Release of Prostaglandins From the Rabbit Perfused Kidney: Effects of Vasoconstrictors

Gagnon, Denis; Gauthier, Rémy; Regoli, Doménico

doi:10.1111/j.1476-5381.1974.tb08588.x

Cited by 30 publications

(11 citation statements)

References 11 publications

(12 reference statements)

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“…These results are similar to results of studies on the rat kidney in which both indomethacin and meclofenamate decreased responses to renal nerve stimulation. 6 These data are not in agreement with the studies of Gagnon et al 27 on the isolated rabbit kidney perfused with Krebs' solution. However, differences in experimental design may be involved since in the present study the kidney was autoperfused in vivo and the pressor hormones were injected, whereas in the other study, the kidney was isolated and the hormones were infused.…”

Section: ^12contrasting

confidence: 55%

“…However, differences in experimental design may be involved since in the present study the kidney was autoperfused in vivo and the pressor hormones were injected, whereas in the other study, the kidney was isolated and the hormones were infused. 27 In the present study, the prostaglandin precursor, arachidonic acid, produced dose-dependent decreases in systemic arterial pressure and renal perfusion pressure and these responses were decreased markedly by indomethacin, whereas dilator responses to PGE 2 and nitroglycerin were not diminished. These data suggest that the precursor is transformed into dilator substances in the systemic vascular bed and the kidney and that biosynthesis of these substances, presumably prostaglandins, is inhibited by indomethacin.…”

Section: ^12mentioning

confidence: 75%

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Influence of prostaglandin E2, indomethacin, and reserpine on renal vascular responses to nerve stimulation, pressor and depressor hormones.

Fink

Chapnick

Goldberg

et al. 1977

Circulation Research

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The effects of prostaglandin E, (PGE 2), indomethacin, and reserpine were evaluated in the rabbit renal vascular bed in situ under conditions of controlled blood flow. Intrarenal infusion of PGE 2 , 0.03 and 0.3 fig/min, decreased responses to renal nerve stimulation, intra-arterial norepinephrine, and angiotensin. Responses to nerve stimulation were decreased to a greater extent than responses to norepinephrine. At lower concentrations the effects of PG£ 2 on pressor responses and on vascular resistance could be separated. Reserpine decreased the histochemical evidence of adrenergic innervation and reduced the response to renal nerve stimulation, enhanced the response to norepinephrine, and was without effect on the response to angiotensin. Indomethacin decreased depressor responses to arachidonic acid, produced a small increase in renal vascular resistance but did not enhance renal pressor responses. The increase in renal vascular resistance after indomethacin was not modified by reserpine pretreatment. Indomethacin enhanced the renal response to bradykinin. These data show that PGE 2 possesses the ability to modulate pressor responses in the kidney. However, experiments with indomethacin suggest that endogenous prostaglandins neither modulate pressor responses nor mediate the response of the renal vascular bed to bradykinin. In addition, these data suggest that the increase in renal resistance after indomethacin is not dependent on the adrenergic nervous system.

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Section: ^12contrasting

confidence: 55%

Section: ^12mentioning

confidence: 75%

Influence of prostaglandin E2, indomethacin, and reserpine on renal vascular responses to nerve stimulation, pressor and depressor hormones.

Fink

Chapnick

Goldberg

et al. 1977

Circulation Research

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“…18 Briefly, this method consisted of mixing at 4°C 25 jtl of rat serum with 2 ^1 of a 3 M tris buffer containing 0.3 M EDTA, pH 7.2 and 3 M l of a 1:100 dilution of the antiangiotensin I serum. This mixture was incubated at 37°C for 15-40 minutes, and returned to a 4°C ice bath.…”

Section: Methodsmentioning

confidence: 99%

Saralasin-induced renin release: its blockade by prostaglandin synthesis inhibitors in the conscious rat.

