Experiments were performed to evaluate the effects of dietary available phosphorus (aP) and PTH infusion rates on avian urinary inorganic phosphate (Pi) excretion. In experiment I, female domestic fowl were fed diets containing low (0-45%) or high (0·83%) aP for 2–4 weeks prior to renal function studies. Pi excretion was significantly higher for birds fed the high-aP diet than for birds fed the low-aP diet. PTH was infused (60–240 units kg body mass−1 h−1) unilaterally into the renal portal system. Para-aminohippuric acid (PAH), included in the unilateral infusate as a marker for effective renal portal perfusion, indicated that PTH must have been delivered to the peritubular surfaces of the infused kidney. However, bilateral but not unilateral phosphaturia occurred, and there were no significant differences in the phosphaturic responses to PTH when low-and high-aP diet treatment groups were compared. In experiment II, PTH was infused at rates of l–5 units h−1. Infusing PTH at 5 units h−1 caused a unilateral increase in urine flow but the phosphaturic response was still bilateral. It appears unlikely that unilateral renal portal PTH infusions can be used to trigger unilateral phosphaturia in domestic fowl.

The renal handling of inorganic phosphorus (Pi) has been studied extensively in mammals and birds. Plasma Pi undergoes glomerular filtration and can be reabsorbed by a proximal tubular Na+/Pi cotransport system (Renfro & Clark, 1984; Gmaj & Murer, 1986). Parathyroid hormone (PTH) inhibits Pi reabsorption, leading to increased Pi excretion (Wideman & Braun, 1981; Wideman, 1984b; Hammerman, 1986). In addition to tubular reabsorption, conclusive evidence exists for a tubular Pi secretory mechanism in birds, although there is no compelling evidence for a Pi secretory flux in mammals (Levinsky & Davidson, 1957; Martindale, 1973; Wideman et al. 1980; Wideman & Braun, 1981; Wideman, 1984a). PTH stimulates avian Pi secretion, but the source of the secreted Pi is not known, and the secretory mechanism does not appear to transport Pi directly from peritubular blood into the tubular lumen (Wideman & Braun, 1981; Wideman, 1984b, 1987). Current evidence suggests intracellular phosphate pools within the kidneys serve as a source for secreted Pi (Wideman, 1984a, 1987).

To evaluate direct effects of PTH on avian tubular Pi transport, several investigators have exploited a technique described by Sperber (1946). In birds, venous blood returning from the leg can enter the renal portal circulation, suffusing the peritubular surfaces of proximal and distal tubules (Wideman et al. 1981). By infusing substances into the portal system of one kidney, ipsilateral (portal-infused) and contralateral (control) kidney function can be compared to identify direct tubular responses (Sperber, 1946). Using this technique, Levinsky & Davidson (1957) and Buchanan (1961) reported unilateral increases in Pi excretion and unilateral net Pi secretion during renal portal infusions of parathyroid extract (PTE). This model potentially could be highly useful for evaluating mechanisms of tubular Pi transport and as a bioassay for endogenous avian PTH. However, in a more recent study both exogenous PTH infusion and endogenous PTH from parathyroid tissue transplanted into the thigh muscle of one leg failed to stimulate unilateral phosphaturia (Kissell & Wideman, 1985). The explanation for these discrepancies remains unclear, but may be related to dietary levels of available phosphorus (aP), hormone infusion rates, or the tubular efficiency for extracting PTH from peritubular blood (Kissell & Wideman, 1985).

Dietary aP significantly influences both basal and PTH-induced Pi excretion in mammals. Using a variety of techniques, low-and high-aP diets have been shown to decrease and increase, respectively, urinary Pi excretion (Sutton et al. 1978; Kempson & Turner, 1979; Shah et al. 1979; Stoll et al. 1979a,b;,Barrett et al. 1980; Bonjour & Fleisch, 1980; Mizgala & Quamme, 1985; Gmaj & Murer, 1986). Micropuncture studies indicate this mammalian renal adaptation to dietary aP occurs primarily in proximal tubules (Muhlbauer et al. 1977; Ullrich et al. 1977; Brazy et al. 1980; Knox et al. 1982; Pastoriza-Munoz et al. 1983), where Pi reabsorption and secretion have both been reported to occur in birds (Laverty & Dantzler, 1982). Differences in dietary aP are known directly to alter urinary Pi excretion in domestic fowl (Wideman et al. 1985), so the possibility clearly exists that such adaptation may alter the phosphaturic responses obtained during unilateral renal portal infusions of PTH.

