Presence of platelet-activating factor in blood from humans and experimental animals. Its absence in anephric individuals

Caramelo, Carlos; Fernandez-Gallardo, S.; Marín-Cao, D; Iñarrea, Pedro; Santos, Juan Carlos; López‐Novoa, José M.; Crespo, Mariano Sánchez

doi:10.1016/s0006-291x(84)80176-x

Cited by 96 publications

(39 citation statements)

References 12 publications

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“…In fact, there is evidence suggesting that under normal conditions, the kidney is a major source of the PAF found in blood (6)(7)(8)(9). Consequently, it has been speculated that PAF concentrations within the kidney may be sufficient to modulate renal hemodynamics.…”

Section: Introductionmentioning

confidence: 99%

Vasodilator and constrictor actions of platelet-activating factor in the isolated microperfused afferent arteriole of the rabbit kidney. Role of endothelium-derived relaxing factor/nitric oxide and cyclooxygenase products.

Juncos¹,

Ren²,

Arima³

et al. 1993

J. Clin. Invest.

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It has been suggested that platelet-activating factor (PAF) plays a prominent role in the control of glomerular hemodynamics in various physiological and pathological conditions. We examined the direct effect of PAF on rabbit glomerular afferent arterioles (Af-Arts) microperfused in vitro and tested whether endothelium-derived relaxing factor/nitric oxide (EDNO) and cyclooxygenase products are involved in its actions. In nanomolar concentrations PAF caused dose-dependent constriction of Af-Arts, with the maximum constriction being 34±10% at 4 x 10-M (n = 9, P < 0.001). The constriction was blunted by cyclooxygenase inhibition (11±6%, n = 7, P < 0.05) but augmented by EDNO inhibition (76±14%, n = 8, P < 0.005). To study a possible vasodilator effect of PAF, Af-Arts were preconstricted with norepinephrine and increasing concentrations of PAF added to the lumen. At picomolar concentrations (lower than those that caused constriction), PAF produced dose-dependent vasodilation that was unaffected by cyclooxygenase inhibition but was abolished by EDNO synthesis inhibition. Both PAF-induced constriction and dilation of Af-Arts were blocked by a PAF receptor antagonist. This study demonstrates that PAF has a receptor-mediated biphasic effect on rabbit Af-Arts, dilating them at low concentrations while constricting them at higher concentrations. Our results suggest that PAF's vasodilator action may be due to production of EDNO, while its constrictor action is mediated at least in part through cyclooxygenase products. (J. Clin. Invest. 1993. 91:1374-1379 Key words: renal circulation * microvasculature * endothelium-derived relaxing factor. prostaglandins * thromboxane Introduction Platelet-activating factor(PAF) l, or I -0-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine, is a unique phospholipid with a broad range of biological activities. It is not only an important mediator in allergic and inflammatory reactions ( 1 ) but also a very potent hypotensive lipid with complex effects on the cardiovascular system ( 1, 2).

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Section: Introductionmentioning

confidence: 99%

Vasodilator and constrictor actions of platelet-activating factor in the isolated microperfused afferent arteriole of the rabbit kidney. Role of endothelium-derived relaxing factor/nitric oxide and cyclooxygenase products.

Juncos¹,

Ren²,

Arima³

et al. 1993

J. Clin. Invest.

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“…Duplicate assays show that the mean variation of PAF production by cultures derived from the same vein was ±5%. Chromatography in a second TLC system (16) showed that [3H]acetate-labeled lipids elicited by histamine, bradykinin, or ATP migrated with authentic 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine. Treatment of each of these radiolabeled lipids with Crotalus adamanteus phospholipase A2 (10) showed that at least 90% of the radioactivity was incorporated into the sn-2 5) while the resting tension was stabilized at 2 g. Agents were tested by stopping this flow, adding the agent to the 10-ml organ bath that was continuously bubbled with the 02/CO2 mixture, and recording the strain gauge output with a strip-chart recorder.…”

Section: Introductionmentioning

confidence: 99%

Cultured endothelial cells synthesize both platelet-activating factor and prostacyclin in response to histamine, bradykinin, and adenosine triphosphate.

