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Splanchnic metabolism of nitrogenous compounds and urinary nitrogen excretion in steers fed alfalfa under conditions of increased absorption of ammonia and L-arginine supply across the portal-drained viscera^1,2,3

S. A. Maltby, C. K. Reynolds^*,4, M. A. Lomax^,5 and D. E. Beever^,6

^* ARS, USDA, Beltsville, MD 20705; and Department of Biochemistry and Physiology, The University of Reading, Whiteknights, Reading, RG6 2AJ U.K.; and and School of Agriculture, Policy, and Development, The University of Reading, Earley Gate, Reading, RG6 6AR U.K.

	Abstract

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Effects of increased ammonia and/or arginine absorption across the portal-drained viscera (PDV) on net splanchnic (PDV and liver) metabolism of nitrogenous compounds and urinary N excretion were investigated in six catheterized Hereford x Angus steers (501 ± 1 kg BW) fed a 75% alfalfa:25% (as-fed basis) corn-soybean meal diet (0.523 MJ of ME/[kg BW^0.75•d]) every 2 h without (27.0 g of N/kg of dietary DM) and with 20 g of urea/kg of dietary DM (35.7 g of N/kg of dietary DM) in a split-plot design. Net splanchnic flux measurements were obtained immediately before beginning and ending a 72-h mesenteric vein infusion of L-arginine (15 mmol/h). For 3 d before and during arginine infusion, daily urine voided was measured and analyzed for N composition. Feeding urea increased PDV absorption (P < 0.01) and hepatic removal (P < 0.01) of ammonia N, accounting for 80% of increased hepatic urea N output (P < 0.01). Numerical increases in net hepatic removal of AA N could account for the remaining portion of increased hepatic urea N output. Arginine infusion increased hepatic arginine removal (P < 0.01) and hepatic urea N output (P < 0.03) and switched hepatic ornithine flux from net uptake to net output (P < 0.01), but numerical changes in net hepatic removal of ammonia and AA N could not account fully for the increase in hepatic urea N output. Increases in urine N excretion equaled quantities of N fed as urea or infused as arginine. Estimated salivary urea N excretion was not changed by either treatment. Urea cycle regulation occurs via a complex interaction of mechanisms and requires N sources other than ammonia, but the effect of increased ammonia absorption on hepatic catabolism of individual AA in the present study was not significant.

Key Words: Amino Acids • Arginine • Bovidae • Liver • Urea

	Introduction

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Ruminants fed legumes and cool-season grasses typically absorb a high proportion of dietary N as ammonia, which is subsequently converted to urea by the liver and either recycled to the gut via blood and saliva or excreted in the urine (Reynolds, 1992). This excretion of dietary N in the urine can represent a substantial loss of N to the environment and may increase the energy requirement for ureagenesis (Milano et al., 2000), potentially contributing to the inefficient utilization of dietary N and energy in cattle fed many forages (Beever et al., 1988; Reynolds et al., 1991) or excess protein (Tyrrell et al., 1970). In addition to potential effects on energy metabolism, it has been hypothesized that excessive ammonia aborption causes increased hepatic catabolism of AA to provide the aspartate N required for urea synthesis (Reynolds, 1992; Lobley et al., 1996; Parker et al., 1996).

Function and regulation of the urea cycle has been extensively described in rodents (Meijer et al., 1990; Waterlow, 1999), but less is known about the control of ureagenesis in ruminants (Lobley and Milano, 1997). In particular, the role of arginine has been well documented as both a cytosolic intermediate and a powerful activator of mitochondrial n-acetyl glutamate synthetase (EC 2.3.1.1). Therefore, it would be predicted that increasing arginine supply to the liver would increase the efficiency of incorporation of ammonia into carbamoyl phosphate and urea synthesis, which may ameleorate effects of ammonia on AA catabolism. Arginine infusion into the abomasum of beef heifers resulted in increased body N retention and decreased arterial concentrations of AA (Davenport et al., 1990a), responses that may have been mediated in part by changes in liver metabolism. Our objectives were to investigate effects of increased ammonia and arginine supply to the liver on N metabolism in ruminants and the implications of increased ureagenesis for splanchnic metabolism of AA and other nutrients.

