The selfish brain hypothesis of high blood pressure 
(Seminars)
3 May 2011
4 - 5pm
Venue: Room 505, Building 501, Faculty of Medical and Health Sciences, Grafton Campus, The University of Auckland
A special Physiology–Bioengineering research seminar by Professor Julian Paton, Professorial Research Fellow in Physiology, School of Physiology and Pharmacology, University of Bristol
Why is blood pressure 120/80 mmHg (mean 93 mmHg)? And, how is this level maintained to ensure it does not dip to cause fainting or rise triggering a stroke? These questions are topical yet remain controversial. The enormity of the question is reflected by the inability to drug-control BP in approximately 23% of patients with hypertension. Does this suggest we do not fully understand what controls blood pressure? Whilst the heart and kidneys play a role in BP regulation, we believe this is not the whole story. Our idea is that brain blood flow itself determines the ‘set-point’ of blood pressure. A mean blood pressure of ~90 mmHg provides optimal perfusion of our organs, particularly the brain - being the most vital.
Exceptionally, the upright adult giraffe has an aortic pressure of 280 mmHg, which is needed to overcome gravity and provide the critical perfusion pressure of 90 mmHg at the base of the brain. Intriguingly, in many hypertensive patients and hypertensive rodent models cerebral vascular resistance is high. Is this a consequence of high pressure or is it causal? Contrary to current dogma, I believe the latter.
In my lecture, I will provide proof-of- principle evidence to support the notion that a reduction in blood flow to the brain triggers hypertension: the selfish brain hypothesis. I will present a new structural model of the vertebrobasilar circulation and explain how, through iterative interactions, this may guide experiments aimed at re-modelling the vertebrobasilar circulation to normalise vascular conductance. I will discuss putative underlying mechanisms that may cause the increased vascular resistance in the posterior cerebral circulation that are not a consequence of high arterial pressure. These will include raised sympathetic nerve activity and vasculo-neural inflammation, both of which are present before hypertension develops. I will end by discussing some novel ideas on alternative treatment strategies for hypertension.
