Role of K-ATP(+) channels in regulation of systemic, pulmonary, and coronary vasomotor tone in exercising swine

The role of ATP-sensitive K+ (K-ATP(+)) channels in vasomotor tone regulati on during metabolic stimulation is incompletely understood. Consequently, w e studied the contribution of K-ATP(+) channels to vasomotor tone regulatio n in the systemic, pulmonary, and coronary vascular bed in nine treadmill-e xercising swine. Exercise up to 85% of maximum heart rate increased body O- 2 consumption fourfold, accommodated by a doubling of both cardiac output a nd body O-2 extraction. Mean aortic pressure was unchanged, implying that s ystemic vascular conductance (SVC) also doubled, whereas pulmonary artery p ressure increased almost in parallel with cardiac output, so that pulmonary vascular conductance (PVC) increased only 25 +/- 9% (both P< 0.05). Myocar dial O-2 consumption tripled during exercise, which was paralleled by an eq uivalent increase in O-2 supply so that coronary venous PO2 was maintained. Selective K-ATP(+) channel blockade with glibenclamide (3 mg/kg iv), decre ased SVC by 29 +/- 4% at rest and by 10 +/- 2% at 5 km/ h (both P< 0.05), w hereas PVC was unchanged. Glibenclamide decreased coronary vascular conduct ance and hence myocardial O-2 delivery, necessitating an increase in O-2 ex traction from 76 +/- 2% to 86 +/- 2% at rest and from 79 +/- 2% to 83 +/- 1 % at 5 km/h. Consequently, coronary venous PO2 decreased from 25 +/- 1 to 1 7 +/- 1 mmHg at rest and from 23 +/- 1 to 20 +/- 1 mmHg at 5 km/h (all valu es are P< 0.05). In conclusion, K-ATP(+) channels dilate the systemic and c oronary, but not the pulmonary, resistance vessels at rest and during exerc ise in swine. However, opening of K-ATP(+) channels is not mandatory for th e exercise-induced systemic and coronary vasodilation.