Effect of nifedipine on cyclosporine A-induced nephrotoxicity, urinary endothelin excretion and renal endothelin receptor number

Brooks, David P.; Ohlstein, Eliot H.; Contino, Lisa C.; Storer, Barbara; Pullen, Mark; Caltabiano, Madelyn M.; Nambi, Ponnal

doi:10.1016/0014-2999(91)90132-a

Cited by 36 publications

(13 citation statements)

References 7 publications

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“…The extraction and radioimmunoassay for endothelin have been described previously (Brooks et al, 1991). The antiserum used had 100% cross-reactivity with endothelin-1, -2 and -3 and <0.001% cross-reactivity with porcine proendothelin (1-39) or human proendothelin (1-38).…”

Section: Methodsmentioning

confidence: 99%

“…There is growing evidence that endothelin is involved in a variety of acute renal disorders including cyclosporine A nephrotoxicity. Thus, an endothelin antibody can attenuate cyclosporine Ainduced renal vasoconstriction (Kon et al, 1990;Perico et al, 1990) and there is increased endothelin binding (Nambi et al, 1990) and urinary excretion (Brooks et al, 1991) in rats and man (Deray et al, 1991) with cyclosporine A-induced nephrotoxicity. Since endothelin is a powerful renal vasoconstrictor and causes proliferation of mesangial cells in culture (Simonson et al, 1989;Jaffer et al, 1990), it may also be involved in chronic renal disease.…”

Section: Introductionmentioning

confidence: 99%

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Increased endothelin excretion in rats with renal failure induced by partial nephrectomy

Brooks¹,

Contino

Storer

et al. 1991

British J Pharmacology

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1 Six weeks following partial nephrectomy in rats, significant increases in serum urea nitrogen and serum creatinine concentration and a significant decrease in creatinine clearance were observed. 2 Measurement of systolic blood pressure by tail plethysmography indicated that animals that had undergone partial nephrectomy were hypertensive. 3 Compared to sham-operated animals, there were 4 fold increases in both urinary protein excretion and urinary endothelin excretion. 4 There was a significant correlation between urinary protein and urinary endothelin excretion (r = 0.77). There was also a correlation (r = 0.65) between urinary endothelin excretion and systolic blood pressure.5 Plasma endothelin concentrations were not different in sham-operated and partially nephrectomized rats.6 The data indicate that there is an increased renal endothelin production in rats with chronic renal failure.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increased endothelin excretion in rats with renal failure induced by partial nephrectomy

Brooks¹,

Contino

Storer

et al. 1991

British J Pharmacology

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“…The exact role played by ET in CsA-induced vasoconstriction is uncertain. A number of investigators have demonstrated an increase in urinary ET excretion in rats after acute CsA infusion (10,11). The study of Bunchman et al ( 12) showing concentration-dependent CsA induction of ET synthesis in cultured endothelial cells would indicate that CsA may directly stimulate increased ET activity in the systemic or renal vasculature.…”

Section: Introductionmentioning

confidence: 99%

Effects of endothelin receptor antagonist on cyclosporine-induced vasoconstriction in isolated rat renal arterioles.

