The insulin-like growth factor family of peptides, binding proteins and receptors: their potential role in tissue regeneration.
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Age Factors↗
Biomedical subjects
A Haramati
Publications and source records attributed to A Haramati.
Altered expression of insulin-like growth factor-I (IGF-I) and IGF receptor genes after unilateral nephrectomy in immature rats.
There is a developmental difference in the initial phase of compensatory renal growth (CRG) following unilateral nephrectomy (UNX), in that CRG is GH-dependent in adult rats and GH-independent in immature rats. Furthermore, CRG in immature rats is associated with an increase in renal IGF-I mRNA, an effect not seen in adult rats. In this study we have examined the age-related differences in expression of the insulin-like growth factor-I (IGF-I) and IGF-II genes as well as in IGF-I and IGF-II receptors and membrane binding after UNX. Immature (22-24 days of age) and adult (4 months of age) male Wistar rats underwent a sham operation or left UNX and were killed 24 or 48 h later. Levels of mRNA for IGF-I and IGF-II and their receptors were determined in the left (control) and right (compensated) remnant kidneys using solution hybridization/RNase protection assays. Steady state levels of IGF-I mRNA as well as IGF-I receptor and IGF-II/mannose-6-phosphate receptor mRNAs were increased 3- to 4-fold in immature remnant kidneys, but not in adult kidneys. The findings related to IGF-I gene expression were confirmed by in situ hybridization to immature and adult kidney slices. The increase in IGF-I gene expression in the immature remnant kidneys was localized to the thick ascending limbs of the loops of Henle. Furthermore, in concert with the changes in mRNA levels, membrane binding studies showed significant increases in specific binding to IGF-I in cortical membranes and increases in specific binding to IGF-II in whole kidney membranes from immature, but not adult, rats. Thus, these findings demonstrate that the initial phase of CRG in the immature rat is associated with increased renal IGF-I gene expression as well as enhanced specific renal binding of IGF-I and IGF-II to plasma membranes and support the notion that this period of rapid renal growth in the immature UNX rat may involve the paracrine influence of the IGFs.
Animals↗
Effect of a growth hormone-releasing factor antagonist on compensatory renal growth, insulin-like growth factor-I (IGF-I), and IGF-I receptor gene expression after unilateral nephrectomy in immature rats.
We have recently reported that pulsatile GH secretion is elevated 24 h after unilateral nephrectomy (UNX) in adult rats. In addition, suppression of the increase in GH with an antagonist to GH-releasing factor (GRF-AN) significantly attenuated compensatory renal growth (CRG) in adult rats. The present study examined the role of GH in CRG in immature animals. Pulsatile GH release was determined 24 h post-UNX in immature (26-28 days of age) sham-operated and UNX male Wistar rats. In contrast to the adult UNX rats, no increase in GH secretion was seen in the immature UNX rats compared with that in the controls. When pulsatile GH release was suppressed with GRF-AN, there was preferential growth of the remnant kidney despite the attenuated gain in whole body weight. In addition, insulin-like growth factor-I (IGF-I) and IGF-I receptor mRNA levels were elevated 3-fold in the remnant kidneys of GRF-AN-treated rats, despite the suppression of pulsatile GH release. These findings suggest that the initial phase of CRG is GH independent in the immature rat and, further, that CRG is associated with an increase in IGF-I and IGF-I receptor gene expression that is independent of episodic GH secretion.
Animals↗
Atrial natriuretic peptide and renal cGMP in rats with experimental heart failure.
