Dietary sodium chloride and potassium have effects on the pathophysiology of hypertension in humans and animals.

A diet high in NaCl can raise blood pressure in susceptible people and animals, probably by similar mechanisms. The possibly harmful effects of a high-NaCl diet are not unexpected because both prehistoric humans and mammals evolved in a low-NaCl environment. Evolutionary forces molded mammals to adapt well to a low sodium intake; modern high NaCl intakes go against this adaptation. A high-NaCl diet can cause premature mortality by raising blood pressure in susceptible people. We have new evidence that in hypertension, a high-NaCl diet can cause a great increase in mortality even though it does not cause a further blood pressure rise, partially because of multiple small cerebral infarcts. Recent evidence also indicates that a high-potassium diet reduces the rise of blood pressure caused by a high-NaCl diet, whereas a low-normal potassium intake encourages an NaCl-induced blood pressure rise. The combination of a tendency by the kidneys to retain NaCl together with a high NaCl intake can produce a blood pressure rise. This combination tends to cause NaCl retention, which can trigger blood pressure rises in susceptible humans and animals. Such blood pressure rises can augment renal NaCl excretion and regain the previous NaCl balance. In Dahl salt-sensitive rats several renal abnormalities encourage sodium retention. By analogy, renal "abnormalities" are probably present in people susceptible to hypertension.