Editor's Note: This article was originally written by Charles Whitcomb, M.D.
High blood pressure has been related to salt intake for over two thousand years. Chinese physicians described "Hardening of the pulse" after excessive salt ingestion in their writings before the time of Christ. Salt restriction has been a cornerstone of hypertension management for a century, and diuretics (which increase sodium excretion through the kidney) remain a mainstay in the treatment of hypertension. What is it about sodium and high blood pressure?
Blood pressure is defined by the relationship between the amount of blood ejected from the heart with each heartbeat and the resistance against which it ejects. Systolic blood pressure is the peak pressure generated by the volume of blood ejected and diastolic pressure the pressure in blood vessels during the period between heartbeats (the time the heart fills with blood between beats is called "diastole"). The cardiac output is determined by the amount of blood in the heart at the beginning of a beat and so is dependent on the total blood volume.
The physiologist Arthur Guyton postulated the theory of "pressure natriuresis". It basically states that every patient with high blood pressure has a disorder of salt handling by the kidney. The appropriate response to increased blood pressure is increased salt excretion through the kidney. The subsequent reduction in blood volume would lead to reduced blood pressure. A large body of experimental data does indeed point to abnormal salt excretion by the kidney as an important component of human hypertension.
Sodium is the primary determinant of blood volume. Salt restriction (or diuretic treatment) reduces blood volume-this is one way to lower pressure. In the last decade another mechanism by which sodium increases blood pressure has been described. A family of compounds called glycosides is produced by the brain and the adrenal gland in response to increased sodium. These compounds stimulate the smooth muscle cells in the walls of blood vessels to contract and thereby increase vascular resistance. So salt gets your blood pressure up both by increasing blood volume (and cardiac output) and increasing vascular resistance.
Finally salt plays a role in the way that some of the most commonly used drugs for hypertension lower blood pressure. ACE (angiotensin converting enzyme) inhibitors and ARBs (angiotensin receptor blockers) work by inhibiting the action of angiotensin. The level of angiotensin and its metabolic partners is inversely related to blood volume and to salt excretion. Hence, diuretics (which are very commonly used in fixed dose combination with ACE inhibitors and ARBs) raise the level of angiotensin and by doing so increase the effectiveness of these drugs. On the flip side, angiotensin stimulates the kidney to absorb more sodium. This is a common reason for these drugs to lose their efficacy in blood pressure control.
The role of salt restriction in blood pressure management was tested in the landmark DASH trial. This trial performed in the 1990s conclusively demonstrated that salt restriction lowered blood pressure by up to 8-10 mm Hg. There was a close relationship between the degree of sodium restriction and the amount of blood pressure reduction. In that same era the largest hypertension trial ever performed-ALLHAT-suggested diuretics were as good as any other class of drugs in reducing the vascular complications of high blood pressure.
Recent findings have suggested that while salt restriction remains a reasonable non-drug strategy diuretics may not be optimal therapy for all patients. The recently reported ACCOMPLISH trial looked at the benefit of adding a diuretic to ACE inhibitor therapy (see above) versus adding the vasodilator drug amlodipine (formerly Norvasc) in reducing heart attack and stroke. This trial was stopped before completion due to better event reduction in the patients receiving the ACE inhibitor/amlodipine. This study adds to the controversy over whether "new" treatments for hypertension (ACE inhibitors and their cousins and calcium channel blockers) are better at reducing vascular events than "old" therapies-- beta blockers and diuretics.
So be careful with that salt shaker-and maybe also with those diuretics.