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F₀F₁ ATP synthase activity is differently modulated by coronary reactive hyperemia before and after ischemic preconditioning in the goat

¹Sezione di Fisiologia, Dipartimento di Neuroscienze and Dipartimento di Scienze Cliniche e Biologiche, Università di Torino, 10100 Turin; ²Dipartimento di Scienze e Tecnologie Biomediche and Centro di Eccellenza Microgravity, Aging, Training, and Immobility, Università di Udine, 33100 Udine; and ³Dipartimento di Medicina, Chirurgia, e Odontoiatria, Università di Milano, 20100 Milan, Italy

Submitted 6 April 2004 ; accepted in final form 22 June 2004

The amplitude of coronary reactive hyperemia (CRH), elicited by 15 s of ischemia, is reduced in hearts subjected to 5 min of ischemic preconditioning (IP). F₀F₁ ATP synthase activity and ATP concentration are also altered by IP. We hypothesized that F₀F₁ ATP synthase is differently modulated by the inhibitor protein IF₁ during CRH elicited before (CRH_np) and after (CRH_prec) IP. Hemodynamic parameters were recorded in 10 anesthetized goats. Myocardial biopsies were obtained before IP (C_np), during CRH_np, 4 and 6 min after the onset of CRH_np, after IP (C_prec), during CRH_prec, and 4 min after CRH_prec. F₀F₁ ATP synthase activity, ATP concentration, and ATP-to-ADP ratio (ATP/ADP) were determined. Compared with CRH_np, IP blunted CRH_prec. F₀F₁ ATP synthase activity transiently increased during CRH_np, decreased 4 min after CRH_np, and returned to control 2 min later; it was lower after IP (C_prec) and did not change during and after CRH_prec. All these changes in activity were modulated by IF₁. During CRH_np, ATP concentration and ATP/ADP were reduced compared with C_np and began to rise 6 min thereafter. During C_prec, both parameters were transiently reduced but increased during and after CRH_prec. Hence, during CRH_np, F₀F₁ ATP synthase activity transiently increases and then decreases significantly. The short-lasting inhibition of the enzyme may explain why a few seconds of occlusion do not induce IP. After IP, F₀F₁ ATP synthase activity is blunted, and it is not affected by a subsequent 15 s of occlusion, which induces a blunted CRH_prec. These results suggest that postischemic long-lasting inhibition of F₀F₁ ATP synthase activity may be a feature of the preconditioned heart. The increase in ATP concentration after preconditioning is in agreement with previous reports of reduced ATP hydrolysis by cytoplasmic ATPases.

coronary circulation; energy metabolism; ischemia; mitochondria

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