Campbell¹,

Jackson²,

Graham³

1979

Hypertension

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SUMMARY The angiotensin antagonist, saralasin, (10 and 30 rag/kg), increased serum renin activity (SRA) in normal, conscious rats from 2.7 ± 0.4 to 16.2 ± 3.7 and 22.5 ± 2.4 ng/ml/hr (p < 0.001), respectively, without markedly altering blood pressure or heart rate. Indomethacin, in a dose which inhibited the urinary excretion of prostaglandin E, (PGE,) by 75%, and arachidonate-induced hypotension by 83%, failed to alter basal SRA but inhibited saralasin-induced renin release by 99% and 87% at the 10 and 30 mg/kg doses, respectively. Indomethacin failed to alter basal hemodynamics or the hemodynamic response to saralasin. Prorjranolol (1.5 mg/kg) inhibited saralasin-induced renin release by 93% and enhanced the suppressant effect of indomethacin from 79% to 100%. Meclofenamate, another prostaglandin synthesis inhibitor, also blocked saralasin-induced renin release by 99% and 72% at the 10 and 30 mg/kg doses, respectively (p < 0.001). In sodium-depleted rats, saralasin (03 mg/kg) increased SRA from 12 ± 2 to 119 ± 6 ng/ml/hr (p < 0.001) and decreased blood pressure by 6% (p < 0.01). In these animals, indomethacin failed to alter basal SRA, but inhibited saralasin-induced renin release by 82%, urinary excretion of PGE, by 79%, and arachidonate-induced hypotension by 81%.These findings suggest 1) that saralasin-induced renin release is mediated by renal prostaglandins, and 2) an interrelationship exists between the receptor controlling All-mediated inhibition of renin release, which is blocked by saralasin, and the juxtaglomerular beta-adrenergic receptor. angiotensin system, suppresses the release of renin by a negative feedback mechanism resulting from its direct action on the juxtaglomerular cells.

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“…It is possible that the increased availability of EPA or DHA or both may lead to an enhanced formation of resolvins, protectins and maresins that could have reversed the development of AAA. Yet, the other possibility that needs to be considered is the action of angiotensin-II on the formation of proinflammatory prostaglandins (PGs), thromboxanes (TXs) and leukotrienes (LTs) from AA, [7][8][9][10] an n-6 PUFA. It is likely that the supplementation of EPA and DHA displaced AA from the cell membrane phospholipid pool that can lead to an increased formation of LXA4 (see figure 3) and decreased formation of pro-inflammatory PGs, TXs and LTs (from AA).…”

Section: Pufas and Their Metabolites Angiotensin-ii Aa And Aaamentioning

confidence: 99%

Is aortic aneurysm preventable?

Das¹

2017

Journal of Translational Internal Medicine

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Abdominal aortic aneurysm (AAA) is a chronic inflammatory condition, triggered by the local accumulation of macrophages, oxidative stress and damage to the aortic wall. Pro-inflammatory eicosanoids seem to play a significant role in AAA. The pro-inflammatory events seen in AAA could be due to a deficiency of anti-inflammatory eicosanoids such as lipoxin A4 (LXA4), resolvins, protectins and maresins as a result of reduced tissue concentrations of their precursors: arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Thus, an imbalance between pro- and anti-inflammatory eicosanoids may underlie AAA. Angiotensin-II (Ang-II), a pro-inflammatory molecule, seems to have a role in AAA. I propose that AAA is due to the local (abdominal aortic wall) deficiency of AA and other PUFAs and their anti-inflammatory metabolites especially LXA4. The beneficial action of EPA and DHA reported in the animal experimental models of AAA induced by Ang-II infusion can be attributed to their (EPA and DHA) ability to enhance the formation of not only resolvins, protectins and maresins but also LXA4. It is likely that abdominal aortic tissue (endothelial cells, smooth muscle cells and other cells) may be deficient in AA, EPA and DHA, and have defective activity of 5-, 12-, and 15-lipoxygenases and cyclooxygenase, especially COX-2 resulting in decreased formation of LXA4, resolvins, protectins and maresins. Thus, methods designed to enhance the formation of LXA4 and other anti-inflammatory eicosanoids may form a new approach to prevent and manage AAA.

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Release of Prostaglandins From the Rabbit Perfused Kidney: Effects of Vasoconstrictors

Cited by 30 publications

References 11 publications

Influence of prostaglandin E2, indomethacin, and reserpine on renal vascular responses to nerve stimulation, pressor and depressor hormones.

Influence of prostaglandin E2, indomethacin, and reserpine on renal vascular responses to nerve stimulation, pressor and depressor hormones.

Saralasin-induced renin release: its blockade by prostaglandin synthesis inhibitors in the conscious rat.

Is aortic aneurysm preventable?

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