Lanese¹,

Conger²

1993

J. Clin. Invest.

203

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Recent evidence suggests that the potent constrictor peptide, endothelin (ET) has a mediating role in cyclosporine A (CsA)-related renal vasoconstriction. However, the nature of the CsA-ET interaction and effect on the renal vasculature is uncertain. The purpose of the present study was twofold: (a) to determine if CsA exposure caused direct local release of ET from the endothelium of the renal microvasculature and (b) to determine if locally generated ET has paracrine effects on the underlying vascular smooth muscle to induce vasoconstriction. Experiments were performed in isolated rat renal arterioles. First it was determined that both afferent arteriole (AA) and efferent arteriole (EA) exhibited concentration-dependent decreases in lumen diameter to increasing molar concentrations of CsA. The AA was more sensitive to the vasoconstrictive effects of CsA than the EA. Next, the blocking effect of a recently synthesized putative ETA receptor antagonist was verified in both the AA and EA, where it was found that the cyclic peptide cyclo D-Asp-L-Pro-D-Val-L-Leu-D-Trp totally inhibited the vasoconstriction observed with ET addition. Finally, the role of locally stimulated ET in CsA-induced vasoconstriction was tested by determining the effect of the ETA receptor antagonist on CsA-induced AA and EA constriction. In the AA the vasoconstrictor effect of 1011 M CsA was completely blocked by the ETA receptor antagonist. However, in contrast to AA, 10 1 M CsA in EA in the presence of the ETA receptor antagonist decreased EA lumen diameter by a mean of 41% from baseline (4.80±0.75 ,um vs 7.80±0.84 ,tm, P < 0.05). This change in lumen diameter was similar to that induced by CsA alone. These data suggest that CsA directly constricts renal microvessels. This effect is mediated by ET in the AA but not the EA. (J.

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“…Recently, investigators have focused on the possibility that endothelin may play a role in the response to radiocontrast media. Endothelin (ET), first discovered by Yanagisawa et al [5], is the most potent vasoconstrictor agent yet identified [5][6][7], Two subtypes of ET receptors (ETA and ETB) have been identified, cloned and sequenced [8,9] and there is growing evidence that ET and its receptors may play an important role in a number of renal diseases including ischemia-induced acute renal failure [10][11][12][13][14], cyclosporine A nephrotoxicity [15][16][17], and progressive glomerular disease [18][19][20], Evi dence for a role of ET in radiocontrast media-induced nephrotoxicity includes observations that radiocontrast media increases plasma and urinary endothelin [21][22][23] and an ET receptor antagonist can decrease the effect of iothalamate on renal blood flow [4], Furthermore, many radiocontrast media arc high osmolar and evidence indi cates that hyperosmolality can regulate both ET-1 produc tion and ET-1 mRNA expression in kidney cells or the inner medullary collecting duct in vitro [24][25][26]. In the present study, we have therefore studied the effect of the novel nonpeptide endothelin receptor antagonist, SB 209670, on the renal effects of Hypaque in anesthe tized dogs.…”

Section: Introductionmentioning

confidence: 99%

Blockade of Radiocontrast-lnduced Nephrotoxicity by the Endothelin Receptor Antagonist, SB 209670

1996

Nephron

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The effect of the novel nonpeptide endothelin (ET) receptor antagonist, ( ± )-SB 209670, on the renal effects of the high osmolar tri-iodinated ionic contrast media, Hypaque, was evaluated in anesthetized dogs in the presence or absence of the cyclooxygenase inhibitor, indomethacin (10 mg/kg, i.v.). Hypaque alone (5 ml/kg, i.v.) resulted in a marked diuresis and natriuresis but little change in either renal blood flow or renal vascular resistance. When the ET receptor antagonist, ( ± )-SB 209670, was infused into the renal artery at a dose that inhibited ET-induced renal vasoconstriction, Hypaque resulted in a significant increase in renal blood flow and decrease in renal vascular resistance. In the presence of indomethacin, Hypaque caused a significant increase in renal vascular resistance which was abolished by ( ± )-SB 209670. The data indicate that the radiocontrast media, Hypaque, can cause renal vasoconstriction which may be mediated by ET.

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Effect of nifedipine on cyclosporine A-induced nephrotoxicity, urinary endothelin excretion and renal endothelin receptor number

Cited by 36 publications

References 7 publications

Increased endothelin excretion in rats with renal failure induced by partial nephrectomy

Increased endothelin excretion in rats with renal failure induced by partial nephrectomy

Effects of endothelin receptor antagonist on cyclosporine-induced vasoconstriction in isolated rat renal arterioles.

Blockade of Radiocontrast-lnduced Nephrotoxicity by the Endothelin Receptor Antagonist, SB 209670

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