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The Cause of High Blood Pressure Revealed By Computer Modelling

Computer simulations show that high blood pressure can be entirely explained by arterial stiffening as we age, say researchers

High blood pressure dramatically increases the risk of a stroke or heart attack and so is one of the biggest silent killers in the Western world.

But while there are several known mechanisms that cause high blood pressure, some 90% of cases are entirely unexplained. Physicians believe that various factors increase the risk of high blood pressure, such as age, family history, lack of exercise and so on. But the actual mechanism that causes the increase is hotly debated.

Today, Klas Pettersen at the Norwegian University of Life Science and a few pals say they have solved the mystery. These guys have created a computer model of the way that major blood vessels stiffen as they age and say this process can entirely account for the measured increases in the population in general.

When measured, blood pressure is usually given as the ratio between the systolic and diastolic pressures. The former is the pressure when the heart forces blood into the vascular system. The latter is the lower pressure that occurs when the heart refills.

In most people, the systolic blood pressure rises throughout their lives. By contrast the diastolic blood pressure tends to remain constant or begins to decline after middle age. The result is that many people over the age of 50 experience an increase in pulse pressure.

The human body has a well understood mechanism for monitoring blood pressure changes, consisting of sensors embedded in the major arterial walls that monitor changes in pressure and then trigger other changes in the body to increase or reduce the pressure as necessary, such as the regulation of the volume of fluid in the blood vessels. This is known as the baroreceptor reflex.

So an interesting question is why this system does not respond appropriately as the body ages. Why, for example, does this system not reduce the volume of fluid in the blood to decrease the pressure when it senses a high systolic pressure in an elderly person?

The theory that Pettersen and co have tested is that the sensors in the arterial walls do not directly measure pressure but instead measure strain, that is the deformation of the arterial walls.

As these walls stiffen due to the natural ageing process, the sensors become less able to monitors changes in pressure and therefore less able to compensate.

The computer model that these guys have developed simulates this stiffening and how much it ought to increase blood pressure as a result of the body’s inability to compensate. That gives them a model of how blood pressure ought to increase with age.

They then compare the simulated results with the actual numbers from large-scale population surveys such as the Framingham Heart Study which has measured the way blood pressure changes in thousands of people for the last 60 years.

Pettersen and co say their model exactly reproduces the observed changes in blood pressure. “We demonstrate quantitatively that arterial stiffening seems sufficient to explain age-related emergence of hypertension,” they say.

That’s an important result with significant implications for future treatments blood pressure. “The results support the view that a major target for treating chronic hypertension in the elderly is the reestablishment of a proper baroreflex response,” say Petterson and co.

An interesting possibility is that the machinery for blood pressure monitoring in the body is entirely intact in people who suffer high blood pressure. It’s simply the stiffening that’s the problem.

So the target for therapy ought to be the arterial stiffening. Reduce this and the ordinary process of blood pressure regulation ought to kick in again. Just how this can be done, is the million dollar question, of course.

If Pettersen and colleagues are correct, this gives other researchers an important goal to concentrate on for future treatments.

Ref: arxiv.org/abs/1305.0727: Arterial Stiffening Provides Sufficient Explanation for Primary Hypertension

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