Renal Prostaglandins in Renal Hypertensive Dogs

Dighe, K.K.; Smith, Gardner W.; Ungar, A.; Whelpdale, P.

doi:10.1042/cs0540561

Cited by 5 publications

(4 citation statements)

References 25 publications

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“…Prostaglandin determination. The ethanol-extracted material was further extracted with ethyl acetate and assayed for PGF-a, PGE or 6-oxo-PGF-la by radioimmunoassay (Dighe, Emslie, Henderson, Rutherford & Simon, 1975;Dighe, Smith, Ungar & Whelpdale, 1978;Dighe, Jones & Poyser, 1978). Details of the cross-reactivities of the antisera have been reported previously (Poyser & Scott, 1980;Lytton & Poyser, 1982).…”

Section: Methodsmentioning

confidence: 99%

Changes in prostaglandin levels in the sensitized and non-sensitized uterus of the mouse after the intrauterine instillation of oil or saline

Milligan¹,

Lytton²

1983

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Intrauterine instillation of oil, but not saline, induced both a decidual cell reaction and a marked elevation in the uterine PGF-alpha content of suitably sensitized ovariectomized mice. Uterine PGF-alpha concentrations were elevated within 5 min of the oil instillation, reached maximal levels within 30-60 min and then declined to near baseline levels again by 3 h. A similar increase in uterine PGF-alpha content in response to oil instillation was seen in non-sensitized females, although no decidual cell reaction developed. No significant changes in PGE or 6-oxo-PGF-1 content were observed. These results suggest that although the increase in uterine PGF-alpha content is not solely due to the distension of the uterus after intrauterine injection, the increase is not necessarily sufficient to induce a decidual cell reaction.

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Section: Methodsmentioning

confidence: 99%

Changes in prostaglandin levels in the sensitized and non-sensitized uterus of the mouse after the intrauterine instillation of oil or saline

Milligan¹,

Lytton²

1983

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“…The finding that several experimental models of glomerular damage show certain common quantitative and qualitative alterations in AA metabolism suggests the importance of this modulatory pathway in glomerular pathophysiology (17)(18)(19). Glomerular production of TxB2 might be one of the factors responsible for the altered glomerular filtration rate in disease (8).…”

Section: Discussionmentioning

confidence: 99%

Increased glomerular thromboxane synthesis as a possible cause of proteinuria in experimental nephrosis.

Remuzzi¹,

Imberti²,

Rossini³

et al. 1985

J. Clin. Invest.

161

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Altered glomerular metabolism of arachidonic acid (AA) has already been demonstrated in experimental nephrotoxic nephritis. The Isolated glomeruli from nephrotic rats studied 14 or 30 d after a single intravenous injection of adriamycin (7.5 mg/kg) when animals were heavily proteinuric generated significantly more TxB2, the stable breakdown product of TxA2, than normal glomeruli. No significant changes were found in the other major AA metabolites formed through cyclooxygenase. Urinary excretion of immunoreactive TxB2 was also significantly higher in nephrotic than in normal animals. Administration of a selective Tx synthetase inhibitor, UK-38,485, from day 14 to day 18 after adriamycin resulted in a significant reduction of proteinuria compared with pretreatment values. Glomerular synthesis and urinary excretion of TxB2 were normal during the UK-38,485 treatment. Additional experiments showed that elevated glomerular synthesis and urinary excretion of TxB2 were not a consequence of increased substrate availability. Maximal stimulation of the renin-angiotensin axis with furosemide increased glomerular TxB2 synthesis in normal rats, which was significantly lower than in nephrotic animals. Finally, experiments using a unilateral model of adriamycin nephrosis indicated that the enhancement of glomerular TxB2This work was presented in part at the American Society of Nephrology Annual Meeting in Washington, DC, 1983. Received for publication 23 January 1984 and in revised form 23 July 1984.synthesis is not simply a consequence of the nephrotic syndrome.We conclude that: there is an abnormality of glomerular AA metabolism in nephrotic syndrome, which leads to increased TxA2 production; the increased Tx generation correlates with protein excretion and might be responsible for altering the glomerular basement membrane permeability to protein; and the alteration found in isolated glomeruli probably reflects a modification in vivo, in that urinary excretion of immunoreactive TxB2 is also consistently increased in adriamycin nephrosis.

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“…Conversely, sodium restriction increases renal production of PGE in the rabbit (Stahl, Attallah, Bloch & Lee, 1979). In a previous study from this laboratory on Goldblatt two-kidney hypertension in conscious dogs results suggested that there is an increase in the concentration of PGE in renal venous blood from the intact kidney after the early phase of hypertension associated with the spontaneous excretion of retained sodium and water (Dighe et al, 1978). Since in this study the accumulated salt and water was removed by dialysis, the failure of the concentration of PGE in renal venous blood to increase implies that the PGE released by the untouched kidney is involved in sodium excretion, and would be consistent with the suggestion that PGE produced within the kidney exerts a natriuretic action, and that its release from the intact kidney is triggered by the retention of sodium and water.…”

Section: Urinary Outputmentioning

confidence: 87%

“…Previous results from this laboratory of studies of Goldblatt two-kidney hypertensive dogs suggested that increased prostaglandin E (PGE) pro- duction by the untouched kidney several days after the partial occlusion of the contralateral renal artery mediated the excretion of salt and water that had been retained over the first 4 days (Dighe, Smith, Ungar & Whelpdale, 1978). In the present study, to test this hypothesis further, salt and water that accumulated during the 2 days after the partial occlusion of one renal artery was removed by haemodialysis.…”

Section: Introductionmentioning

confidence: 98%

Effects of Salt and Water Depletion on the Early Phase of Hypertension in Goldblatt two-Kidney Hypertensive Dogs

et al. 1981

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1. Hypertension was induced in dogs by partial occlusion of one renal artery, the opposite kidney remaining intact, and the changes in blood pressure, plasma renin activity, aldosterone and prostaglandin E (PGE) were monitored. 2. Two days after induction of hypertension, the retained sodium and water were removed by haemodialysis and the animals were then maintained on a low dietary intake of sodium for the following 7 days. 3. Removal of the accumulated sodium and water had no immediate effect on blood pressure, but during the ensuring 7 days there was a small decrease in blood pressure, which again increased after re-institution of a normal sodium intake. 4. Plasma renin activity and aldosterone increased during development of hypertension and remained elevated during the period of sodium restriction. 5. Sodium and water retained during the development of hypertension was not responsible for the elevated blood pressure. 6. The concentration of PGE in arterial plasma and renal venous plasma from the unclamped kidney were unchanged during the study, although we have previously shown that in the absence of sodium depletion, PGE rises. 7. PGE released from the kidney may be important in mediating the excretion of sodium and water that is retained during the development of renal hypertension.

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Renal Prostaglandins in Renal Hypertensive Dogs

Cited by 5 publications

References 25 publications

Changes in prostaglandin levels in the sensitized and non-sensitized uterus of the mouse after the intrauterine instillation of oil or saline

Changes in prostaglandin levels in the sensitized and non-sensitized uterus of the mouse after the intrauterine instillation of oil or saline

Increased glomerular thromboxane synthesis as a possible cause of proteinuria in experimental nephrosis.

Effects of Salt and Water Depletion on the Early Phase of Hypertension in Goldblatt two-Kidney Hypertensive Dogs

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