Abstract
Hypertension and cerebral artery: Hypertensive damage of cerebral artery occurs in the densely innervated artery; brain base vascular nets and perforating arteries, and is characterized by medial cell necrosis (moth-eaten cell atrophy and necrosis). The pilar circumflex artery, which has less frequent innervation than the perforating artery, is not involved with hypertension. A hypertensive cerebral hemorrhage is not induced by the rupture of a microaneurysm (angionecrosis), but is due to a direct rupture at the bifurcation of a hypertensively involved perforating artery. The microaneurysm indicates a recanalisation state after a subclinical rupture of a small artery less than 200μ in diameter. Hypertension may also accelerate a lipid accumulation in the intima even in the arterioles of the perforating branches demonstrating both a luminal narrowing by intimal thickening and/or dilation due to medial cell necrosis. The former causes cerebral thrombosis in the basal ganglia, while the latter loses a vascular function by earthen pipe phenomenon in the artery. They can, thus induce a disturbance of the autoregulation system regarding intracerebral circulation. As a result, leukoaraiosis occurs and extends to the white matter of the cerebrum (Bin-swanger type dementia).
Hypertension and the coronary artery: As for atherogenesis, hypertension is suppressed in the coronary artery, but coronary spasms frequently occur in variant angina which histologically reflects the adventitial inflammation of coronary artery located in the subepicardium. Accumulated inflammatory cells (lymphocytes and monocyte/macrophages) may also directly stimulate medial smooth muscle cells, and/or do so through the vascular nerve fibers in adventitia where they are densely distributed. Repeated coronary spasms may also accelerate atherosclerosis in the intima by an increased insudation of the same artery.
Hypertension and renal artery: Hypertensive vascular damage occurs in the interlobular and afferent arteries measuring 50-100μ in diameter, which are densely innervated by adrenergic & cholinergic fibers, demonstrating with either medial cell necrosis or moth-eaten atrophy. Those changes thus result in a reduced autoregulation system for glomerular circulation, and may also induce glomerulosclerosis by both ischemic and glomerular hypertension (hyperfiltration) mechanisms.
