Researchers investigate how fat causes high blood pressure (hypertension) and they say the findings could one day help identify which obese people, and maybe some lean ones too, are at risk for high blood pressure.

The researchers have found that deleting or mutating the gene PTP1B puts mice at risk for high blood pressure by interfering with an endogenous mechanism that should help prevent it.

"In a normal individual gaining weight, PTP1B should increase and they would be protected in theory from hypertension," says Dr. David Stepp, the study's corresponding author.

"But if you don't have a good copy of PTP1B and you become obese, then you are going to have a problem. So in theory this gene can segregate the obese people who will become hypertensive and those who won't."

A key player is the hormone leptin, produced by fat cells. Overweight individuals generally produce more of the hormone that essentially revs up the body, suppressing appetite and increasing metabolism so you won't get fatter. But leptin also increases blood pressure by activating the sympathetic nervous system, the so-called fight-or-flight response. Mutated or missing PTP1B dramatically increases leptin's negative effects.

Scientists studying how blood pressure got the message to increase found leptin also provides protection against high pressures by turning off the signaling pathway that squeezes blood vessels and drive pressures up in a process called adrenergic desensitization.

"Normally, if you give someone leptin, his blood pressure would probably not go up because he would have this protective mechanism intact that would basically turn off his blood pressure signaling pathway," Dr. Stepp says. "His blood pressure would be regulated differently, but it would not be high."

But the combination of missing or mutated PTP1B and too much leptin means increases in constriction are too strong to turn off.

Mice missing PTP1B tend to have lower body fat but high blood pressure, not usually what you see in people, Dr. Stepp notes. While this single gene can't explain every combination of body size and blood pressure found in nature, it could help explain why some skinny people are hypertensive and why others who get fat are as well.

"It's a vulnerability gene," he says. "If you stimulate leptin in individuals who can't activate their protective mechanisms, they are going to get high blood pressure.”

And what about those people who have great blood pressure? They likely have well-functioning PTP1B, he notes. Interestingly, PTP1B often is over expressed in obese people, which is good for the blood pressure but bad for leptin's positive effect on metabolism.

"I think we have identified at least a couple of new pieces of information that clarify the relationship between obesity and hypertension," Dr. Stepp says. "We have identified a gene that, if it's not functional, will greatly increase the extent to which a metabolic signal from leptin translates into a cardiovascular signal. We also have identified a protective mechanism that, if it's not working, contributes to hypertension."

Now the scientists want to develop markers so one day people determine their PTP1B expression through a blood test.

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References:
1. David W. Stepp,, et al. Protein Tyrosine Phosphatase 1B, a Major Regulator of Leptin-Mediated Control of Cardiovascular Function. Circulation. 2009;120:753-763. doi: 10.1161/CIRCULATIONAHA.109.853077.

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