Arterial muscle contraction and potassium movement in vitro

¹ Department of Physiology, University of Michigan, Ann Arbor, Michigan

Rings of dog carotid 2–3 mm in width were placed in a physiological salt solution, equilibrated, under 1 g of tension, at 37 C for 2 hr and were then stimulated electrically or with epinephrine, or norepinephrine. Tension development was recorded. At given time intervals following stimulation, rings were removed and analyzed for potassium content. Maximum loss of potassium, averaging 10% of original content, occurred 5–15 min after electrical stimulation. After stimulation by either epinephrine or norepinephrine a consistent slight increase in potassium content occurred. Thus net potassium efflux (and membrane depolarization?) is not an essential part of vascular muscle contraction in response to catecholamine stimulation. The reported loss of potassium from artery wall following catecholamine stimulation in vivo suggests another, perhaps indirect, action of these agents.