	Materials and Methods

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This study was conducted with the approval of the USDA Beltsville Agricultural Research Center Animal Care Committee. Six Hereford x Angus steers (501 ± 1 kg BW) from the Beltsville beef nutrition herd were surgically prepared with chronic indwelling catheters in the portal, hepatic, and mesenteric veins and caudal aorta as described by Huntington et al. (1989). The steers had previously completed a diet comparison study (Reynolds et al., 1992) and had been catheterized at approximately 300 kg BW. The steers were kept in a tie-stall barn under constant temperature (18°C), relative humidity (60%), and light:dark cycle (16:8 h), given daily exercise when not undergoing sampling, and allowed free access to water. They were fed a pelleted diet containing 75% alfalfa:25% ground corn and soybean meal (0.523 MJ of ME/[kg BW^0.75•d]) without or with the inclusion of urea (20 g/kg of DM; Table 1). The diets were introduced gradually over a 5-d period and were fed in 12 equal meals delivered at 2-h intervals using automatic feeders. Intakes were adjusted for BW changes weekly and fixed 4 d before the start of each 6-d sampling period.

Individual blood samples were analyzed for PAH, packed cell volume, urea N, -amino N, and ammonia N (Reynolds et al., 1988a). Glutamate, glutamine, and alanine were determined enzymatically on pooled, deproteinized, neutralized blood extracts (Guerino et al., 1991), and free plasma AA were measured on deproteinized, pooled plasma using a Beckman 6300 high-performance AA analyzer (Beckman Instruments Ltd., High Wycombe, U.K.), as described by Metcalf et al. (1996). Excluding plasma AA, all blood and plasma analyses were conducted on the day of sampling. Daily urine samples were kept frozen (–10°C) until analyzed for total N content by macro Kjeldahl analysis and for urea N and ammonia N contents using previously described methods for analysis of these metabolites in blood.

Measurements were averaged for each steer during each sampling period before statistical analysis. Rates of net tissue metabolism of nutrients (mmol/h) were calculated as the product of blood or plasma flow and venous-arterial concentration difference as described by Guerino et al. (1991). Because effects of diet and arginine on net nutrient fluxes to a large extent reflect those observed in venous-arterial differences, the latter data are not presented. Positive values represent a net release or production by the tissue, and negative values represent net removal or uptake of nutrients by the tissue bed. Estimates of salivary urea N transfer to the rumen were obtained by subtracting urinary urea N excretion from total splanchnic urea N output (Huntington, 1989). As a result of an electrical power failure, one steer was not sampled during arginine infusion when the control diet was fed; thus, least squares means calculated using the GLM procedure of SAS (SAS Inst., Inc., Cary, NC) and the SEM for n = 5 are presented. In the ANOVA model used, diet period, steer, and diet were evaluated as whole-plot effects and were tested using the error mean square for their interaction, whereas the effect of subplot infusion period (arginine infusion) and arginine infusion x diet interaction were tested using the residual error mean square. Diet composition, DMI, and BW were analyzed for effects of diet using a simple crossover design and a model testing effects of animal, whole-plot period, and diet using residual error mean squares. In interpreting the results of the statistical analyses, differences were considered significant at P < 0.10 and a trend at P < 0.20.

	Results

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The steers exhibited no apparent adverse effects as a result of feeding urea or mesenteric vein infusion of arginine. Dry matter intake for the urea diet was higher due to the slightly higher DM content of this diet (Table 2). This resulted in slightly higher estimated ME intakes for the urea diet. Feeding urea increased N intake by 56 g/d compared with the control diet (Table 2). There was a small increase in average BW when urea was fed (Table 2). Although not measured, steers were observed to consume more water when fed urea. Arginine infusion decreased arterial packed cell volume (P < 0.01; Table 3), and this decrease occurred to a greater extent with the control diet (diet x arginine interaction; P < 0.04). This is likely to be more a result of blood removal during sampling than arginine infusion per se. There was no effect of diet or arginine infusion on portal vein or hepatic blood flow, and across all treatments, the contribution of portal flow to hepatic flow averaged 89% (Table 3). There was, however, a decrease in hepatic plasma flow (P < 0.05) with urea treatment that also was observed as a trend (P < 0.17) for hepatic blood flow. In addition, arginine infusion tended to increase portal plasma flow (P < 0.12). The difference in flow rate between plasma and blood values amounted on average to 31%, which was approximately equivalent to packed cell volume.

	Discussion

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Feeding urea increased direct transfer of urea N to the PDV from blood by 15.6 g/d, which, if converted to absorbed ammonia, could account for 30% of the increase in net PDV ammonia N appearance (Table 11). On average, 27.5% (±1.19) of hepatic urea N output was transferred to the PDV via blood, with little change in this proportion due to increased N intake. Ruminants also transfer urea to the rumen via saliva, the rate of which would depend on both the arterial concentration of urea and flow of saliva (Egan et al., 1984; Huntington, 1986). In the present study, there was no effect of diet on estimated daily salivary urea N excretion, although as a proportion of the hepatic output, considerably less urea was transferred to the rumen via saliva with the urea-supplemented diet (12% compared with 22% on the control diet), in spite of the increase in arterial urea concentration when urea was fed. This may be a result of an increase in ruminal ammonia concentration when urea was fed, which can inhibit salivary flow rate (Oltjen et al., 1969).

