The adverse renal effects of prostaglandin-synthesis inhibitors in the newborn rabbit

2002 ◽  
Vol 26 (6) ◽  
pp. 398-405 ◽  
Author(s):  
Jean-Pierre Guignard
Keyword(s):  
Prostaglandin Synthesis ◽  
Renal Effects ◽  
Newborn Rabbit ◽  
Prostaglandin Synthesis Inhibitors

Effect of prostaglandin synthesis inhibitors on morphine-induced gastric protection in rats

1988 ◽  
Vol 20 ◽  
pp. 353
Author(s):  
G.M. Scoto ◽  
G. Pagano ◽  
C. Parenti ◽  
C. Spadaro ◽  
R. Arrigo-Reina
Keyword(s):  
Prostaglandin Synthesis ◽  
Prostaglandin Synthesis Inhibitors

Mechanism of bradykinin, ADH, and cAMP interaction in rabbit cortical collecting duct

1985 ◽  
Vol 249 (5) ◽  
pp. F645-F653 ◽  
Author(s):  
V. L. Schuster
Keyword(s):  
Collecting Duct ◽  
Prostaglandin Synthesis ◽  
Regulatory Subunit ◽  
Cortical Collecting Duct ◽  
Camp Generation ◽  
Osmotic Water ◽  
Transepithelial Voltage ◽  
Collecting Tubules ◽  
Prostaglandin Synthesis Inhibitors ◽  
Osmotic Water Flow

Vasopressin (ADH) and bradykinin (BK) have been shown to stimulate prostaglandin synthesis in rabbit cortical collecting tubules. We studied ADH and BK effects on osmotic water flow (Lp), Na transport (JNa), and transepithelial voltage (VT). Bath BK but not lumen BK blunted subsequent ADH hydroosmotic responses. This BK effect was prevented by ibuprofen or pertussigen pretreatment and was overcome with exogenous cAMP, suggesting that BK, via prostaglandins, interferes with ADH action on Lp at the cAMP generation step. In contrast, bath BK had no effect on bath-to-lumen (Jb-1Na) or lumen-to-bath (Jl-bNa) Na flux or on VT. As reported by others, ADH lowered Jl-bNa and depolarized VT; however, prostaglandin synthesis inhibitors neither prevented nor reversed these ADH effects. Together, these BK and ADH data do not support regulation of JNa by peptide-stimulated prostaglandins. Moreover, cAMP alone depolarized VT but had no effect on Jl-bNa. Therefore, ADH-induced depolarization of VT may at least partly owe to cAMP effects on VT independent of accompanying changes in JNa. As with Lp, bath BK blunted subsequent ADH effects on VT and, to a lesser extent, Jl-bNa; these BK effects on ADH action were also prevented by ibuprofen or pertussigen pretreatment. The data are consistent with the following model: 1) ADH depolarizes VT and increases Lp via cAMP; 2) ADH decreases JNa via neither cAMP nor prostaglandins; and 3) BK, via prostaglandins, inhibits the actions of ADH on Lp and VT at the inhibitory guanyl-nucleotide regulatory subunit of adenylate cyclase.

Renal effects of endogenous prostaglandin synthesis promoter ONO-3122

1992 ◽  
Vol 262 (6) ◽  
pp. F1047-F1054
Author(s):  
T. Takabatake ◽  
H. Hara ◽  
Y. Ishida ◽  
H. Ohta ◽  
K. Kobayashi
Keyword(s):  
Proximal Tubule ◽  
Prostaglandin Synthesis ◽  
Fluid Replacement ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Distal Nephron ◽  
Water Reabsorption ◽  
Renal Vasculature ◽  
Renal Effects ◽  
Collecting Tubules

The renal effects of a prostaglandin synthesis agonist, 1-iodo-3-aminomethyl-5,6,7,8-tetrahydro-2-naphthol (ONO-3122), were investigated in anesthetized rats. ONO-3122 (0.3 mg/kg + 0.3 mg.kg-1.h-1 iv) doubled the urinary excretion of the main metabolites of prostaglandin F, and induced transient increases in renal blood flow and glomerular filtration rate (GFR) with a marked, stable natriuresis. Indomethacin suppressed the natriuresis. When the diuretic fluid losses were replaced, micropuncture showed an unaltered reabsorption of sodium in the proximal tubule but reductions in the loop of Henle (86 +/- 1 vs. 76 +/- 1%) and in the more distal segments (98 +/- 1 vs. 83 +/- 3%) with comparable reductions in water reabsorption. Potassium secretion was seen in the distal and collecting tubules. Without fluid replacement, sodium reabsorption was reduced in the loop and more distal nephron but increased in the proximal tubule. Differences between proximal and distal nephron GFR were unaffected by systemic ONO-3122. Loop perfusion with ONO-3122 did not change tubuloglomerular feedback responses, which were, however, completely suppressed by furosemide. It is concluded that ONO-3122 stimulates renal prostaglandin biosynthesis, transiently dilates renal vasculature, and induces natriuresis mainly by suppressing sodium and water reabsorption in the loop of Henle and the more distal nephron. Luminal ONO-3122 does not affect the tubuloglomerular feedback.

Histamine tachyphylaxis in canine airways despite prostaglandin synthesis inhibition

1988 ◽  
Vol 65 (5) ◽  
pp. 1944-1949 ◽  
Author(s):  
P. J. Antol ◽  
S. J. Gunst ◽  
R. E. Hyatt
Keyword(s):  
Smooth Muscle ◽  
Dose Response ◽  
Prostaglandin Synthesis ◽  
Response Curves ◽  
Synthesis Inhibition ◽  
High Concentrations ◽  
Alpha Chloralose ◽  
Prostaglandin Synthesis Inhibitors

Tachyphylaxis to aerosolized histamine was studied in dogs anesthetized with thiamylal after pretreatment with prostaglandin synthesis inhibitors. Three consecutive histamine dose-response curves were obtained in nine dogs pretreated with 5 mg/kg indomethacin; two of these nine were also pretreated with 10 mg/kg indomethacin. Seven of the nine dogs were pretreated with 4 mg/kg sodium meclofenamate; four of these seven were also pretreated with 12 mg/kg. All dogs had tachyphylaxis at high concentrations of histamine regardless of inhibitor used. Pretreatment with indomethacin while the dogs were under alpha-chloralose-urethan anesthesia gave similar results. Histamine tachyphylaxis was also studied both in the presence and in the absence of indomethacin in tracheal smooth muscle strips obtained from seven additional dogs. A decrease in the median effective dose to histamine was observed in the indomethacin-treated strips, but tachyphylaxis to histamine remained. We conclude that prostaglandin synthesis inhibition does not reverse histamine tachyphylaxis either in vivo or in vitro. Thus the mechanism of histamine tachyphylaxis remains unexplained.

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