The finding of a rat study backs the theory that hypertension could arise from problems in the blood vessels of the brain.
Up to 60 per cent of patients with hypertension continue to have a high BP after treatment, say the researchers from the University of Bristol.
Their research centres on a molecule called junctional adhesion molecule-1 (JAM-1) that is believed to obstruct blood flow through vessels in the brain.
JAM-1 forms part of the tight junction between endothelial cells lining blood vessels, making it part of the blood–brain barrier.
The researchers found that JAM-1 was overexpressed in the brain stem of rats genetically engineered to have hypertension.
The latest study compared levels of JAM-1 messenger RNA (mRNA) in rats that were spontaneously hypertensive and normal rats.
Higher levels of JAM-1 mRNA were found in a number of brain areas, particularly in the nucleus tractus solitarii area of the brain stem, which is known to affect arterial pressure. This region had nearly three times the level of JAM-1 mRNA in hypertensive than control adult rats.
When normal rats were induced to overexpress JAM-1, systolic BP increased from 120 to 132mmHg.
Lead researcher Professor Julian Paton, head of cardiorespiratory research, said: ‘We are concerned that something is altering in the brain that is causing high BP.’
Overexpression of JAM-1 may cause hypertension by inducing inflammation of the blood vessels or because the molecule traps leukocytes in the blood vessels. This could obstruct blood flow and lead to poor oxygen uptake in the brain.
‘We know that if you make a brain ischaemic you cause high BP. The reason is that the brain is selfish and it’s trying to shunt blood flow to itself,’ explained Professor Paton.
The researchers are now examining brain tissue from people who have died from hypertension to measure levels of JAM-1 expression.
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