When the control diet was supplemented with urea, the liver removed an additional 51 g/d ammonia N and produced an additional 64 g/d urea N, but the increment in urea N production not accounted for by increased ammonia removal (13 g/d) was not associated with an increase in -amino N removal. As observed in previous studies (Reynolds, 1992), the net hepatic removal of ammonia N and -amino N on all treatments was less than hepatic urea N output (82 to 94%). This is due in part to the contribution of N in AA side chains to hepatic urea synthesis. Indeed, when the total N content of plasma free AA removed by liver is accounted for then measurements of net hepatic removal of ammonia and free AA N account for 108% hepatic urea N output before arginine infusion in the present study (Table 11). On an incremental basis, numerical changes in net hepatic removal of ammonia and free AA N accounted for 106% of the increase in hepatic urea N output when urea was fed. Arginine made the largest contribution to hepatic N uptake of the AA measured accounting for 45% of the numerical increase in net hepatic removal of free AA N when urea was fed, although this increase in hepatic removal of arginine was only a trend (P < 0.19). On a total splanchnic basis, free AA N release before arginine infusion was numerically decreased by feeding urea from 27 to 0 g/d (calculated from Table 11), but this change was not significant (Table 8; P = 0.21).

In contrast to the present study, 0.5-h mesenteric vein infusion of NH₄HCO₃ in sheep caused a decrease in net hepatic removal of arginine, and an increase in hepatic ornithine removal and glutamate release (Milano and Lobley, 2001), but these studies did not allow time for adaptation. With longer-term (4 d) infusions at more physiological rates (Milano et al., 2000), increased liver removal of NH₃N accounted for all of the measured increase in urea synthesis. These and other studies in vitro (Luo et al., 1995) do not support the hypothesis that excess ammonia absorption in ruminants requires AA transamination for urea synthesis (Reynolds, 1992; Parker et al., 1996). In the present study, increased ammonia absorption did not account fully for increased hepatic urea synthesis, but the requirement for additional urea N was relatively small, and there were no effects on net hepatic removal of individual AA.

The observation that when steers were fed the urea-supplemented diet, they consumed more water was con-firmed by the increase in the daily weight of urine voided. In association with this, total urinary N loss was also higher, primarily due to an increase in urea N excretion. Feeding 56 g of urea N/d increased urinary urea N excretion by 50.9 g/d and total urinary N excretion by 58.6 g/d. Thus 104% of the incremental N fed as urea could be accounted for as increased urinary N excretion with no apparent change in body N retention, assuming fecal N excretion was not affected.

The net hepatic output of glutamate was decreased by feeding urea, suggesting increased glutamate transamination to produce aspartate to support the higher rate of hepatic urea synthesis (Reynolds, 1992). Replacing soybean meal with urea in a semipurified diet fed to sheep increased the capacity of liver glutamate dehydrogenase (EC 1.4.1.3) for asparatate synthesis from glutamate (Chalupa et al., 1970), but in a similar study in calves, liver glutamate dehydrogenase activity was not affected (Salem et al., 1973). An alternative explanation for the decrease in liver glutamate release measured in the present study would be a decrease in glutamate synthesis resulting from a decrease in the ratio of NADP to NADPH due to ammonia activation of the pyrophosphate pathway (Prior et al., 1970) or by a decrease in the transamination of ornithine to glutamate (Katunuma et al., 1966; Salem et al., 1973).

Effects of Increased Arginine Absorption
Arginine is unique in that it contains four N molecules; hence, arginine infusion resulted in a substantial increase in daily N supply (20.16 g). This was not detected in the net PDV appearance of -amino N primarily because the -amino N assay only measures one of the four N supplied by arginine and because changes in the net metabolism of other AA may have opposed increases in arginine supply. However, by summation of all the net PDV fluxes of individual plasma AA, a numerical increase in the net PDV appearance of total AA was observed that was approximately equal to the amount of arginine infused (108%), and largely due to increased net PDV appearance of arginine. Arginine infusion decreased arterial concentration of a number of AA, as observed previously in growing cattle (Davenport et al., 1990a). These decreases in arterial concentrations of essential AA were accompanied by a decrease in their removal by the liver, suggesting increased utilization of these AA in other body tissues.