Additionally, the rate and duration of PTH infusion may affect the phosphaturic response to unilateral renal portal infusions of PTH. Levinsky & Davidson (1957) infused PTE at rates of 3 or 5 units h−1 in 2–2·5 kg domestic fowl, resulting in unilateral phosphaturia (3 units h−1) and unilateral net Pi secretion (5 units h−1). These investigators suggested that higher PTE infusion rates may obscure any unilateral effect as systemic blood levels of PTH become sufficiently elevated to have an equally phosphaturic impact on the contralateral kidney (Levinsky & Davidson, 1957). Subsequently, Buchanan (1961) reported bolus injections of 150 units of PTE caused unilateral phosphaturia. However, Kissell & Wideman (1985) infused exogenous PTH at a rate of 1 unit kg body mass−1 min−1 and observed bilateral but not unilateral phosphaturia. The objectives of the present study were to evaluate the effects of dietary aP on basal and PTH-stimulated Pi excretion, to evaluate the effects of PTH infusion rate and duration of PTH infusion on Pi excretion, and to manipulate these variables in an attempt to stimulate unilateral net Pi secretion.

Experimental animals

In experiment I, female Single Comb White Leghorns (SCWL) were raised on commercial grower ration (approximately 0·5 % aP) and were given water ad libitum. At 8 weeks of age, they were randomly divided into two groups and were fed diets containing either low (0·45%) or high (0·83%) levels of aP. The diets were formulated to have similar levels of protein, methionine, calcium, sodium, potassium, vitamins, metabolizable energy and trace mineral premix. Samples of each diet were analyzed to confirm total phosphorus and calcium levels (low: 0·55% total P, 1·1% Ca2+; high: 0·93% total P, 0·9% Ca2+). These diets were fed ad libitum until the birds reached 10–12 weeks of age, when renal function studies were performed. In experiment II, SCWL cockerels were raised on commercial grower diet (approximately 0·5 % aP) ad libitum until 14 weeks of age, when renal function studies were performed.

General surgical procedure

A surgical plane of anesthesia was maintained throughout each experiment by injecting birds intramuscularly with allobarbital (Dial, quarter strength, 3·5 ml kg−1, Ciba Pharmaceutical). Additionally, 2% lidocaine was injected as a supplemental local anesthetic at all incision sites. An anterior tibial vein was cannulated for unilateral infusion into the renal portal system. A carotid artery was cannulated for arterial blood sampling. The ureters were prepared as previously described to allow separate urine sample collection from the left and right kidneys (Wideman & Braun, 1982). A wing (brachial) vein was cannulated for systemic intravenous infusion.

Experimental protocol

In experiment I, control solution containing 2·5% mannitol, 200 mg 100 ml−1 para-aminohippuric acid (PAH) and 200 mg 100 ml−1 inulin was infused unilaterally at a rate of 0·2 ml kg body mass−1 min−1 during a 30-min equilibration period. Urine sample collection began during control solution infusion (three consecutive 10-min clearance periods), followed by infusion for 120 min with the same solution containing either 5 or 10 units ml−1 PTH (synthetic bovine 1–34 PTH, 6000 units mg−1, Sigma Chemical Co., lot 55F-04361) at the same infusion rate (12 Consecutive 10-min clearance periods). Gelatin (0·05%, USP Gelatin 250A, diagnostic reagent grade, Clinical Assays, Inc.) was added to PTH solutions to prevent surface adsorption of the hormonal peptide. Blood samples were collected every 30 min.

The protocol of experiment II closely matched that used by Levinsky & Davidson (1957). An intravenous bolus of 100mg inulin in 80ml of 0·45 % NaCl was given, followed by unilateral renal portal infusion (tibial vein) of a solution containing 0·45 % NaCl, 120 mg 100 ml−1 inulin and 100 mg 100 ml−1 PAH at a rate of 1ml min−1. After a 30-min equilibration period, control urine samples were collected for 30min (two consecutive 15-min clearance periods), followed by consecutive 60–80 min infusions with PTH added to deliver 1, 3 or 5 units h−1 (consecutive 20-min clearance periods). Blood samples were collected every 30 min.

