Abstract
BackgroundWe have previously shown that there is a novel control pathway between physiological levels of intracranial pressure (ICP) and blood pressure via the sympathetic nervous system. Increases in ICP of up to 20 mmHg over a 30‐minute infusion period were matched by increases in mean arterial pressure such that cerebral perfusion pressure remained constant. However, whether this ‘intracranial baroreflex’ is altered in hypertension is not known. Hence, in the present study we tested the hypothesis that the intracranial baroreflex is attenuated in a group of hypertensive animals.MethodsExperiments were conducted in two groups of adult ewes which either underwent unilateral renal artery clipping for three weeks (n=6) or sham surgery (n=6). Three weeks later, the mean arterial pressure and renal blood flow response to intracerebroventricular infusion of saline was determined.ResultsIntracerebroventricular infusion of saline produced a ramped increase in ICP of up to 20 mmHg over a 30‐minute infusion period (baseline 4.3±1.1 mmHg) in the normotensive group of animals. The ICP increase was matched by an increase mean arterial pressure in the normal animals such that cerebral perfusion pressure remained constant. Direct recordings of renal blood flow indicated that renal blood flow did not change but renal vascular conductance decreased with increasing ICP. In the hypertensive group, while intracerebroventricular infusion of saline produced similar ramped increases in ICP, the increase in mean arterial pressure was significantly attenuated such that cerebral perfusion pressure decreased. Administration of the ganglionic blocker, hexamethonium, prior to the infusion of saline abolished the increase in blood pressure in both groups.DiscussionIn conclusion, we have shown that the ‘intracranial baroreflex’ ensures increases in mean arterial pressure during physiological increases in intracranial pressure to maintain cerebral perfusion. This reflex is attenuated in hypertension.Support or Funding InformationHealth Research Council of New Zealand
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