Arginine infusion increased net PDV removal of urea in part through increased arterial urea N concentration. Similarly, abomasal infusion of arginine increased plasma urea concentration in both sheep and beef heifers (Davenport et al., 1990a,b). Nitrogen transferred to the PDV as urea may be reabsorbed (primarily as ammonia or AA) or excreted in the feces, depending in part on the site of transfer into the gut lumen (Lapierre and Lobley, 2001). Increased PDV removal of urea N resulting from arginine infusion did not increase net PDV absorption of nitrogenous compounds measured and was not balanced by an equivalent change in calculated salivary urea N recycling. It is therefore possible that the increase in transfer of urea N from blood to the PDV increased the loss of endogenous N in the feces, although the studies of Davenport et al. (1990a, b) reported no such effect. In the present study, total net PDV release of ammonia and total AA N was equal to 70.7% of N intake as feed or infused arginine (calculated from Table 11), a proportion similar to previous measurements of the apparent digestion of the control diet fed in the present study at maintenance intake (69.6%; Reynolds et al., 1991).

Infusion of arginine increased hepatic urea N output by 17% on both dietary treatments, which amounted to 19.6 and 30.7 g of N/d on the control and urea diets, respectively. On the control diet, the increment in daily hepatic urea N output could be accounted for by the additional N infused as arginine; however, on the urea-supplemented diet, N infused as arginine could only account for 66% of the increase in hepatic urea N output. Net hepatic removal of ammonia N was unaffected by the infusion of arginine and therefore, as a consequence of the increase in hepatic urea synthesis, the maximum contribution of ammonia N to urea N was decreased with both the control (71 to 61%) and urea (75 to 66%) diets. This finding suggests that arginine infusion stimulated hepatic urea synthesis from non-ammonia sources.

Ion of L-arginine increased hepatic removal of plasma arginine; on the control diet, 72.4% of the incremental PDV appearance of arginine was removed compared with 97.8% on the urea diet. This and the trend toward increased net hepatic removal of arginine when urea was fed implies an increased arginine requirement by the liver in association with the stimulation of urea cycle activity by feeding urea. The metabolism of arginine in the liver is primarily by enzymatic cleavage to ornithine and urea as catalyzed by arginase (EC 3.5.3.1), but it is also an essential precursor of polyamines and is involved in the synthesis of creatine and guanidoacetic acid (Visek, 1979). Although only two of the N molecules of arginine are used directly for the synthesis of urea, the remainder are likely to be indirectly available through other metabolic pathways. Therefore, assuming all hepatic arginine N removed was able to contribute to urea production, it could maximally account for 74 and 59% of the increment in hepatic urea N output on the control and urea diets, respectively. Thus, on the urea-supplemented diet it was evident that despite a higher proportion of the PDV supply of arginine being removed by the liver, it accounted for a lower proportion of the increment in hepatic urea synthesis due to arginine infusion. For both diets, measurements of net ammonia and free AA N removal accounted for 97% of hepatic urea N output when arginine was infused compared with 108% before arginine infusion (Table 11). On an incremental basis, changes in net hepatic removal of ammonia and total free AA N accounted for only 33% of the increase in hepatic urea N output when arginine was infused. This finding suggests that stimulation of the urea cycle by infusing arginine increased the hepatic requirement for alternative N sources to support ureagenesis. There may have been a subtle change in the ratio of protein synthesis to protein degradation within the liver, or changes in the metabolism of export proteins or other nitrogenous compounds.

Concurrent with the increase in hepatic urea production due to arginine infusion was a switch in the hepatic flux of plasma ornithine from net removal to net output. Arginine metabolized in the cytosol as part of the urea cycle produces urea and ornithine, of which the latter is translocated across the mitochondrial membrane and reported to be channelled directly into the ornithine carbamoyl transferase (EC 2.1.3.3) complex, resulting in the production of citrulline (Cohen et al., 1989). In rats injected intraperitoneally with an exogenous load of arginine, its hepatic conversion to ornithine was shown to be both rapid and complete, as was the subsequent metabolism of the resultant ornithine (Stewart and Walser, 1980). However, in the present study, because there was no effect of arginine upon the net hepatic flux of citrulline, it suggests that ornithine metabolism to citrulline was limited under conditions of arginine-induced ureagenesis. On the basis of the stoichiometry of the urea cycle reactions, the increment in hepatic arginine removal that was apparently directly cleaved to ornithine could only account for 20% of the increment in urea N output resulting from arginine infusion.

