Abstract
We have previously shown that elevations in intracranial pressure (ICP) within physiological ranges in normotensive animals increase arterial pressure; termed the intracranial baroreflex. Hypertension is associated with alterations in reflexes which maintain arterial pressure however, whether the intracranial baroreflex is altered is not known. Hence, in the present study, we tested the hypothesis that in hypertension, physiological increases in ICP would not be accompanied with an increase in arterial pressure. Renovascular hypertension was associated with no change in heart rate, renal blood flow or ICP levels compared to the normotensive group. ICV infusion of saline produced a ramped increase in ICP of 20 ± 1 mmHg. This was accompanied by an increase in arterial pressure (16 ± 2 mmHg) and a significant decrease in renal vascular conductance. ICV infusion of saline in the hypertensive group also increased ICP (19 ± 2 mmHg). However, the increase in arterial pressure was significantly attenuated in the hypertensive group (5 ± 2 mmHg). Ganglionic blockade abolished the increase in arterial pressure in both groups to increased ICP. Our data indicates that physiological increases in ICP lead to increases in arterial pressure in normotensive animals but this is severely attenuated in renovascular hypertension.
Highlights
Arterial pressure Heart rate Intracranial pressure Cerebral perfusion pressure Renal blood flow Renal vascular conductance interested in the response of the contralateral kidney to hypertension
The increase in Intracranial pressure (ICP) was accompanied by an increase in arterial pressure; the magnitude of which was almost matched to the increase in ICP (16 ± 2 mmHg)
Clipping of the renal artery was associated with a significant increase in arterial pressure but there was no change in baseline heart rate or renal blood flow to the contralateral kidney (Table 1)
Summary
ICV infusion of saline in the hypertensive group increased ICP over the 30-min infusion period to similar levels as the normotensive group (19 ± 2 mmHg). The attenuated increase in arterial pressure meant that cerebral perfusion pressure decreased in the hypertensive group during the ICV saline infusion. Ganglionic blockade abolished the increase in arterial pressure in the normotensive group to increased ICP and was associated with a significant decrease in cerebral perfusion pressure (Fig. 5). Similar to the normotensive group, ganglionic blockade abolished the increase in arterial pressure and this meant cerebral perfusion pressure decreased in response to the ICV infusion of saline in the hypertensive group. Baroreflex mediated increases in arterial pressure led to significant decreases in heart rate and renal blood flow. The change in arterial pressure with ICV infusion was lower and there were no significant changes in heart rate or renal blood flow during the ICV infusion
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