A Phenol Red test was performed as described previously (Wideman & Braun, 1981) during the intial equilibration period and following the last urine sample collection period for each bird. In all cases, substantially higher Phenol Red excretion by the portal-infused kidney than by the contralateral kidney confirmed effective peritubular delivery of the unilateral infusate. Birds were killed with an overdose of 20% urethane at the end of experiments.

Sample handling and analysis

Urine samples were collected in preweighed tubes for gravimetric determination of urine volume. Immediately after each urine volume had been recorded, 0–2 mi of whole urine was mixed with 0–2 ml of 0–5 mol l−1 lithium hydroxide to dissolve uric acid precipitates. This diluted urine was used for analysis. After adding ammonium heparin (200 units ml−1), blood samples were centrifuged to separate the plasma. Whole urine and plasma osmolalities were measured immediately after collection (Wescor Inc. vapor pressure osmometer, model 5100C). Urine and plasma samples were stored frozen (−4°C) until analysis.

Colorimetric techniques were used to assay inorganic phosphate (Fiske & Subbarow, 1925), PAH (Brun, 1957) and inulin (Waugh, 1977). Sodium and potassium were measured by flame photometry (Instrumentation Labs model 443). Calcium was measured by atomic absorption spectrophotometry (Instrumentation Labs model 551).

Calculations and statistical analysis

The clearance of inulin (CIn) was used to determine glomerular filtration rates. The clearance of PAH (CPAH) was calculated for both kidneys, but only CPAH for the contralateral kidney estimates effective renal plasma flow, as CPAH for the portal-infused kidney reflects proximal tubular extraction of PAH delivered directly to the peritubular surfaces with the unilateral infusate. Fractional Pi excretion (FEP) was calculated by dividing the clearance of Pi by the clearance of inulin. FEP values exceeding 10 reflect net Pi secretion, whereas FEP values less than 1·0 reflect net Pi reabsorption. All results are reported as means ±S.E.M. Infused and uninfused kidneys were compared using Student’s t-tests, and in cases with paired observations (portal-infused vs contralateral kidneys within a single clearance period) a paired t-test was used. Group comparisons were analyzed using one-or two-way analysis of variance (SAS Users Guide, 1979). Values were considered to differ significantly at P⩽0·05.

With the exception of CPAH, no significant differences were detected when left vs right or portal-infused vs uninfused kidneys were compared within diet treatment groups during control clearance periods (data not shown). Consequently, values for both kidneys were pooled for intergroup comparisons. As shown in Table 1, Pi excretion and fractional Pi excretion were significantly lower, whereas plasma Pi was significantly higher, for birds fed the low-aP diet than for birds fed the high-aP diet. Birds fed the low-aP diet also had significantly lower glomerular filtration rates (GFR), urine flow rates, osmolal clearances (Cosm) and total plasma calcium concentrations than the group fed the high-aP diet (Table 1).

Table 1.

Control values for low and high available phosphorus (aP) diet treatment groups

Control values for low and high available phosphorus (aP) diet treatment groups
Control values for low and high available phosphorus (aP) diet treatment groups

Fig. 1 is representative of responses obtained in experiment I when birds fed either low-or high-aP diets were unilaterally infused with either 5 or 10 units ml−1 PTH. Urine samples 1–3 were pooled to generate mean control values for portal-infused and contralateral kidneys (30 min values, Fig. 1). Birds fed the low-aP diet receiving a unilateral PTH infusion of 10 units ml−1 at a rate of 0·2 ml kg BM−1 min−1 (BM, body mass) exhibited bilateral increases in Pi excretion (PEC) and GFR that were significant within 30 min after the start of hormone infusion (60 min values, Fig. 1) and these remained significantly elevated for up to 90 min (GFR: 120 min values) or 120 min (PEC: 150 min values) after PTH infusion began. Urine flow increased bilaterally over control values within 20 min after PTH infusion began, and urine flow from the infused kidney was significantly higher than for the contralateral kidney 60–90 min after the start of hormone infusion (Flow rate: 90–130 min values). The clearance of PAH (CPAH) by the infused kidney was always significantly higher than for the uninfused kidney, indicating successful delivery of the unilateral infusate to the peritubular surfaces of the infused kidney.

