Comparisons of avian renal responses to bovine parathyroid extract, synthetic bovine (1–34) parathyroid hormone, and synthetic human (1–34) parathyroid hormone

Wideman, Robert F.; Youtz, Sandra L.

doi:10.1016/0016-6480(85)90231-x

Cited by 8 publications

(4 citation statements)

References 22 publications

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“…Previous studies have shown that PTX causes decreased P ; excretion and hypercalciuria, and these effects are reversed by PTH (Clark et al, 1976;Clark and Wideman, 1977;Mok, 1982;Wideman and Youtz, 1985;Stanton, 1987). Hypercalciuria was not observed following PTX in the present study, possibly because exogenous PTH was administered before this effect could be observed.…”

Section: Discussionmentioning

confidence: 93%

Effect of Gray Strain Infectious Bronchitis Virus and High Dietary Calcium on Renal Function of Single Comb White Leghorn Pullets at 6, 10, and 18 Weeks of Age

1988

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Experiments were designed to evaluate the effects of Gray strain infectious bronchitis virus (IBV) and high dietary calcium (Ca), alone and in combination, on renal function in pullets. Eight hundred female Single Comb White Leghorn chicks were raised on starter ration. Five hundred chicks were inoculated intravenously with Gray strain IBV at 4 wk of age; the remaining chicks were not exposed to IBV. At 6 wk of age, IBV-inoculated and uninoculated chicks were randomly divided into two diet treatment groups. Half the chicks were fed commercial grower ration (approximately 1.0% Ca, .6% available P) and half were fed commercial layer ration (approximately 3.25% Ca, .5% available P). Birds remained on their respective diets until 18 wk of age. Kidney function studies were conducted on anesthetized birds at 6 wk of age prior to initiation of the diet treatments, at 10 wk of age, and at 18 wk of age. The layer ration increased Ca excretion, decreased inorganic phosphate excretion, and decreased urine hydrogen ion concentration in 10-wk-old pullets in comparison with the grower ration. These diet effects on kidney function were attenuated when the pullets reached 18 wk of age. The layer ration also caused an 11.5% incidence of urolithiasis, and significantly increased kidney asymmetry in 18-wk-old pullets relative to the effects of the grower ration. Gray strain IBV exposure significantly increased kidney asymmetry in 18-wk-old pullets, but had no gross effect on kidney function clearly related to the etiology of urolithiasis. Gray strain IBV did not enhance the incidence of urolithiasis in any of the age groups.

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Section: Discussionmentioning

confidence: 93%

Effect of Gray Strain Infectious Bronchitis Virus and High Dietary Calcium on Renal Function of Single Comb White Leghorn Pullets at 6, 10, and 18 Weeks of Age

1988

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“…In the chicken, this peptide has previously been demonstrated as effective as bovine parathyroid extract and synthetic bovine PTH-(1-34) in several parameters, including effects on glomerular filtration rate, renal plasma flow rates, urine pH, and fractional excretion of sodium, potassium, chloride, calcium, magnesium, and P i (45). Fractional excretion of P i was greatest with hPTH compared with the other peptides.…”

Section: Discussionmentioning

confidence: 96%

Regulation of transepithelial phosphate transport by PTH in chicken proximal tubule epithelium

