Acute increases in arterial blood pressure, beyond the autoregulatory capacity of cerebral blood vessels, produce an increase in cerebral blood flow, passive dilatation of cerebral arterioles and venules, and disruption of the blood-brain barrier (BBB). Stimulation of sympathetic nerves during acute hypertension attenuates the increase in cerebral blood flow and protects the BBB. It has been assumed that the protective effect of sympatheic stimulation is accomplished by constriction of large cerebral arteries, protecting downstream arterioles and capillaries. We have found, however, that sympathetic stimulation does not attenuate increases in pial arteriolar pressure accompanying acute hypertension. We now suggest that the protective effect of sympathetic stimulation may be accomplished by attenuation of increases in pial venous pressure. In chronic hypertension, blood pressure is sufficiently elevated that one might expect an increase in cerebral blood flow and disruption of the BBB. However, cerebral blood flow is normal and the BBB is intact in chronic hypertension. Protection of the cerebral circulation during chronic hypertension is accomplished in part by a trophic effect of sympathetic nerves, which promotes hypertrophy of cerebral blood vessels. Vascular hypertrophy attenuates increases in microvascular pressure accompanying hypertension. Thus, stimulation of sympathetic nerves protects cerebral vessels during acute hypertension, perhaps by attenuation of increases in cerebral venous pressure, and a trophic effect of sympathetic nerves promotes vascular hypertrophy and protect cerebral vessels during chronic hypertension.
|Original language||English (US)|
|Issue number||1 II SUPPL. 1|
|State||Published - 1987|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)