Decreased O2 consumption by PMNL from humans and rats with CRF: Role of secondary hyperparathyroidism

Decreased O2 consumption by PMNL from humans and rats with CRF: Role of secondary hyperparathyroidism. Bactericidal ability of polymorphonuclear leukocytes (PMNL) is impaired in chronic renal failure (CRF). This function of PMNL is mediated by the generation of oxidizing radicals and the latter even...

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Bibliographic Details
Published in:Kidney international 1992-09, Vol.42 (3), p.602-609
Main Authors: Kiersztejn, Maciej, Smogorzewski, Miroslaw, Thanakitcharu, Prasert, Fadda, George Z., Massry, Shaul G.
Format: Article
Language:English
Subjects:
Adult
Animals
Biological and medical sciences
Calcium - metabolism
Female
Humans
Hyperparathyroidism - etiology
Hyperparathyroidism - metabolism
Kidney Failure, Chronic - complications
Kidney Failure, Chronic - metabolism
Kidney Failure, Chronic - therapy
Life Sciences & Biomedicine
Male
Medical sciences
Middle Aged
N-Formylmethionine Leucyl-Phenylalanine - pharmacology
Nephrology. Urinary tract diseases
Nephropathies. Renovascular diseases. Renal failure
Neutrophils - metabolism
Oxygen Consumption - drug effects
Rats
Rats, Sprague-Dawley
Renal Dialysis
Renal failure
Science & Technology
Time Factors
Urology & Nephrology
Verapamil - pharmacology
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Summary:Decreased O2 consumption by PMNL from humans and rats with CRF: Role of secondary hyperparathyroidism. Bactericidal ability of polymorphonuclear leukocytes (PMNL) is impaired in chronic renal failure (CRF). This function of PMNL is mediated by the generation of oxidizing radicals and the latter event requires O2 consumption by these cells. The present study examined both basal and FMLP-stimulated rise in cytosolic calcium ([Ca2+]i) and O2 consumption of PMNL from normal subjects and hemodialysis patients and from CRF rats, and evaluated the potential role of secondary hyperparathyroidism of CRF on these properties of PMNL. Basal levels of [Ca2+]i were significantly higher, and FMLP-induced increments in [Ca2+]i were significantly lower in PMNL of both humans and rats with CRF than in normals. Basal and FMLP-stimulated O2 consumption were significantly lower in CRF subjects and rats than in normals. These derangements were prevented by prior parathyroidectomy of CRF rats or by their treatment with verapamil from day one of CRF. Also, therapy of rats with pre-existing CRF with this drug reversed the abnormalities in [Ca2+]i and in O2 consumption of PMNL. The data indicate that: (1) CRF is associated with derangements in the homeostasis of [Ca2+]i of PMNL and their oxygen consumption, (2) these abnormalities are, most likely, mediated by the state of secondary hyperparathyroidism of CRF, and (3) verapamil, which blocks the PTH-induced entry of calcium into cells, and prevents as well as reverses these PMNL dysfunctions. These results implicate the excess PTH of CRF in the genesis of the defective bactericidal function of PMNL, and assign a new dimension to PTH toxicity in CRF.
ISSN:0085-2538
1523-1755
DOI:10.1038/ki.1992.324