Dudas

Villalobos

Gocek-Sutterlin

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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2001.-The effect of parathyroid hormone (PTH) and activation of protein kinase C (PKC) and protein kinase A (PKA) on transepithelial Pi transport was examined in monolayers of chick proximal tubule cells in primary culture (PTCs). Acute exposure of the PTCs to PTH (10 Ϫ9 M, basolateral side) significantly decreased the net reabsorption of Pi by ϳ66%. There was no effect after the addition of PTH to the luminal side. Activation of PKC by phorbol 12-myristate 13-acetate (PMA; 0.1 M) dramatically decreased net P i reabsorption by ϳ60%. Bisindolylmaleimide I (BIM; 1 M), a highly selective PKC inhibitor, prevented PMA-induced inhibition. Activation of adenylate cyclase/PKA by forskolin (10 M) mimicked the effect of PTH by significantly reducing net P i reabsorption by one-half. Addition of H-89 (10 M), a potent inhibitor of PKA, abolished forskolin-induced inhibition. PTH inhibition was blocked by either BIM or H-89. Tissue electrophysiology remained stable after all treatments. There was a decreased immunoreactivity of the luminal Na ϩ -Pi cotransporter NaPi-IIa after PTH treatment. These data indicate that PTH inhibition of Pi reabsorption in this in vitro system is mediated by PKC and PKA. primary cultures; reabsorptive flux; secretory flux; luminal sodium-inorganic phosphate cotransporter NaPi-IIa; protein kinase C; protein kinase A THE STUDY OF RENAL FUNCTION in birds and other nonmammalian vertebrates has provided valuable insights into the regulation of renal phosphate (P i ) excretion. In mammals, filtration and reabsorption provide sufficient control of P i excretion; however, in birds, which generally have lower and more variable glomerular filtration rates (46), the capacity for net tubular P i secretion has been reported (3). P i can be excreted by the avian kidney in quantities severalfold higher than the filtered load (21). Because avian kidneys possess this additional level of control for renal P i handling, comparative studies of its regulation should further our understanding of P i homeostasis.In both the avian and mammalian renal proximal tubule, P i reabsorption occurs via secondary, Na ϩ -dependent electroneutral transport across the luminal membrane [brush-border membrane (BBM)] (15, 34) coupled to an undefined exit process in the basolateral membrane (BLM) (1). In both mammals and birds, parathyroid hormone (PTH) has been found to be the major regulator of this process (28,24). PTH decreases BBM Na ϩ -P i cotransport activity in both mammals and birds and, in the latter, additionally stimulates net P i secretion (1, 34), which likely occurs through a unique Na ϩ -independent, voltage-and K ϩ -dependent transporter in the BBM (1, 35).Studies with the opossum kidney cell line (OK cells) have shown that PTH exerts its effects through activation of both protein kinase A (PKA) and protein kinase C (PKC) (7, 32), resulting in inhibition of BBM Na ϩ -P i cotransport. Other studies indicated the phosphaturic effect of PTH involves endocytic retrieval followed by lysosomal degradation of the BBM Na ϩ -P...

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“…The reduced phosphate reabsorption appears to be secondary to an inhibition of sodium transport at this site (Agus, Gardner, Beck & Goldberg, 1973;Aurbach & Chase, 1976). Bovine PTHO-84) and hPTH(l-84) stimulated urinary sodium excretion in chicks in vivo (Wideman & Youtz, 1985). A prolonged sodium loss of this nature could be detrimental to the animal.…”

Section: Discussionmentioning

confidence: 99%

Response of adrenal cells to parathyroid hormone stimulation

Rosenberg¹,

Pines²,

Hurwitz³

1987

Journal of Endocrinology

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Dispersed adrenal cells of avian and bovine origin were incubated with human (h) 1-34 parathyroid hormone (PTH(1-34)), bovine (b) PTH(1-84), bPTH(3-34), avian (a) PTH, and with ACTH. Kidney tubular cells, the established target cells for PTH, were used for comparison. Cyclic AMP (cAMP) accumulation and steroid hormone (aldosterone and corticosterone) secretion were measured in response to the hormones. In the bovine adrenocortical cells PTH of both bovine and avian origin stimulated cAMP production, but the aPTH action was more pronounced. The maximal cAMP response of avian adrenocortical cells to aPTH was 15-fold greater than that of ACTH, but a 20-times higher concentration of aPTH was required to reach half-maximal response. Avian PTH stimulated steroid hormone secretion in the chick adrenocortical cells, but the induced secretion was similar to that induced by ACTH, despite the difference in cAMP accumulation. Human PTH(1-34) and bPTH(1-84), which stimulated cAMP production in kidney cells, and the conventional antagonist bPTH(3-34) inhibited aPTH stimulation of cAMP accumulation in avian adrenocortical cells, but did not interfere with ACTH action. Furthermore, cAMP stimulation by aPTH and ACTH in avian adrenal cells was additive. The results establish the adrenal as a target organ for PTH, and suggest that the PTH acts through specific receptors, distinct from those for ACTH.

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Comparisons of avian renal responses to bovine parathyroid extract, synthetic bovine (1–34) parathyroid hormone, and synthetic human (1–34) parathyroid hormone

Cited by 8 publications

References 22 publications

Effect of Gray Strain Infectious Bronchitis Virus and High Dietary Calcium on Renal Function of Single Comb White Leghorn Pullets at 6, 10, and 18 Weeks of Age

Effect of Gray Strain Infectious Bronchitis Virus and High Dietary Calcium on Renal Function of Single Comb White Leghorn Pullets at 6, 10, and 18 Weeks of Age

Regulation of transepithelial phosphate transport by PTH in chicken proximal tubule epithelium

Response of adrenal cells to parathyroid hormone stimulation

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