in attempts to prevent coronary heart disease by antihypertensive drugs.
Bondjers
G
G
Wallenberg Laboratory for Cardiovascular Research, University of Gothenburg, Sweden.
Glukhova
M
M
Hansson
G K
GK
Postnov
Y V
YV
Reidy
M A
MA
Schwartz
S M
SM
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology* / Q000276:immunology; D002462:Cell Membrane / Q000502:physiology; D004730:Endothelium, Vascular / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D010641:Phenotype; D011519:Proto-Oncogenes; D015290:Second Messenger Systems / Q000502:physiology