Cerebral metabolism and its relationship with sympathetic nervous activity in essential hypertension

Abstract

To examine Dickinson's hypothesis in mild essential hypertension, in which neurogenic mechanisms are believed to be particularly relevant, by combining measures of cerebral oxygen consumption with the concurrent assessment of sympathetic nervous activity. Twenty-five untreated essential hypertensive subjects and 28 healthy age-matched volunteers underwent direct blood sampling using percutaneously inserted catheters advanced into the internal jugular vein, with cerebral blood flow scans to differentiate between cortical and subcortical venous drainage of the brain. Venoarterial blood gas measurements and internal jugular vein blood flows were used to calculate cerebral respiratory quotients and cerebral oxygen utilization. The total body rate of noradrenaline spillover into plasma was measured to assess relationships between cerebral oxidative metabolism and sympathetic nervous activity. Compared with controls, the hypertensive subjects exhibited reductions in internal jugular vein blood flow (482 +/- 29 versus 410 +/- 15 ml/min), cerebral oxygen consumption (27 +/- 2 versus 23 +/- 1 ml/min) and cerebral oxygen supply (93 +/- 6 versus 78 +/- 3 ml/min). The cerebral respiratory quotients were identical (1.00 +/- 0.04 in normotensives and 0.98 +/- 0.03 in hypertensives). Technetium blood flow scans revealed that the reductions in internal jugular blood flow and cerebral oxygen consumption in the hypertensive patients were confined to cortical brain regions. Cortical blood flow was quantitatively linked to the matching respiratory quotient and oxygen consumption, neither of which bore any relation to the level of sympathetic nervous activity. The spillover of noradrenaline into the plasma for the body as a whole did not differ between the two groups. In accord with Dickinson's hypothesis, we have established a reduction in internal jugular vein blood flow and cerebral oxygen utilization in hypertension. These reductions were confined to cortical brain regions. However, cerebral respiratory quotients in our hypertensive study group were no different from those in our controls, suggesting that glucose remained as the major cerebral metabolic substrate in hypertension. We were not able to establish a link between cerebral metabolism and blood pressure or sympathetic nervous activity in mildly hypertensive patients.