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Vasoconstrictor responses to norepinephrine were determined during constant flow perfusion with warm Krebs solution in dog mesenteric arteries. The arteries were then stored 20−24 hours at 3°C in one of the following isosmotic solutions: Krebs, complex K (KC1, CaCl2, KHCO3 and glucose), NaCl, KCl, sucrose, or mannitol. After storage, arteries were again perfused with warm Krebs solution, and vasoconstrictor responses to norepinephrine compared to prestorage control responses. Tissue levels of Na+ and K+ were determined before cold storage and after 0−35 minutes of poststorage perfusion with warm Krebs solution. Storage of arteries in mannitol or sucrose solution reduced their Na+ and K+ content, and during poststorage perfusion with warm Krebs solution their responsiveness gradually improved as they rapidly (within 5 minutes) regained Na+ and slowly regained K+. Arteries stored in NaCl solution were initially more responsive than those stored in electrolyte- free solutions during poststorage perfusion with warm Krebs solution, and their responsiveness also improved as they regained K+. Arteries cold-stored in K+ containing media (KCl and complex K solutions) quickly regained Na+, and their responsiveness exceeded prestorage values with 11 minutes of poststorage perfusion with warm Krebs solution. Since these data indicate that artery responsiveness may be related to tissue levels of both Na++ and K+ efforts were made to establish minimal levels of each ion required for “normal” responsiveness. The critical level of Na+ appears to be approximately 30 μEq Na/g dry weight; the minimal effective K+ content is apparently near 20 μEq K/g dry weight. If arteries contain at least minimal levels of K+ and an excess (over 100 μEq/g) of Na+ the magnitude of theft responses to vasoconstrictor stimuli is exaggerated

Influence of Sodium and Potassium Content on Arterial Responsiveness