GROWTH, NITROGEN-METABOLISM, AND CARDIAC RESPONSES TO CLENBUTEROL ANDKETOCLENBUTEROL IN RATS AND UNDERFED CATTLE

Two beta-adrenoceptor agonists, clenbuterol and ketoclenbuterol, were examined for their effects on growth and cardiac tissue. In female rat s, clenbuterol caused a 48% increase in weight gain (P < .05), with im proved feed efficiency (26%; P < .1) and increased muscle mass (9%; P < .1). Ketoclenbuterol had less effect on weight gain (30%) and feed e fficiency (16%) and did not increase muscle mass. Next we studied the adverse cardiovascular effects of these compounds. Neither drug increa sed the force of contraction of isolated rat ventricular papillary mus cle. Clenbuterol was potent at causing an increase in the rate of cont raction of isolated rat atria, and when fed to cattle over 2 d, the dr ug caused heart rate to increase by 92 to 117%. In contrast, ketoclenb uterol was not a potent stimulator of atrial rate in the rat, and in c attle it caused a smaller increase in heart rate than clenbuterol (12 to 27%). Finally, cattle that were underfed to simulate dry-season tro pical pasture conditions were treated with clenbuterol or ketoclenbute rol for 35 d. Ketoclenbuterol caused no beneficial changes in N metabo lism. The results obtained with clenbuterol were equivocal, and might have been confounded partly by the refusal of some treated animals to eat all the feed offered. Although clenbuterol did not cause a reducti on in total urinary N output relative to control animals, marked reduc tions in plasma urea concentrations and in urea synthesis were observe d (23 to 53%; P < .001). We conclude that ketoclenbuterol is not effec tive for attenuation of dry-season protein loss in cattle. Clenbuterol seems to be less effective in underfed cattle than in well-fed cattle , and further evidence is required to judge whether compounds of this nature are likely to benefit tropical cattle under harsh grazing condi tions.