Rats with chronic aortocaval (AV) fistula, an experimental model of congestive heart failure, display high plasma levels of atrial natriuretic factor (ANF) and a blunted natriuretic response to ANF infusion. We previously reported that rats with AV fistula either develop progressive sodium retention (urinary sodium excretion, UNaV less than 100 microeq/24 h) or compensate (UNaV greater than 1,200 microeq/24 h). To gain further insight into the mechanism of renal hyporesponsiveness to ANF, we evaluated the effect of ANF on renal guanosine 3',5'-cyclic monophosphate (cGMP) production in sham-operated control rats and in the two groups of rats with AV fistula. Infusion of synthetic ANF-(99-126) (at either 10 or 50 micrograms.kg-1.h-1) resulted in a reduced fractional sodium excretion (P less than 0.05) in both compensated rats (0.7 +/- 0.2 and 7.9 +/- 1.6%) and sodium-retaining rats (0.3 +/- 0.1 and 0.5 +/- 0.1%) compared with controls (8.5 +/- 1.2 and 13.7 +/- 2.3% for low and high doses, respectively). Similarly, urinary cGMP excretion corrected by glomerular filtration rate (UcGMPV/GFR) during low-dose ANF infusion was significantly reduced (P less than 0.05) in both groups with AV fistula (compensated: 39 +/- 10 pmol/ml; sodium-retaining: 55 +/- 13 pmol/ml) compared with controls (115 +/- 16 pmol/ml). During high-dose ANF infusion, compensated rats, but not sodium-retaining rats, displayed a significant increase in UcGMPV/GFR. The differences in UcGMPV/GFR are probably not due to variations in urine flow because furosemide infusion to a separate group of rats with AV fistula increased urine flow approximately eightfold but did not increase UcGMPV/GFR.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Suppression of growth hormone release restores phosphaturic response to PTH in immature rats.
Immature rats display a blunted rise in urinary phosphate but not adenosine 3',5'-cyclic monophosphate (cAMP) excretion in response to parathyroid hormone (PTH), perhaps as a consequence of the increased demand for phosphate during growth. Because a major driving force for growth is growth hormone (GH), and in view of the fact that GH has been shown to promote renal phosphate retention in the immature animal, it is possible that GH may attenuate the phosphaturic effect of PTH. The objective of this study was to determine whether suppression of pulsatile GH release, during administration of a synthetic peptide antagonist to GH-releasing factor, i.e., [N-acetyl-Tyr1-D-Arg2]-GRF-(1-29)-NH2 (GRF-AN), alters the renal response to increasing doses of PTH (1.5-15.0 micrograms.100 g-1.h-1) in the acutely thyroparathyroidectomized immature rat. Baseline fractional excretion of phosphate (FEPi), before administration of PTH, was negligible in all groups (less than 0.05%). Infusion of PTH resulted in an attenuated rise in FEPi in immature control rats compared with adult control rats (from 3.8 +/- 1.4% at lowest PTH dose to 16.7 +/- 3.1% at highest dose in immature rats vs. 21.1 +/- 3.5 to 31.9 +/- 4.4% in adult rats, P less than 0.05). In contrast, immature rats treated for 2 days with GRF-AN (100 micrograms/kg, twice daily) displayed an enhanced phosphaturic response (FEPi from 12.0 +/- 4.2 to 42.9 +/- 3.7%, P less than 0.05) compared with immature control rats, which was not different from that observed in control adult rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Renal IGF-1 mRNA levels are enhanced following unilateral nephrectomy in immature but not adult rats.
The increase in IGF-1 gene expression following unilateral nephrectomy (UNX) in adult rats is controversial. In this study we have examined whether developmental differences exist in the effect of UNX on IGF-1 gene expression. Immature (23 days) and adult (4 months) Wistar rats underwent a sham operation or left UNX, and were sacrificed 24 or 48 hrs later. IGF-1 mRNA levels were determined in left (control) and right (compensated) kidneys using solution hybridization/RNase protection assays. By 48 hrs post-UNX, remnant kidneys had grown 20 +/- 1% in adult rats (P less than 0.05), and 69 +/- 5% in immature rats (P less than 0.05). IGF-1 mRNA levels were not increased in the adult compensated kidneys at either 24 or 48 hrs post-UNX. In contrast, kidneys from immature rats 24 and 48 hrs post-UNX had an average 4-fold increase (P less than 0.05) in exon 1 IGF-1 mRNA levels, and an average 3-fold increase (P less than 0.05) in exon 2 mRNA levels. Thus, these findings suggest that there is an age-dependent difference in the effects of UnX on IGF-1 gene expression, and provide the first evidence that IGF-1 gene expression increases following unilateral nephrectomy in immature rats.
Aging↗
Regulation of renal phosphate reabsorption during development: implications from a new model of growth hormone deficiency.
