Potential role of potassium as a determinant of morbidity and mortality in patients with systemic hypertension and congestive heart failure.

Prehistoric animals and humans consumed a diet low in sodium but high in potassium, and thus, evolutionary forces fostered the development of physiologic systems that conserved sodium and excreted potassium. With the advent of civilized societies, food cooking and processing have greatly increased the sodium but decreased the potassium content of the diet. However, there has been little time for physiologic systems to adapt. The resulting excess of sodium has been implicated as an important factor in the development of hypertension and congestive heart failure. This traditional focus on sodium has ignored the potential role that an inadequate dietary intake of potassium might play in the degenerative diseases of the heart, brain and kidney. Yet dietary potassium may be as powerful a determinant of cardiovascular morbidity and mortality as dietary sodium. In experimental and clinical hypertension, an increased intake of potassium (without a change in dietary sodium) can reduce blood pressure, may suppress the activity of the sympathetic nervous and renin-angiotensin systems, and can prevent the development of vascular injury; conversely, potassium depletion has been associated with an increase in stroke and sudden death. In patients with chronic heart failure, potassium can modify both the mechanical and electrical properties of the heart, it can exert diuretic effects, and it can reduce the frequency and complexity of potentially lethal ventricular tachyarrhythmias. Given this central role, the effects of many pharmacologic interventions on the morbidity and mortality of patients with hypertension or chronic heart failure can be enhanced or diminished by the effect that these treatments might have on potassium homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)