J F Gerkens

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A major limitation in the use of amphotericin B is its potential to cause nephrotoxicity. In animals, increased dietary sodium reduces renal toxicity. Experience with five patients in whom impaired renal function developed early during amphotericin B therapy is reported. In four of the patients, there was evidence of sodium depletion due to low sodium(More)
Administration of the antifungal agent amphotericin B causes a pronounced reduction in renal blood flow (RBF). Since amphotericin B induced renal vasoconstriction may contribute to the clinical nephrotoxicity of this drug, the purpose of these studies was to investigate the mechanism of amphotericin B induced renal vasoconstriction. To determine if the(More)
The polyene antibiotic, amphotericin B, causes an acute reduction in renal blood flow and glomerular filtration rate. The purpose of this study was to evaluate the hypothesis that the renal vascular response to amphotericin B can be blocked by aminophylline. Toward this end, the effect of aminophylline on the renal response to amphotericin B in(More)
The relationship between renal prostaglandin (PG)I2 biosynthesis and renin release was examined in conscious dogs before and during renal artery constriction. Dogs were chronically instrumented with femoral vein, femoral artery and left renal vein catheters and an inflatable cuff and electromagnetic flow probe were positioned on the left renal artery. After(More)
Three groups of rats were fed a low-sodium diet. Groups 1 drank water and was treated with cyclosporine, 100 mg kg-1 48 h-1 p.o. for 3 weeks (low-salt-treated group). Group 2 drank 0.15 M saline and was also treated with cyclosporine (high-salt-treated group). Group 3 drank water and was treated with the vehicle (low-salt-vehicle group). Measurements were(More)
Rat tail artery segments were cannulated both ends, immersed in an organ bath filled with Krebs solution, and perfused at a constant 3 ml/min with Krebs solution from a reservoir or arterial blood from a donor conscious rat. Donor rats had chronic indwelling exteriorized silastic cannulas in a carotid artery and jugular vein. Blood withdrawn from the(More)
The renal vascular effects of prostaglandin E2 (PGE2), 6-keto-PGE1, and PGI2 were investigated in indomethacin-pretreated rats. These prostanoids were infused directly into the left renal artery at rates ranging from 0.01 to 1.0 microgram/min, while renal blood flow and mean arterial blood pressure were constantly monitored. PGE2, 6-keto-PGE1, and PGI2(More)
The influence of intra-renal infusions of prostaglandin (PG) I2, PGE2 and PGD2 on renin secretion and renal blood flow was investigated in renally denervated, beta-adrenergic blocked, indomethacin treated dogs with unilateral nephrectomy. All three prostaglandins when infused at doses of 10(-8) g/kg/min and 10(-7) g/kg/min resulted in marked renal(More)
  • J F Gerkens
  • 1989
Clinical use of the immunosuppressant cyclosporine A (CyA) is associated with nephrotoxicity and hypertension of unknown mechanisms. Because the vascular endothelium is now known to influence vascular tone by release of relaxing factors and CyA can damage endothelial cells, it was of interest to determine if CyA could induce a rise in blood pressure (BP) in(More)