It has been hypothesized that the high rate of renal phosphate (Pi) reabsorption in the immature animal is a consequence of the increased demand for Pi associated with the rapid rate of growth. Although growth hormone (GH) has been proposed to play a role in this process, investigations of the relationship between GH, growth and the renal Pi transport have been hampered by the lack of methods available to specifically alter circulating GH levels. This review summarizes the findings from recent studies using a newly developed peptidic antagonist to GH-releasing factor (GRF-AN) as a method of specifically inhibiting GH release. Systemic injection of GRF-AN was effective in suppressing the pulsatile release of GH, and in significantly attenuating the rate of growth, in both immature and adult rats. However, the inhibition of growth was associated with a reduction in net Pi retention only in immature rats, resulting in a doubling in the urinary excretion of Pi. GRF-AN treatment of immature rats lead to a decrease in the maximum tubular capacity to transport Pi-down to the level seen in adult rats. However, GRF-AN treatment did not alter renal Pi reabsorption in adult rats. We conclude that chronic administration of an antagonist to GRF in rats provides a new model of GH deficiency with which to study the interrelationships between growth, GH and other physiological systems. Furthermore, the findings suggest that the pulsatile release of GH, directly or indirectly, contributes to the high rate of renal Pi reabsorption in young, growing animals and may play a critical role in regulating Pi homeostasis during development.
Animals↗
Atrial natriuretic peptide in the recovery from high-output congestive heart failure.
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Aged↗
Effect of converting-enzyme inhibition on renal response to ANF in rats with experimental heart failure.
Increased activity of the renin-angiotensin system is thought to play a major role in the pathogenesis of salt retention and edema formation in congestive heart failure. The present study evaluates the effects of chronic inhibition of angiotensin-converting enzyme on the response to infusion of exogenous atrial natriuretic factor (ANF) in salt-retaining rats with chronic arteriovenous (a-v) fistula, an experimental model of high-output congestive heart failure. Administration of ANF in incremental doses (5-50 micrograms.kg-1.h-1) to Inactin-anesthetized, sham-operated control rats resulted in dose-dependent increases in urine flow, sodium excretion, and glomerular filtration rate, and significant decreases in mean arterial blood pressure. These effects of atrial peptide were markedly attenuated in salt-retaining rats with a-v fistula. However, chronic oral treatment with the angiotensin-converting-enzyme inhibitor enalapril restored the natriuretic response of sodium-retaining rats with a-v fistula to high doses of ANF. At a dose of 50 micrograms.kg-1.h-1, fractional excretion of Na (FENa) in a-v fistula rats given enalapril was 4.0 +/- 0.5%, which was significantly greater than that in a-v fistula rats without enalapril (0.5 +/- 0.4%, P less than 0.05) and not different from the response in sham-control rats (4.9 +/- 0.7%). The improvement in the natriuretic response after enalapril was not associated with a significant increase in GFR and occurred despite a decrease in mean arterial pressure. Moreover, chronic enalapril treatment did not significantly alter the plasma levels of immunoreactive ANF in either the sham controls or in the rats with a-v fistula.(ABSTRACT TRUNCATED AT 250 WORDS)
Angiotensin-Converting Enzyme Inhibitors↗
Renal adaptation to changes in dietary phosphate during development.
The present study tested the hypothesis that the influence of dietary phosphate (Pi) on the renal handling of Pi changes during development. We evaluated whether variations in the dietary Pi content would alter the tubular capacity of Pi reabsorption [Max RPi/glomerular filtration rate (GFR)] in immature rats, which have a relatively greater Max RPi/GFR compared with adult rats. Then we examined the response of immature and adult Pi-deprived rats to dietary Pi replenishment. Studies were performed in acutely thyroparathyroidectomized Wistar rats at three different stages of development: immature (3- to 4-wk old), young (6- to 7-wk old), and adult (12- to 13-wk old). Animals were fed either low (0.07%)-, normal (0.7%), or high (1.8%)-phosphate diet (LPD, NPD, and HPD, respectively) for 4 days and were then prepared for renal clearance experiments to determine the Max RPi/GFR. On all dietary regimens, the Max RPi/GFR was highest in immature rats and decreased progressively with age. When fed LPD, immature rats, with an already elevated rate of phosphate transport, displayed a remarkable 68 +/- 13% increase in the Max RPi/GFR (from 5.58 +/- 0.29 to 9.47 +/- 0.76 mumol/ml, P less than 0.01). This was significantly greater than the 38 +/- 3% increase observed in adult rats (from 3.50 +/- 0.18 to 4.81 +/- 0.09 mumol/ml). Conversely, in response to HPD, the decrease in the Max RPi/GFR was smallest in immature rats (-42 +/- 2%) compared with the decrement in either young (-54 +/- 3%) or adult (-61 +/- 6%) rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Absorption↗
Antagonist to GH-releasing factor inhibits growth and renal Pi reabsorption in immature rats.
