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Ghrelin Plays a Minor Role in the Physiological Control of Cardiac Function in the Rat

Department of Experimental and Environmental Medicine and Biotechnology (A.T., E.B., R.A., I.B., F.B., V.L.), University of Milano-Bicocca, 20052 Monza, Italy; Institute of Pharmacological Sciences (G.R.), University of Milano, 20129 Milano, Italy; Department of Biomedical Sciences and Biotechnology (G.T., D.C.), University of Brescia, 25100 Brescia, Italy; and Europeptides (R.D.), 95108 Argenteuil, France

Address all correspondence and requests for reprints to: Dr. Antonio Torsello, DIMESAB, University of Milano-Bicocca, via Cadore 48, 20052 Monza, Italy. E-mail: antonio.torsello{at}unimib.it.

We have previously reported that a 7-d pretreatment with hexarelin, a synthetic ligand of the GH secretagogue receptor (GHS-R), largely prevented damages induced by ischemia and reperfusion in isolated rat hearts. Our aim was to ascertain whether ghrelin, an endogenous ligand of the GHS-R, is physiologically endowed with cardioprotective activity. Hypophysectomized rats were treated in vivo for 7 d with either ghrelin (320 µg/kg) or hexarelin (80 µg/kg), and their hearts were subjected in vitro to the ischemia and reperfusion procedure. Ghrelin was far less effective than hexarelin in preventing increases in left ventricular end-diastolic pressure (15% and 60% protection for ghrelin and hexarelin, respectively), coronary perfusion pressure (10% and 45% reduction), and release of creatine kinase in the heart perfusate (15% and 55% reduction). In the second experiment, normal rats were passively immunized against ghrelin for 21 d before the ischemia and reperfusion procedure. In these isolated hearts, the ischemia-reperfusion damage was not significantly increased compared with control rats. After hypophysectomy, CD36 mRNA levels significantly increased, whereas those of atrial natriuretic factor significantly decreased. We conclude that: 1) ghrelin plays a minor role in the control of heart function; and 2) hexarelin effects are mediated in part by the GHS-R and largely by interactions with the CD36.

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