Objective: Brainstem neurovascular contact (NVC) may interfere with central autonomic regulation and contribute to essential hypertension. We have previously shown that patients with autosomal-dominant hypertension, brachydactyly, and NVC feature extreme phenylephrine hypersensitivity due to impaired baroreflex buffering. We tested the hypothesis that similar abnormalities are present in patients with essential hypertension who have NVC.
Methods: Six patients with NVC and essential hypertension and five patients with NVC and monogenic hypertension and brachydactyly were studied. Responses to incremental phenylephrine doses were assessed before and during ganglionic blockade with trimethaphan.
Results: Supine blood pressure was 172 +/- 8.8/89 +/- 6.1 mmHg before ganglionic blockade. Blood pressure decreased 47 +/- 5/18 +/- 3 mmHg with trimethaphan (16 +/- 4.4/4 +/- 4.0 mmHg in autosomal-dominant hypertension, P < 0.05). Before ganglionic blockade, 25 microg phenylephrine increased systolic blood pressure 17 +/- 4 mmHg in patients with essential hypertension and 30 +/- 3 mmHg in patients with autosomal-dominant hypertension (P < 0.05). During ganglionic blockade, the same dose increased systolic blood pressure 32 +/- 1 and 33 +/- 4 mmHg in patients with essential and with autosomal-dominant hypertension, respectively (NS).
Conclusions: Phenylephrine hypersensitivity due to baroreflex dysfunction is uncommon in patients with essential hypertension and NVC. This finding may suggest that the effect of NVC on autonomic regulation is heterogeneous. An alternative explanation is that radiological NVC is not necessarily functionally relevant.