Compared with adult rats, the immature rat has an enhanced tubular capacity for phosphate reabsorption, which presumably facilitates the growth process. Since the main driving force for growth is thought to be the pulsatile release of growth hormone, we examined the possibility that the adaptation in phosphate handling by the immature kidney is promoted by growth hormone (GH). To address this issue, we used a synthetic peptide antagonist to GH-releasing factor (GRF-AN) that we have shown blocks episodic GH secretion, and attenuates somatic growth. Immature male Wistar rats (4-5 wk of age) were catheterized with Silastic jugular cannulas and placed in metabolic cages. The rats were injected intravenously with either saline or GRF-AN (100 micrograms/kg) twice daily for 4 days. On the 4th day, they were prepared for renal clearance experiments to assess the maximum capacity for phosphate transport (TmPi). In animals treated with GRF-AN, there was an attenuated gain in body weight over 4 days of treatment (5 +/- 2 vs. 23 +/- 2% in saline controls, P less than 0.01). The suppressed growth was associated with a doubling of daily urinary phosphate excretion, and a reduction in the TmPi (3.3 +/- 0.1 vs. 4.6 +/- 0.3 mumol/ml in controls, P less than 0.01). A single injection of the antagonist to a separate group of immature rats did not alter TmPi. Thus injections of this new antagonist to GH-releasing factor over a 4-day period inhibit the pulsatile release of GH and significantly attenuate growth. The decline in growth of the immature rat was associated with a decrease in the renal capacity for phosphate reabsorption, down to levels seen in normal adult rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Absorption↗
Restoration of a phosphaturic response to parathyroid hormone in the immature rat.
Recent studies have shown that immature rats display a diminished sensitivity to the phosphaturic effects of parathyroid hormone (PTH), and that the responsiveness to PTH increases with age. The attenuated phosphaturia may reflect an inability of the neonate to respond to the hormone because of functional immaturity of the developing kidney. Alternatively, PTH may actually inhibit tubular phosphate reabsorption in the neonate but, due to other phosphate conservation mechanisms, no phosphaturia occurs. Our objective was to determine whether a phosphaturic response to PTH would be elicited in immature rats during infusion of moderate amounts of phosphate (Pi). Clearance experiments were performed on 26 acutely thyroparathyroidectomized immature Wistar rats (3-5 wk of age) fed a normal Pi diet (0.63%). In response to infusion of either Pi (1 mumol/min.100 g) (group I) or PTH (8.3 ng/min.100 g) (group II) alone, the fractional excretion of phosphate rose minimally (from 0.01 +/- 0.01% to 4.9 +/- 1.9% and from 0.12 +/- 0.12% to 2.9 +/- 1.4% for groups I and II, respectively). However, when Pi and PTH were combined either Pi first followed by PTH (group III) or PTH first followed by Pi (group IV), the fractional excretion of Pi rose dramatically (from 0.01 +/- 0.01 to 21.8 +/- 3.5% and from 0.04 +/- 0.04 to 27.7 +/- 3.3% for groups III and IV, respectively). A significant increase in urinary cAMP excretion occurred during infusion of PTH even when Pi excretion was minimal, but there was no further increase in urinary cAMP during the combined infusion of Pi and PTH.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Inhibition of pulsatile growth hormone (GH) secretion and somatic growth in immature rats with a synthetic GH-releasing factor antagonist.
