Cerebrovascular Abnormalities Supporting the Selfish Brain Hypothesis of Human Hypertension

Abstract

The selfish brain hypothesis of hypertension suggests that brainstem hypoperfusion triggers increased sympathetic activity (SNA) and blood pressure (BP) as a mechanism to maintain cerebral perfusion. We assessed: 1) prevalence of anatomical variations in the posterior cerebral circulation, which may cause brainstem hypoperfusion, 2) relationships of SNA to cerebral vascular resistance (CVR) in hypertensive (HTN) vs normotensive (NTN) humans. The vertebral arteries (VA) and Circle of Willis (CoW) were imaged in 121 HTN (MR angiography). VA hypoplasia (VAH), defined as <2mm diameter, together with CoW morphology were compared to known standards in >50 NTN. In a cohort of HTN (n=50) and NTN (n=40), muscle SNA (MSNA, microneurography), blood flow in the internal carotid arteries (ICA) and VA (MR phase contrast), and BP were recorded.Prevalence of VAH and incomplete posterior CoW was higher in HTN vs NTN (51 vs 27% and 62 vs 38%, p<0.05). Of the posterior CoW variants, complete disconnection of anterior/posterior CoW was higher in HTN (31 vs 10%, p<0.05). Prevalence of having both VAH and incomplete posterior CoW variant was higher in HTN vs. NTN (38 vs 10%, p<0.05). Total CVR and CVR in VA was higher in HTN vs. NTN (2.6 ±0.1 vs 1.1±0.1 and 9.5±0.1 vs 6.7±0.1 mmHg/mL/dl.tissue/min). CVR was related to MSNA in both groups (HTN; r=0.40, NTN; r=0.38, P<0.05). CVR was more closely related to MSNA in the VA vs ICA in HTN (r=0.40 vs r=0.30, P=0.05).The higher prevalence of VAH and incomplete posterior CoW may cause the observed increase in CVR in HTN. The higher CVR in the posterior circulation was linked to higher MSNA in HTN, supporting the hypothesis of brainstem hypoperfusion as a driver of neurogenic hypertension.BHF.