Cerebral vascular bed in hypertension and consequences for the brain
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The internal carotid artery of spontaneously hypertensive rats and stroke-prone spontaneously hypertensive rats has a thicker media than that of normotensive Wistar Kyoto rats as early as 15 days of age; furthermore, the media-to-lumen ratio is increased in the larger pial arteries. Since several studies have indicated that the mean arterial pressure is slightly elevated in spontaneously hypertensive rats during the early postnatal period, these vascular alterations may to some extent be related to an increased pressure load. However, it seems likely that pressure-independent genetic factors are also involved. In adult spontaneously hypertensive rats the media-to-lumen ratio in the cerebral arteries is increased over a large spectrum of vessel sizes, including the brain basal arteries. The cortical surface arteries, measured through a closed cranial window in vivo, have a smaller inner diameter in spontaneously hypertensive rats than in Wistar Kyoto under resting conditions as well as during hypercapnic vasodilation. In the relaxed cerebrovascular bed the cerebral blood flow is lower in spontaneously hypertensive rats than in Wistar Kyoto at the same perfusion pressure, which is probably due mainly to a decreased internal radius in spontaneously hypertensive rats. Since the blood flow is proportional to the fourth power of the luminal radius, the lumen reduction of cerebral arteries in spontaneously hypertensive rats and stroke-prone spontaneously hypertensive rats is a potential risk factor under conditions of impending ischemia such as systemic hypotension or distal to an arterial occlusion. On the other hand, the increased media-to-lumen ratio reduces the arterial wall tension, increases the capacity to autoregulate at high blood pressure levels, and protects the blood-brain barrier.