Rat arterial muscle cells show an elevated Ca 2+ -dependent K + efflux during the established phase of hypertension. This association of enhanced K + efflux with high arterial pressure implies that changes of in vivo blood pressure can alter the level of K + channel current in arterial membranes. We directly tested this hypothesis by comparing K + current density between patch-clamped aortic muscle membranes of normotensive Wistar-Kyoto (WKY) rats, spontaneously hypertensive rats (SHR), and SHR treated with the angiotensin-converting enzyme inhibitor ramipril (3.5 mg/kg per day PO) to normalize blood pressure. Peak macroscopic K + current was measured during progressive depolarizing steps (10 mV) from -60 and +60 mV in cells diaryzed with pipette solution containing 10" 6 mol/L calcium to amplify Ca 2+ -dependent K + current. With the use of this approach, maximum K + current density in aortic muscle membranes of untreated SHR was 2.6-fold higher than in untreated WKY rats (SHR, 31 ±3 pA/pF; WKY, 12±1 pA/pF) C alcium-dependent K + efflux is increased in arteries from genetic and renal rat models of established hypertension.1 -6 It has been proposed that this enhanced K + current is a consequence of high blood pressure and is a compensatory mechanism activated during the development of hypertension to counteract arterial excitability and prevent further vasoconstriction. 79 However, increased arterial K + current has been described only in the established phase of hypertension, 5 and there is little direct evidence to link changes in blood pressure amplitude with dynamic modulation of K + current levels in arterial muscle membranes.To explore the relation between blood pressure changes and arterial K + current density, we compared K + current density between patch-clamped aortic muscle cell membranes of adult spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto (WKY) rats, and SHR after antihypertensive treatment with the angiotensin-converting enzyme inhibitor ramipril. In addition, parallel measurements of tension were recorded in isolated vessel rings to determine whether K + current suppressed aortic contraction in these preparations. Thus, we investigated for the first time whether a potential link exists between blood pressure regression and modulation of K + current in arterial muscle membranes of hypertensive rats.From the Department of Physiology, Medical College of Wisconsin, Milwaukee.Correspondence to Nancy J. Rusch, PhD, Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, Wl 53226. and was predominantly blocked by 2 mmol/L tetraethylammonium. K + current density in SHR aortic membranes was unchanged after 1 week of ramipril therapy, but it was reduced 42% (to 18±1 pA/pF) after 2 weeks of treatment. Parallel tensionrecording studies showed that untreated SHR aortic segments but not aortic segments from WKY rats or ramipril-treated SHR constricted strongly after block of Ca 2+ -dependent K + channels by tetraethylammonium. Our findings imply...