We previously reported that systemic administration of the recently described GRF peptide antagonist (N-Ac-Tyr1,D-Arg2)GRF-(1-29)-NH2 to adult male rats would suppress the pulsatile release of GH. In the present study, we have sought to determine whether this same antagonist would be efficacious in immature male rats to block spontaneous GH secretion and, as a result, retard several parameters of somatic growth. Indwelling Silastic catheters were placed into the jugular veins of immature male rats (120-140 g) at 29 days of age. After a recovery period of 48 h, beginning at 1000 h, 100-400 micrograms/kg GRF antagonist or its vehicle (controls) were injected iv immediately after withdrawing an initial blood sample from conscious undisturbed animals. Subsequent samples were obtained every 20 min until 1520 h. Red blood cells were resuspended in a restorative volume of saline and reinjected after each blood sample. Results showed that both doses of antagonist prevented the two major periods of episodic GH release observed in controls. For example, mean plasma GH (+/- SEM; nanograms per ml) at 1120 h was 9.0 +/- 2.7 in antagonist-treated rats and 37.1 +/- 5.1 in controls (P less than 0.05). Mean plasma GH (+/- SEM) at 1340 h was 10.8 +/- 3.7 in antagonist-treated rats and 38.8 +/- 9.6 in controls (P less than 0.05). Injection of 400 micrograms/kg of the structurally related VIP antagonist (N-Ac-Tyr1,D-Phe2)GRF-(1-29)-NH2, iv failed to suppress spontaneous GH release. GRF antagonist (100 micrograms/kg) was next administered twice daily iv for 4 days to 31-day-old rats in metabolic cages. This treatment essentially arrested the normal rapid body weight gain, significantly suppressed increases in body and tail lengths, and reduced increases in heart and kidney weights (P less than 0.01). Food intake and fecal output were unchanged by antagonist treatment and, therefore, did not contribute to the observed effects. These results support the idea that a number of tissues and organs are stimulated by the pulsatile secretion of GH and that a peptidic GRF receptor antagonist is useful in blocking episodic GH release in immature animals. As a consequence, this specific antagonist is effective in suppressing numerous aspects of somatic growth.
Animals↗
Effects of atrial natriuretic factor in rats with experimental high-output heart failure.
The effects of atrial natriuretic factor (ANF) were evaluated in rats with chronic aorto-caval (A-V) fistula. In this experimental model of high-output heart failure, the animals display elevated atrial pressure and systemic vasodilation, but avidly retain sodium. Experiments were performed on Munich-Wistar rats, 8 to 14 days after placement of an infrarenal surgical anastomosis (side-to-side, 0.9 +/- 0.2 mm) and on sham operated controls. Infusion of synthetic ANF (3-28) intravenously (5 micrograms/kg prime; 0.17 microgram/kg.min) resulted in increases in urine flow (V) and fractional sodium excretion (FENa) and decreases in blood pressure (BP) that were significantly attenuated in rats with A-V fistula compared to controls. To control for the lower baseline BP that was present in rats with A-V fistula, a second series of studies was performed in which renal perfusion pressure was reduced in normal rats to 110 mm Hg with a servocontrolled pneumatic cuff. ANF infusion to this group led to significant increases in glomerular filtration rate (GFR), V and FENa that were greater than those seen in rats with A-V fistula (FENa = 2.7 +/- 0.3% vs. 0.48 +/- 0.12%, P less than 0.05). Thus, the moderately reduced BP in rats with A-V fistula did not account for the blunted response to ANF. To investigate whether the renal sensitivity to ANF is altered in this model, an additional series of experiments were performed in which ANF was infused over a range of doses (0.08 to 2.5 micrograms/kg.min) to both groups of rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Hormonal determinants of sodium excretion in rats with experimental high-output heart failure.
The present study evaluates the inter-relationship between the alteration in atrial natriuretic factor (ANF) and the renal handling of Na in rats with chronic aortocaval (a-v) fistula, an experimental model of congestive heart failure. Balance studies in these animals showed two distinct patterns of Na excretion: some rats developed progressive Na retention [urinary sodium excretion (UNaV) less than 100 mueq/24 h], whereas others compensated and returned to normal Na balance (UNaV greater than 1,200 mueq/24 h). Base-line plasma ANF levels were equally elevated in Na-retaining and compensated rats with a-v fistula (588 +/- 70 vs. 621 +/- 114 pg/ml, P, NS). However, the response of the two groups to exogenous administration of synthetic rat ANF-(101-126) in incremental doses varied greatly. ANF infusion increased the fractional Na excretion (FENa) in compensated animals from 0.12 +/- 0.03 to 2.6 +/- 0.5%, whereas the rise in FENa in Na-retaining animals was markedly blunted (0.11 +/- 0.06 to 0.89 +/- 0.35%). A similar pattern of ANF action was observed on the glomerular filtration rate and urine flow. The blunted response to ANF in the Na-retaining animals was associated with a marked increase in plasma renin activity (PRA) (35.6 +/- 6.9 vs. 4.5 +/- 0.7 ng ANG I.ml-1.h-1 in sham control rats, P less than 0.05) and plasma aldosterone levels (729.3 +/- 28.2 vs. 42.6 +/- 18.4 ng/dl in sham control rats, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Aldosterone↗
Developmental changes in the tubular capacity for phosphate reabsorption in the rat.
