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The presence of alpha2-adrenoceptors in membranes from omental and s.c. adipose tissue from gilts and barrows was shown in saturation binding assays with [3H]yohimbine. Four trials tested effects of alpha2-adrenoceptor antagonists (A2AA) on plasma concentrations of NEFA and urea nitrogen (PUN). In Trial 1, barrows were given i.v. injections of saline, 200 microg/kg BW of one of three A2AA (efaroxan, idazoxan, or RX821002), or 25 microg/kg BW of isoproterenol. Concentrations of NEFA were measured in plasma harvested every 15 min from 1 h before to 2 h after treatment. Compared with results for saline-treated pigs, areas under the curve (AUC) for NEFA were increased (P < .05) by efaroxan, RX821002, and isoproterenol. In Trial 2, barrows received i.v. doses of saline, efaroxan (200 or 400 microg/kg BW), or RX821002 (200 or 400 microg/kg BW). Levels of NEFA were quantified in plasma obtained at 15-min intervals through 2 h after treatment. Among pigs treated with RX821002 at 400 microg/kg BW, mean NEFA AUC was more than three times greater (P < .05) than that for saline-treated animals. Trial 3 tested whether NEFA responses to A2AA were due to direct effects on alpha2-receptors or involved beta-adrenoceptor mediation. Pigs were first treated i.v. with saline or propranolol (1 mg/kg BW). One hour later, pigs were treated i.v. with RX821002 (400 microg/kg BW) or the beta-adrenoceptor agonist cimaterol (25 microg/kg BW). Compared to values for pigs treated with saline at both injections, NEFA AUC among pigs treated with saline at the first injection and RX821002 at the second doubled (P > .05). Plasma NEFA AUC among pigs treated with saline then cimaterol rose nearly fourfold (P < .05) compared with saline-treated controls. Mean NEFA AUC among propranolol-treated pigs was similar to values for saline-treated pigs, suggesting beta-adrenoceptor involvement in the effect of A2AA on NEFA. In Trial 4, pigs were treated s.c. 10 times at 8-h intervals with saline, RX821002 (400 microg/[kg BW x injection]), cimaterol (20 microg/[kg BW x injection]) or recombinant porcine somatotropin (rpST; 1 mg/[pig-injection]). After the 10th treatment, only cimaterol increased NEFA AUC compared to saline-treated controls (P < .05). Mean PUN AUC was reduced by RX821002 and rpST compared to controls; PUN among rpST-treated pigs was lower than that among RX821002-treated pigs (P < .05). In summary, A2AA increase lipolysis in swine by potentiating lipolytic effects of endogenous catecholamines on beta-adrenoceptors. Reduced PUN suggests improved nitrogen efficiency may result from treatment with A2AA.

We studied the effects of alpha2-adrenoceptor antagonists (A2AA) on nitrogen (N) partitioning. The diets fed contained 19.8% CP and 1.15% lysine. Pigs were fed the diet as a percentage of BW equaling approximately 90% of voluntary intake. In Trial 1, pigs (n = 11/treatment) were fed a basal diet and injected s.c. at 8-h intervals for 11 d with saline, RX821002 (25 mg/injection), or cimaterol (.6 mg/injection). Compared to saline-treated pigs, urinary N, as a percentage of N eaten, decreased among pigs injected with RX821002 (15%, P < .05) or cimaterol (17%, P < .05). In Trial 2, pigs got saline (n = 6) or 25 mg RX821002 (n = 6) as s.c. injections three times daily, or they were fed a diet containing 150 ppm RX821002 and injected thrice daily with saline (n = 6) for 11 d. The RX821002 lowered apparent DM and N digestibility (P < .05). Compared to controls, RX821002 lowered urinary N, as a percentage of N eaten, 15 and 18% when given by injections or per os, respectively, but effects were not significant. Trial 3 evaluated the effects of RX821002 fed at levels of 0 (n = 6), 37.5 (n = 5), 75 (n = 6), or 150 ppm (n = 6). Contrasts showed linear dose-dependent decreases in gain and apparent N digestibility (P < .05). Compared to untreated controls, urinary N, expressed as a percentage of N consumed, decreased 2, 12, and 10% among pigs fed diets with 37.5, 75, or 150 ppm RX821002, respectively, but effects were not significant. Trial 4 compared N balance in pigs (n = 6/treatment) fed basal diet or diet with 100 ppm RX821002 to that of pigs fed diets with 25 or 100 ppm yohimbine. Treatments reduced apparent N and DM digestibility (P < .05). Urinary N, as a percentage of N consumed, decreased 16 (P > .05), 18 (P < .05), and 24% (P < .05) for 100 ppm RX821002, 25 ppm yohimbine, or 100 ppm yohimbine, respectively. Data from Trials 2, 3, and 4 from control pigs (n = 18) or pigs fed A2AA (all A2AA sources and doses; n = 41) were pooled and analyzed. Feeding A2AA decreased apparent N and DM digestibility (P < .01). The fact that fecal moisture content was higher in pigs fed A2AA suggests rate of digesta passage increased and offers an explanation for reduced N and DM digestibility in treated pigs. Despite adverse effects of A2AA, efficiency of postabsorptive N metabolism increased. As a percentage of N consumed and compared to control pigs, urinary N decreased 15% (P < .01) and retained N increased 12% (P < .05) in animals fed A2AA. Data from these studies show net efficiency of N metabolism is improved in swine given A2AA.