Fig. 1.

Renal responses to unilateral infusion of 10 units ml−1 parathyroid hormone at a rate of 0·2 ml kg body mass−1 min−1 (mean ± S.E.M., N = 12 for 30 min sample, N= 4 for 40–150min samples). ▵, Portal-infused kidney control values; ▴, contralateral kidney control values; ○, portal-infused kidney during PTH infusion; •, contralateral kidney during PTH infusion. GFR, glomerular filtration rate; CPAH, PAH clearance; (PEC), Pi excretion rate. Asterisks, mean values that differed significantly (P<0·05) by paired t-test during individual clearance intervals.

Fig. 1.

Renal responses to unilateral infusion of 10 units ml−1 parathyroid hormone at a rate of 0·2 ml kg body mass−1 min−1 (mean ± S.E.M., N = 12 for 30 min sample, N= 4 for 40–150min samples). ▵, Portal-infused kidney control values; ▴, contralateral kidney control values; ○, portal-infused kidney during PTH infusion; •, contralateral kidney during PTH infusion. GFR, glomerular filtration rate; CPAH, PAH clearance; (PEC), Pi excretion rate. Asterisks, mean values that differed significantly (P<0·05) by paired t-test during individual clearance intervals.

Responses of the remaining three groups (low-aP diet + 5 units ml−1 PTH; high-aP diet + 5 units ml−1 PTH; high-aP diet + 5 units ml−1 PTH; N = 4 birds per group) during unilateral PTH infusion were qualitatively identical to those shown in Fig. 1: Pi excretion increased bilaterally without exhibiting significant differences between infused and contralateral kidneys, the PTH-stimulated diuresis was significantly greater for the infused than for the contralateral kidney, and CPAH by the uninfused kidney always significantly exceeded that of the contralateral kidney. To summarize these data, mean values for infused and contralateral kidneys were calculated for each bird, incorporating all urine samples collected 30-90 min after the start of PTH infusion. Paired i-tests demonstrated no significant differences for GFR, FEP and PEC when individual mean values for infused and contralateral kidneys were compared by individual groups or pooled (Fig. 2). However, paired t-tests demonstrated that CPAH and urine flow (Fig. 2), and sodium and potassium excretion (not shown) were significantly higher for the portal-infused kidney than for the uninfused kidney when compared within groups or pooled.

Fig. 2.

Scatterplots of mean values for infused (ordinate) vs contralateral (abscissa) kidney function of individual birds 30–90 min after the start of unilateral renal portal PTH infusion. ○, low-aP diet, 5 units mF1 PTH; •, low-aP diet, 10 units ml−1 PTH; □, high-aP diet, 5 units ml−1 PTH; ▪, high-aP diet, lOunitsml−1 PTH. Urine flow rate, glomerular filtration rate (GFR) and PAH clearance (CPAH) are measured in ml kg body mass−1; Pi excretion rate PEC in μanol kg body mass−1 min−1; FEP is fractional Pi excretion.

Fig. 2.

Scatterplots of mean values for infused (ordinate) vs contralateral (abscissa) kidney function of individual birds 30–90 min after the start of unilateral renal portal PTH infusion. ○, low-aP diet, 5 units mF1 PTH; •, low-aP diet, 10 units ml−1 PTH; □, high-aP diet, 5 units ml−1 PTH; ▪, high-aP diet, lOunitsml−1 PTH. Urine flow rate, glomerular filtration rate (GFR) and PAH clearance (CPAH) are measured in ml kg body mass−1; Pi excretion rate PEC in μanol kg body mass−1 min−1; FEP is fractional Pi excretion.

Because significant differences existed in Pi excretion rates for the diet treatment groups during control clearance periods (Table 1), intergroup comparisons of the phosphaturic response to PTH were made by calculating the absolute change from control values (experimental PEC minus control PEC) and percentage change from control values [(experimental PEC/control PEC) x 100]. Portal-infused and contralateral kidney values were pooled for this analysis because they did not have significantly different Pi excretion rates. Absolute changes in Pi excretion relative to control values are shown in Fig. 3 for low-AP and high-aP diet treatment groups infused with 5 or 10 units ml−1 PTH. The phosphaturic responses to PTH did not differ significantly for any of the treatment groups (analysis of variance) during individual clearance periods. Similarly, comparisons of percentage change (from control) in Pi excretion failed to reveal significant differences in the phosphaturic response to PTH (Fig. 4).

