Researchers studying how hypertension increases the risk of heart attacks and strokes have discovered a remarkable way in which the body adapts to hypertension by developing a set of \u201cnew senses\u201d. <\/p>\n
The study, conducted by experts in Translational Health Research at the University of Bristol and published today (Tuesday 26 August)\u00a0in \u2018Circulation Research\u2019, could have important implications for developing new therapies to counter the elevated risk of cardiovascular events among people diagnosed with high blood pressure.\u00a0<\/p>\n
Prior to this study, it remained unknown why people on antihypertensive medications were able to successfully reduce their blood pressure and yet remained at high risk of a major cardiovascular event even where they adhered to medication protocols and observed a healthy lifestyle.\u00a0\u00a0<\/p>\n
Researchers from Bristol Medical School surmised from these studies \u2013 one drawing on a large European populace, the other focused on Korea \u2013 that hypertension in these cases may have been merely a symptom rather than the underlying cause of a life-threatening heart attack or stroke.\u00a0<\/p>\n
The answer, as discovered by this latest study, lies in the brain, specifically abnormal activity in the sympathetic nervous system, which is responsible for the body\u2019s flight or fight response to stress.\u00a0\u00a0<\/p>\n
In healthy individuals, this system oversees a variety of functions including elevating the body\u2019s blood pressure and heart rate as a normal response to exercise. However, according to earlier research in a separate study, hypertensive patients\u2019 sympathetic activity does not decrease at rest and is on average 1.5X greater compared to those without hypertension.\u00a0<\/p>\n
In order to pinpoint why that is the case, Bristol\u2019s Professor David Murphy worked with Professor Julian Paton from the University of Auckland turned to the mechanism controlling sympathetic activity in an experimental model of hypertension.\u00a0<\/p>\n
\u201cOne such mechanism is the arterial chemoreflex which continuously monitors our blood for oxygen and sends a powerful signal to the brain to stimulate breathing and make our heart pound, say when we dive or start running out of breath under water,\u201d explains Dr Audrys Pauza, who contributed to the study as part of his PhD and is a lead author on the paper.\u00a0<\/p>\n
\u201cWe found that instead of acting as a quiescent monitor of blood oxygen as it ordinarily does, that very same reflex becomes continuously active in hypertension, leading to chronically elevated sympathetic nerve activity. We found that one of the reasons for this is that the arterial chemoreflex develops new senses to respond to hormone signals circulating in the bloodstream as a result of hypertension.\u201d\u00a0<\/p>\n
The study is the first to describe how the arterial chemoreflex is activated by the melanocortin system, which is traditionally associated with skin pigmentation and the body\u2019s response to stress.\u00a0<\/p>\n
Crucially, the Bristol study adds to the body of work showing that when this reflex is inhibited in hypertensive state, both blood pressure and sympathetic activity is reduced. This work opens an unprecedented opportunity to finally temper the overactive sympathetic drive that fuels cardiovascular risk in hypertension.\u00a0\u00a0<\/p>\n
Audrys now aims to translate these pre-clinical findings to patients living with hypertension, and to ascertain exactly why the arterial chemoreflex becomes sensitive to melanocortin hormones.\u00a0<\/p>\n
\u201cInitiated during my time in Bristol, this study has been a major catalyst for my career and I\u2019m delighted to see the results finally published,\u201d said Audrys, who undertook part of the research during his BHF-funded 4-year PhD programme at Bristol. He has since relocated to New Zealand, where he continues his research with support from the National Heart Foundation of New Zealand, the Health Research Council, and the Partridge Family Foundation.\u00a0<\/p>\n
Paper<\/p>\n