Zimmerman²,

et al. 1985

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Cultured human endothelial cells synthesize prostacyclin (PGI) a potent inhibitor of platelet function, when stimulated with histamine, bradykinin, or ATP. Paradoxically, we report that these agonists also induced the rapid and sustained synthesis of platelet-activating factor (PAF) by endothelial cells. In fact, the synthesis of this potent activator of platelets and neutrophils was induced by stimulation of the same receptor subtype that induced PG12 synthesis: stimulation of a histamine HI or a bradykinin B2 receptor induced both PAF and PGI2 synthesis. However, two physiologically important differences exist between the production of PAF and PGI2 by endothelial cells. The synthesis of PGI2 proceeded for only 7.5 min before the abrupt termination of synthesis, whereas the synthesis of PAF was clearly detectable even 45 min after stimulation. Although

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“…PAF circulates in the peripheral blood at subnanomolar or nanomolar concentrations in humans, rabbits and rats under physiological conditions (Caramelo et al 1984). Domain II of extracellular albumin is an exclusive acceptor for PAF released by cells (Ammit & O'Neill 1997) and binding to it might increase the half-life of PAF.…”

Section: Discussionmentioning

confidence: 99%

Platelet-activating factor acts on cortisol secretion by perfused guinea-pig adrenals via calcium-/phospholipid-dependent mechanisms

Shimada¹,

Hirose²,

Matsumoto³

et al. 2005

Journal of Endocrinology

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Bilateral adrenals of the guinea pig were perfused in situ with an artificial medium equilibrated with 95% O 2 /5% CO 2 . Platelet-activating factor (PAF) induced biphasic cortisol responses, which reached a maximum at 10 nM PAF and declined at 100 nM. The effect of the PAF receptor antagonists CV-3988 and CV-6209 on PAFstimulated cortisol secretion was examined. Prior exposure of adrenal glands to 10 µM CV-3988 or a simultaneous incubation with 10 µM CV-6209 abolished the cortisol response to 10 nM PAF. Lyso-PAF (a PAF precursor and breakdown product) did not affect cortisol secretion. Concentrations of 5-12·5 µM 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), a protein kinase C (PKC) inhibitor, abolished subsequent cortisol secretion in response to 10 nM PAF. N-[2-(Methylamino)ethyl]-5-isoquinoline sulfonamide dihydrochloride (H-8), a protein kinase A inhibitor, was less effective. A calcium ionophore (A23187) at 3·3 and 10 µM increased cortisol secretion, but the activator of PKC, --1-oleoyl-2-acetyl-sn-3-glycerol (OAG), at 50 µM had no effect. When infused simultaneously, OAG (50 µM) and A23187 (3·3 µM) stimulated cortisol secretion synergistically. The secretory response of cortisol to repeated infusions of adrenocorticotrophin (100 pg/ml) or forskolin (10 µM) was essentially reproducible. By contrast, cortisol secretion in response to repeated infusions of PAF (10 nM) or OAG plus A23187 was not reproducible and the second response was diminished compared with the first. Our findings suggest that PAF plays a role in the regulation of steroidogenesis via a mechanism mediated by the PAF receptor and PKC.

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Presence of platelet-activating factor in blood from humans and experimental animals. Its absence in anephric individuals

Cited by 96 publications

References 12 publications

Vasodilator and constrictor actions of platelet-activating factor in the isolated microperfused afferent arteriole of the rabbit kidney. Role of endothelium-derived relaxing factor/nitric oxide and cyclooxygenase products.

Vasodilator and constrictor actions of platelet-activating factor in the isolated microperfused afferent arteriole of the rabbit kidney. Role of endothelium-derived relaxing factor/nitric oxide and cyclooxygenase products.

Cultured endothelial cells synthesize both platelet-activating factor and prostacyclin in response to histamine, bradykinin, and adenosine triphosphate.

Platelet-activating factor acts on cortisol secretion by perfused guinea-pig adrenals via calcium-/phospholipid-dependent mechanisms

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