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We tested the hypothesis that potassium ion (K+) is involved in the local control of the coronary circulation. The left coronary artery was perfused at constant flow in closed-chest, anesthetized dogs. Step increases in heart rate caused transient (six dogs) or sustained (three dogs) increases in coronary sinus plasma [K+] averaging 0.53 mEq/liter. When the effects of vascular transit delay were accounted for, we found that [K+] changes preceded the vasodilation seen with increased heart rate. We used a mathematical model to calculate changes in interstitial [K+] from arterial and venous [K+] and K+ release rate. The magnitude of the changes in interstitial [K+] appeared to be sufficient to account for a considerable portion but not all of the initial changes in coronary vascular resistance associated with increased heart rate. Thus potassium seems to be involved at least transiently, and, in three of nine dogs, for a more sustained period, in heart rate-induced coronary vasodilation. Cessations (for 15 seconds) of coronary blood flow resulted in transient postischemic increases of coronary sinus [K+] averaging 0.55 mEq/liter. In this case, correction for vascular transit disclosed that the recovery of [K+] preceded the return of vascular tone to baseline for only the second half of the recovery, implying only a limited role for potassium in this response. Potassium appears to play a significant but transient role in the local control of the coronary circulation.

The role of potassium in the metabolic control of coronary vascular resistance of the dog.