Endurance training increases natriuretic peptide synthesis in the hypertrophied myocardium of spontaneously hypertensive rats. We examined the effects of 22-week-long treadmill exercise on plasma and tissue atrial natriuretic peptide in Zucker rats, a model of genetic obesity and moderate hypertension without clear cardiac hypertrophy. The blood pressures of the animals were measured by the tail-cuff method, and plasma and tissue samples for the peptide determinations were taken at the end of the study. The training increased heart weight to body weight ratio, while atrial natriuretic peptide contents in the right and left atrium, ventricular tissue, and plasma did not change. The exercise prevented the elevation of blood pressure, which was observed in non-exercised obese Zucker rats, and also reduced blood pressure in the lean rats. In conclusion, these results suggest that in the absence of preceding myocardial hypertrophy, the long-term exercise-induced workload is not deleterious to the heart in experimental obesity, since no changes in plasma and tissue atrial natriuretic peptide were detected.The prevalence of hypertension is high among overweight persons (Landsberg 1992), and physical activity is recommended as a non-pharmacological measure for the treatment of hypertension and obesity (World Hypertension League 1991). The Zucker fatty rat is a well-established model of genetic obesity with autosomal recessive homozygous inheritance (fa/fa), the heterozygous and missing fa gene (Fa/?) producing the corresponding slender control strain, the lean Zucker rat (Argilès 1989). The fatty mutation is characterized by insulin resistance, hyperinsulinaemia, glucose intolerance, hyperlipidaemia (Argilès 1989), and often by the development of moderate hypertension (Kurtz et al. 1989;Baylis et al. 1991;Zeigler & Patel 1991;Kasiske et al. 1992). However, the obese Zucker rat does not show clear left ventricular hypertrophy (Cox & Kikta 1992).The myocardium adapts to increased workload by muscle cell hypertrophy, molecular changes in contractile proteins, and increased synthesis of atrial natriuretic peptide (Ruskoaho 1992). Under normal physiological circumstances, the major site of atrial natriuretic peptide synthesis is in the atria, but under pathophysiological conditions associated with chronic pressure or volume overload, ventricular atrial natriuretic peptide gene expression is also activated (Ruskoaho 1992). Plasma atrial natriuretic peptide has been shown to rise during acute dynamic exercise (Ruskoaho et al. 1989;Schmidt et al. 1990;Vuolteenaho et al. 1992), but even a 55-week-long treadmill exercise does not increase Author for correspondence: Ilkka Pörsti, Medical School, University of Tampere, Department of Pharmacological Sciences, FIN-33014 Tampere, Finland (fax π358 3 215 6170, e-mail ilkka.porsti /uta.fi).plasma atrial natriuretic peptide at rest, or the gene expression of atrial natriuretic peptide in the ventricles of normotensive dogs (Mäntymaa et al. 1994). In contrast, endurance training...