Fig. 3.

Absolute change in Pi excretion (PEC: μmol kg body mass−1 min−1) before (control sample at 30 min) and during (40–150 min samples) infusion of 5 units ml−1 (open symbols) or 10 units ml−1 (closed symbols) PTH, as related to dietary available phosphorus (circles, 0·45% aP; squares, 0·83% aP).

Fig. 3.

Absolute change in Pi excretion (PEC: μmol kg body mass−1 min−1) before (control sample at 30 min) and during (40–150 min samples) infusion of 5 units ml−1 (open symbols) or 10 units ml−1 (closed symbols) PTH, as related to dietary available phosphorus (circles, 0·45% aP; squares, 0·83% aP).

Fig. 4.

Percentage change in Pi excretion (PEC) before (control sample at 30 min) and during (40-150min samples) infusion of 5 units ml−1 (open symbols) or 10 unitsml−1 (closed symbols) PTH, as related to dietary available phosphorus.

Fig. 4.

Percentage change in Pi excretion (PEC) before (control sample at 30 min) and during (40-150min samples) infusion of 5 units ml−1 (open symbols) or 10 unitsml−1 (closed symbols) PTH, as related to dietary available phosphorus.

In experiment II, PTH infusion at rates of 1, 3 or 5 units h−1 failed to cause unilateral phosphaturia. Data for the three experimental groups are presented in Fig. 5 using the same format used for Fig. 2. Within each group during PTH infusion, CPAH for the portal-infused kidney was higher than for the contralateral kidney, and urine flow was significantly unilaterally elevated for the group infused with 5 units ml−1 PTH, but none of the other measured parameters differed significantly for intra-or inter-group comparisons of infused and contralateral kidneys (Fig. 5). The 3 and 5 units h−1 PTH infusion rates caused significant bilateral phosphaturia when compared with initial control samples (data not shown).

Fig. 5.

Scatterplots of mean values for infused (ordinate) vs contralateral (abscissa) kidney function of individual birds 30–90 min after the start of unilateral renal portal PTH infusion. ○, 1 unit PTH h−1; □, 3 units PTH h−1; ▴, 5 units PTH h−1. Urine flow rate, glomerular filtration rate (GFR) and clearance of PAH (CPAH) are measured in ml kg body mass−1min−1; Pi excretion rate (PEC) in μmol kg body mass−1 min−1. FEP is fractional Pi excretion.

Fig. 5.

Scatterplots of mean values for infused (ordinate) vs contralateral (abscissa) kidney function of individual birds 30–90 min after the start of unilateral renal portal PTH infusion. ○, 1 unit PTH h−1; □, 3 units PTH h−1; ▴, 5 units PTH h−1. Urine flow rate, glomerular filtration rate (GFR) and clearance of PAH (CPAH) are measured in ml kg body mass−1min−1; Pi excretion rate (PEC) in μmol kg body mass−1 min−1. FEP is fractional Pi excretion.

The results of the present study demonstrate that avian Pi excretion during control clearance periods is significantly influenced by dietary levels of aP. During control periods in experiment I, birds fed high-aP diets had significantly higher fractional and absolute Pi excretion rates than birds fed low-aP diets. These results are consistent with previous observations for domestic fowl (Wideman et al. 1985) and mammals. Studies with mammalian brush-border membrane vesicles indicate that low-aP diets stimulate Pi reabsorption whereas high-aP diets inhibit Pi reabsorption (Gmaj & Murer, 1986). The adaptive mechanism appears to involve specific changes in proximal tubular transport, independent of changes in the filtered load of Pi (Muhlbauer et al. 1977; Ullrich et al. VHT, Knox et al. 1982; Pastoriza-Munoz et al. 1983). Distal nephron Pi transport may also adapt to dietary phosphorus intake (Boudry et al. 1975; Muhlbauer et al. 1977). Tubular sites and mechanisms of avian renal adaptation to dietary phosphorus intake remain to be determined, but the avian proximal tubular brush-border Na+/Pi cotransport system appears to be functionally similar to that of mammals (Renfro & Clark, 1984).

