Contribution of prostaglandins to the systemic and renal vascular response to frusemide in normal man.

Mackay, I. G.; Muir, A L; Watson, M.

doi:10.1111/j.1365-2125.1984.tb02383.x

Cited by 72 publications

(52 citation statements)

References 34 publications

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“…The acute effects of frusemide on renal haemodynamics and renin release are prostaglandin dependent (MacKay et al, 1984) and thus changes in these parameters may serve as a guide to intrarenal prostaglandin synthesis. Dunn et al (1987) have shown that the effects of All on the glomerulus are modulate by prostaglandins.…”

Section: Discussionmentioning

confidence: 99%

“…Intravenous frusemide induces renal vasodila-down product of prostacyclin (PGI2), 6-keto-tion, an early rise in plasma renin activity, and PGFI,a in normal man (Vorburger, 1964; a less consistent rise in glomerular filtration rate Mackay et al, 1984;Ciabattoni et al, 1979). all of which are dependent on prostaglandin Intravenous frusemide also increases urine synthesis and can be antagonised by indo-dopamine excretion but this is not prostaglandin methacin (Mackay et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

“…all of which are dependent on prostaglandin Intravenous frusemide also increases urine synthesis and can be antagonised by indo-dopamine excretion but this is not prostaglandin methacin (Mackay et al, 1984). Associated dependent (Jeffrey et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

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Frusemide, ACE inhibition, renal dopamine and prostaglandins: acute interactions in normal man.

MacDonald¹,

Craig²,

Watson³

1989

Brit J Clinical Pharma

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1 The acute effects of intravenous frusemide (30 mg) on prostaglandin dependent renal haemodynamics, urinary prostaglandin excretion, urinary dopamine excretion and electrolyte excretion were studied in six salt replete healthy volunteers with and without pretreatment with the angiotensin converting enzyme (ACE) inhibitor, ramipril (5 mg) and compared with the effects of ramipril alone in order to clarify the role of the reninangiotensin system in these responses.2 Frusemide increased natriuresis (UNaV), kaliuresis (UKV), inulin clearance and plasma renin activity (PRA) and ramipril pretreatment significantly enhanced these effects suggesting that the acute generation of angiotensin II (All) may attenuate these actions of intravenous frusemide.3 Frusemide increased para-aminohippurate (PAH) clearance, osmolar clearance and urine flow but did not change filtration fraction or urinary kallikrein excretion. Pretreatment with ramipril did not affect these responses. 4 Frusemide increased the excretion of urinary PGE2 and 6-keto-PGFia. Ramipril pretreatment did not suppress this rise in prostaglandin excretion. Since the frusemide induced prostaglandin dependent renal haemodynamic changes were also not suppressed with ACE inhibition, this suggests that in salt-replete volunteers All does not significantly modulate renal prostaglandin production after frusemide. 5 Urinary free dopamine excretion increased with frusemide alone. With ramipril pretreatment this rise showed a tendency to increase. All may therefore inhibit the rise in urinary dopamine excretion after frusemide. However this requires further study.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Frusemide, ACE inhibition, renal dopamine and prostaglandins: acute interactions in normal man.

MacDonald¹,

Craig²,

Watson³

1989

Brit J Clinical Pharma

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“…Frusemide has acute effects on renal blood flow and glomerular filtration (Mackay et al, 1984) which are unrelated to natriuresis. Frusemide causes acute increases in plasma renin activity (Frolich et al, 1976;Johnston et al, 1986) and prostaglandin excretion (Mackay et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

The effects of cilazapril alone and in combination with frusemide in healthy subjects.

Johnston

Passmore

1989

Brit J Clinical Pharma

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1. In a fourway double‐blind placebo controlled study, the effects of cilazapril, a new angiotensin converting enzyme inhibitor, on renal function and the responses to intravenous frusemide were studied in a group of twelve salt depleted male volunteers. 2. Cilazapril produced an increase in effective renal plasma flow and urinary output of prostaglandin E2 metabolite (PGE2‐M) but no effect on sodium, potassium or water excretion. 3. Pretreatment with cilazapril antagonised the effects of frusemide on glomerular filtration, PGE2‐M and sodium excretion.

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“…Although cytostatics, especially cisplatin, affect renal tissue and function (Von Hoff & Rosencweig, 1979), creatinine clearance in out patients showed little or no change. Furosemide could also have been a factor, because it was reported to increase the output of PGI2 and TxA2 products (Wilson et al, 1983), but this was not confirmed by others (Mackay et al, 1984;Franchi et al, 1987).…”

Section: Discussionmentioning

confidence: 94%

Urinary excretion of prostacyclin and thromboxane degradation products in patients with ovarian malignancy: effect of cytostatic treatment

Aitokallio-Tallberg

Viinikka²,

Ylikorkala³

1989

Br J Cancer

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Summary We studied the effect of ovarian cancer and its chemotherapy on the urinary excretion of prostacyclin (PGI2) and thromboxane A2 (TxA2) hydration and metabolic products. In six patients we measured 6-keto-PGF,a and 2,3-dinor-6-keto-PGF,. (PGI2 products) and thromboxane B2 (TxB2) and 2,3-dinor-TxB2 (TxA2 products) by HPLC followed by radioimmunoassay before, during and after the combined infusion of cisplatin, 4'epi-adriamycin and cyclophosphamide. Before the first cytostatic infusion, the urinary excretion of prostanoids was on average 4.4-5.8 times higher than in patients with ovarian endometriosis (n= 19). The infusion of cytostatics led to a 50-120% rise in the excretion of prostanoids during the first post-infusion 9 hours, but in the subsequent 10 hours their ouput was 25-45% below the initial value and remained low for at least 2 weeks. Following repetitive courses of cytostatics (2-4 per patient), prostanoid excretion tended to normalise. These data suggest that ovarian cancer is associated with increased production of PGI2 and TxA2, and that cytostatics suppress this production. This may be of biological significance in tumour behaviour and in the effect of cytostatics.

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Contribution of prostaglandins to the systemic and renal vascular response to frusemide in normal man.

Cited by 72 publications

References 34 publications

Frusemide, ACE inhibition, renal dopamine and prostaglandins: acute interactions in normal man.

Frusemide, ACE inhibition, renal dopamine and prostaglandins: acute interactions in normal man.

The effects of cilazapril alone and in combination with frusemide in healthy subjects.

Urinary excretion of prostacyclin and thromboxane degradation products in patients with ovarian malignancy: effect of cytostatic treatment

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