For decades, you’ve heard the advice: Cut down on salt because it’s bad for your heart — not to mention your kidneys and other organs.
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But if you follow health news, you know recent research has questioned this conventional wisdom. Several studies show evidence that if you are otherwise healthy, taking drastic measures to reduce salt in your diet may not reduce your risk of heart disease. Some studies even suggest an extremely low-salt diet can do more harm than good.
Does that mean you should pick up a salt shaker and apply generously? Not so fast. The key phrase above is “otherwise healthy.”
For example, if you have high blood pressure (hypertension), you may not need to cut out salt entirely, but how much sodium you eat may still matter. New research from the Lerner Research Institute is shedding light on this mysterious connection.
The sodium-hypertension mystery
Sodium is essential for your body, partly because of its ability to regulate retention of water. This gives it a major role in controlling blood volume and pressure.
“Even if salt intake may be less of a risk than we used to think, there’s still plenty of reasons for people with hypertension to pay close attention.”
Paul DiCorleto, PhD
Lerner Research Institute
But the balance is delicate. Eating too much salt can lead to fluid retention, which has a relationship to blood pressure. However, scientists previously have known little about exactly how this works at a molecular level.
Sadashiva Karnik, PhD, along with colleagues at Cleveland Clinic and the University of Southern California, recently discovered a possible explanation.
Dr. Karnik and team study the hormone angiotensin. Angiotensin helps regulate your blood pressure when it binds with a “receptor” called AT1R and turns it on. The AT1R molecules in cells of your kidneys continuously regulate the level of sodium in the blood. This relationship can be overactive in some people, which leads to high blood pressure.
There’s hope in the form of drugs called AT1R blockers (losartan, for example). True to their name, these drugs block angiotensin from binding with AT1R — and thereby keep blood pressure lower. To make these drugs even more effective, researchers want to understand the molecular structure of AT1R.
That’s exactly what Dr. Karnik and his team have done. In their research, they uncovered the exact structure of AT1R.
But they also made a surprising discovery along the way: AT1R binds not only to angiotensin, but also to sodium. This knowledge suggests — for the first time — that AT1R serves as a sensor of the sodium level in the blood.
What the discovery means for patients
Knowing AT1R’s exact structure offers plenty of possible benefits.
First, it should help drug companies fine-tune AT1R blockers for lowering blood pressure. Second, these types of drugs are also in clinical trials for treating heart failure, diabetic neuropathy, aortic aneurysms and Marfan syndrome. People with hypertension aren’t the only ones who stand to benefit.
But the sodium discovery is a major bonus, even if it wasn’t the team’s primary goal. As Dr. Karnik notes, understanding the connection between sodium and activation of AT1R may help explain whether — and why — salt in our diets affects high blood pressure.
Too much sodium might change your body’s sodium excretion processes at a molecular level. The next step will be further research to explore this change and find out how exactly to reset the sodium sensor function of AT1R in hypertensive patients.
Stay tuned. Even if salt intake may be less of a risk than we used to think, there’s still plenty of reasons for people with hypertension to pay close attention.