In mammals, adaptation of low-phosphorus diets severely blunts the phosphaturic response to PTH (Steele et al. 1976; Steele & DeLuca, 1976; Gloor et al. 1979; Pastoriza-Munoz et al. 1983), an effect that occurs regardless of plasma Pi concentrations or the filtered load of Pi (Gloor et al. 1979). Although differences in dietary aP clearly had a direct impact on Pi excretion during control periods, the phosphaturic response to PTH, evaluated as absolute and percentage change from control, was clearly not blunted by the low-aP diet. Both the low-and high-aP diet groups exhibited net Pi secretion (FEP >1·0) in response to PTH. These data suggest that much lower levels of dietary aP may be necessary to blunt the avian phosphaturic response to PTH, and that the capacity for PTH to stimulate net Pi secretion was not altered by the levels of aP used in the present study.

Owing to the presence of an innervated renal portal valve, blood from leg veins can bypass avian kidneys entirely (valve open), or can flow into the renal portal system (valve closed; Akester, 1967). Consequently, it was necessary to infuse Phenol Red and PAH unilaterally to determine if blood from the cannulated leg vein was, in fact, flowing to the ipsilateral kidney without first entering the systemic circulation. PAH and Phenol Red are organic anions (acids) that are avidly extracted from the peritubular blood and secreted into the tubular fluid by proximal tubule cells (Wideman, 1988). For all birds included in the present study, Phenol Red and PAH were excreted at higher concentrations by the portal-infused kidney than by the contralateral kidney, demonstrating conclusively that the portal-infused kidney was exposed to the unilateral infusate at a much higher concentration than was the contralateral kidney. Therefore, the proximal tubules of the portal-infused kidney must have been exposed to higher exogenous PTH concentrations than the proximal tubules of the contralateral kidney. Avian proximal tubules have been identified as a site of tubular Pi reabsorption and secretion (Laverty & Dantzler, 1982; Renfro & Clark, 1984).

In spite of direct renal portal delivery of exogenous PTH to the peritubular surfaces of the ipsilateral kidney, neither 5 nor 10 units ml−1 PTH (experiment I) consistently caused unilateral phosphaturia, although bilateral phosphaturia did occur, and a significant unilateral diuresis was consistently observed. The 5 unit ml−1 PTH infusion rate was apparently adequate to attain maximal phosphaturia; consequently, further increases in the hormone infusion rate did not further enhance Pi excretion. In experiment II, much lower doses of PTH caused unilateral diuresis (5 units h−1) and bilateral phosphaturia (3 and 5 unitsh−1), but also failed to cause unilateral phosphaturia. The lowest dose used in experiment II failed to cause phosphaturia. Similar bilateral phosphaturic responses were obtained in a previous study when endogenous and exogenous PTH were given unilaterally via the renal portal system, and when exogenous PTH was delivered unilaterally via the renal arteries (Kissell & Wideman, 1985). As renal PTH receptors must be accessible either through the portal or arterial circulations, it must be concluded that failure to achieve unilateral phosphaturia is not due to failure to deliver PTH to the appropriate nephron segments. The occurrence of unilateral diuresis and bilateral phosphaturia demonstrate that infused PTH does retain its potency. Evidently, neither different levels of dietary aP nor differences in hormone infusion rates can account for our inability to duplicate the PTH-induced unilateral phosphaturia reported by Levinsky & Davidson (1957) and Buchanan (1961). It now appears unlikely that unilateral PTH-induced phosphaturia will be demonstrated consistently in domestic fowl, probably because the amount of exogenous PTH bypassing the portal-infused kidney even at low hormone infusion rates (3–5 units h−1) is sufficient to recirculate and trigger equivalent phosphaturia by the contralateral kidney. Apparently, as noted previously (Kissell & Wideman, 1985), the tubular extraction of PTH from peritubular blood is inefficient with regard to the phosphaturic but not the diuretic response. This observation strongly suggests different mechanisms may be responsible for PTH-induced diuresis and phosphaturia.

This work was submitted by TSS in partial fulfilment of the requirements for a Masters of Science Degree in Physiology at The Pennsylvania State University. The technical contributions of Mrs J. L. Satnick are gratefully acknowledged. Paper no. 8100 in the Journal Series of the Pennsylvania Agricultural Experiment Station.

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