Metabolism of ornithine by the urea cycle may be regulated either at the level of the catalyzing enzyme ornithine carbamoyl transferase or by substrate supply (carbamoyl phosphate). In vitro studies in rodents have shown that it is unlikely that ornithine carbamoyl transferase regulation would affect urea cycle activity (Meijer and Hensgens, 1982; Meijer et al., 1990). Synthesis of carbamoyl phosphate has a direct and absolute requirement for ammonia, bicarbonate, and ATP, and an indirect requirement for glutamate and acetyl CoA, which together produce n-acetyl glutamate. Arginine is an allosteric activator of the enzyme n-acetyl glutamate synthetase. Thus, assuming the additional arginine arriving at the liver was able to enter the mitochondria, n-acetyl glutamate synthetase activity should not limit the synthesis of n-acetyl glutamate, provided that adequate glutamate and acetyl CoA are available. Because arginine infusion was not associated with any increase in either net PDV absorption or hepatic removal of ammonia, it is possible that ammonia availability could limit carbamoyl phosphate synthesis, resulting in an accumulation of ornithine when arginine was infused. Thus, as suggested by early investigations of urea cycle regulation, mitochondrial ammonia may be the most important regulator of the urea cycle (Waterlow, 1999). The role of ammonia may be particularly important under conditions of increased flux through carbamoyl phosphate synthetase, as would be expected during arginine infusion.

Further evidence that ammonia may be limiting urea synthesis under arginine-stimulated conditions is the associated increase in hepatic glutamine removal. Glutamine metabolized in the liver may support the urea cycle by supplying N both as aspartate via glutamate and as carbamoyl phosphate from ammonia. Thus, assuming a maximal net contribution to hepatic urea synthesis of two N per mole of glutamine utilized, cumulatively the increment in hepatic removal of arginine and glutamine N could maximally account for 84 and 75% of the increment in hepatic urea N output during arginine infusion on the control and urea diets, respectively. However, these estimates are reduced to an average of 60% of the urea N production during arginine infusion by balancing the arginine N released as ornithine with its potential contribution to urea via glutamate in association with the potential contribution from glutamine.

It is concluded from the present study that both feeding urea and infusing arginine stimulated hepatic urea synthesis but via different mechanisms. Whereas the change in hepatic urea N output when urea was fed could be accounted for by increased hepatic removal of ammonia and AA N, increases in urea N output resulting from arginine infusion could not be totally accounted for by the increment in hepatic ammonia and AA N removal. Thus, alternative N sources not quantified in this study must have been metabolized to urea during arginine infusions. Ultimately, the additional N fed as urea or infused as arginine was excreted by the body in the urine. Therefore, although increments in N intake may equal increases in urinary N loss, the source of excreted N may not be of direct dietary origin.

	Implications

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Ruminants fed ruminally degradable nitrogen sources often absorb large amounts of ammonia, which must be detoxified, largely by conversion to urea in the liver. It has been hypothesized that excess ammonia absorption may increase the deamination of amino acids to support urea synthesis, decreasing the efficiency of dietary amino acid utilization for the production of meat and milk. Data from the present study do not support this hypothesis. These data confirm that ammonia conversion to urea requires additional sources of nitrogen for urea synthesis in the liver, but the effect on net essential amino acid supply by the splanchnic tissues is relatively small. This implies that the inefficient utilization of forages and high-protein diets is caused by factors other than ammonia absorption.

	Footnotes

 
¹ Mention of a trade name, proprietary product, or specific equipment does not constitute a guarantee or warranty by the USDA and does not imply its approval to the exclusion of other products that may be suitable.

² The authors acknowledge student sponsorship for S. A. Maltby from the U.K. Science and Education Research Council.

³ The authors gratefully acknowledge the invaluable assistance of the Beltsville Agric. Res. Center Veterinary Services and Animal Operations for animal care; D. Hucht, M. L. Miner, S. Thurber, and B. Morgan for help in obtaining and analyzing samples, and C. Pippard for amino acid analysis.

⁵ Current address: Dept. of Agric. Sci., Imperial College, Wye, Kent, TN25 5AH, U.K.

⁶ Current address: Richard Keenan & Co., Borris, Co. Carlow, Ireland.

⁴ Correspondence and current address: Dept. of Anim. Sci., The Ohio State Univ., OARDC, 1680 Madison Ave., Wooster 44691-4096 (phone: 330-263-3793; fax: 330-263-3949; e-mail: Reynolds.345 @osu.edu).

Received for publication April 21, 2004. Accepted for publication January 25, 2005.

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