The need for young, immature animals to maintain positive phosphate balance for growth is well known. However, whether this process involves changes in the intrinsic capacity of the kidney to reabsorb phosphate is not clear. In the present study, the maximum capacity of phosphate reabsorption [Max RPi/glomerular filtration rate (GFR)] was measured in four groups of rats at different stages of development, from weanling to adulthood (3-4, 5-6, 10-14, and 52 wk of age). Clearance experiments were performed in acutely thyroparathyroidectomized (TPTX) rats in the presence and absence of fixed levels of parathyroid hormone (synthetic PTH-(1-34), 1 U.kg-1.min-1). Max RPi/GFR was determined with progressive infusions of phosphate (0-6 mumol Pi/min) that raised the filtered load of phosphate. Max RPi/GFR in TPTX 3- to 4- and 5- to 6-wk-old rats (5.55 +/- 0.36 and 4.28 +/- 0.18 mumol/ml, respectively) was significantly greater than in the corresponding 52-wk-old rats (3.51 +/- 0.13 mumol/ml, P less than 0.05). PTH decreased the Max RPi/GFR in all age groups. However, the developmental pattern was maintained, with the highest levels present in the youngest rats (2.79 +/- 0.25 mumol/ml, P less than 0.05) compared with the other age groups (1.92 +/- 0.23, 1.35 +/- 0.11, and 1.15 +/- 0.13 mumol/ml for 5- to 6-, 10- to 14-, and 52-wk-old rats, respectively). These results demonstrate that the tubular capacity for phosphate reabsorption per milliliter GFR is enhanced in immature rats and progressively decreases with age. This PTH-independent adaptation in young rats may contribute to the renal retention of phosphate during growth.
Aging↗
Intrarenal phosphate reabsorption: role of nephron heterogeneity.
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Absorption↗
Effect of dexamethasone on segmental phosphate reabsorption in phosphate-deprived rats.
These experiments were designed to test the hypothesis that avid phosphate reabsorption by the pars recta accounts for the resistance to the phosphaturic effects of acute dexamethasone (DEX) and parathyroid hormone (PTH) infusions in rats fed a low-phosphate diet. Acute infusion of DEX [0.4 mg/(kg X h)] increased the fractional delivery of phosphate (FDPi) to the late proximal tubule from 7.1 +/- 2.1 to 14.4 +/- 3.5%, whereas FDPi to the early distal tubule and urine were not different. PTH alone [1 U/(kg X min)] increased FDPi to the late proximal tubule from 4.0 +/- 1.1 to 15.7 +/- 3.7%, whereas FDPi to the early distal tubule or urine was not different. The combination of DEX and PTH further increased FDPi to the late proximal tubule (32.7 +/- 6.4%) and resulted in an increase in fractional excretion of phosphate (FEPi), in spite of the fact that the FDPi to the early distal tubule was not significantly increased. The increased delivered load of phosphate to the pars recta following inhibition of phosphate transport in superficial proximal convoluted tubules resulted in a comparable increase in phosphate reabsorption in the pars recta, based on linear regression analysis, in rats fed low-phosphate diet but not in rats fed normal phosphate diet. These results demonstrate that acute infusion of DEX or PTH inhibits fractional phosphate reabsorption in the superficial proximal tubule but does not result in an increase in FEPi due at least in part to avid phosphate reabsorption in the superficial pars recta in rats fed low-phosphate diet.(ABSTRACT TRUNCATED AT 250 WORDS)
Absorption↗