Mechanism of shear-induced prostacyclin production in endothelial cells

Bhagyalakshmi, A.; Frangos, John A.

doi:10.1016/s0006-291x(89)80172-x

Cited by 128 publications

(44 citation statements)

References 13 publications

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“…This suggests that flow modulation of the myogenic response is endothelium-dependent in the Af-Art. Since flow is known to stimulate the release of both NO (14,(18)(19)(20) and PGI2 (18,(21)(22)(23)) from endothelial cells, we examined their role using L-NAME and indomethacin, respectively. Like endothelial disruption, L-NAME was found to abolish the difference between free-flow and no-flow Af-Arts whereas indomethacin had no effect, suggesting that NO rather than PGs is involved in flow modulation of the myogenic response in Af-Arts.…”

Section: Discussionmentioning

confidence: 99%

“…In conduit arteries, flow is known to cause vasodilation (13-16), and it has been suggested that such dilation is mediated by nitric oxide (NO) released by the endothelium (7,9,10,17). Indeed, shear stress associated with flow has been shown to be a major stimulus for endothelial release of NO (14,(18)(19)(20) and/or prostaglandins (PGs) (18,(21)(22)(23). On the other hand, microvascular responses to flow are remarkably variable and site specific (24-26).…”

Section: Abstract Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.

Juncos¹,

Garvin²,

Carretero³

et al. 1995

J. Clin. Invest.

107

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IntroductionFlow may be a physiological stimulus of the endothelial release of nitric oxide (NO) and prostaglandins (PGs). We tested the hypothesis that pressure-induced constriction of the glomerular afferent arteriole (Af-Art) is modulated by luminal flow via endothelial production of NO. We microdissected the terminal segment of an interlobular artery together with two Af-Arts, their glomeruli (GL) and efferent arterioles (Ef-Art). The two Af-Arts were perfused simultaneously from the interlobular artery, while one Ef-Art was occluded. Since the arteriolar perfusate contained 5% albumin, oncotic pressure built up in the glomerulus with the occluded Ef-Art and opposed the force of filtration, resulting in little or no flow through the corresponding Af-Art. Thus this preparation allowed us to observe free-flow and no-flow Af-Arts simultaneously during stepwise 30-mmHg increases in intraluminal pressure (from 30 to 120 mmHg). Pressureinduced constriction was weaker in free-flow than no-flow Af-Arts, with the luminal diameter decreasing by 11.1±1.7 and 25.6±2.3% (n = 30), respectively, at 120 mmHg. To examine whether flow modulates myogenic constriction through endothelium-derived NO and/or PGs, we examined pressure-induced constriction before and after (a) disruption of the endothelium, (b) inhibition of NO synthesis with NW-nitro-L-arginine methyl ester (L-NAME), or (c) inhibition of cyclooxygenase with indomethacin. Both endothelial disruption and L-NAME augmented pressure-induced constriction in free-flow but not no-flow Af-Arts, abolishing the differences between the two. However, indomethacin had no effect in either free-flow or no-flow Af-Arts. The myogenic response may be modulated by neural, hormonal and metabolic factors, as well as physical factors such as luminal flow (7-12). In conduit arteries, flow is known to cause vasodilation (13-16), and it has been suggested that such dilation is mediated by nitric oxide (NO) released by the endothelium (7,9,10,17). Indeed, shear stress associated with flow has been shown to be a major stimulus for endothelial release of NO (14,(18)(19)(20) and/or prostaglandins (PGs) (18,(21)(22)(23). On the other hand, microvascular responses to flow are remarkably variable and site specific (24-26). Thus it remains unclear whether flow modulates the myogenic response of the Af-Art, nor do we fully understand the role of the endothelium, NO or PGs in the myogenic response of the Af-Art, a crucial vascular segment to the control of glomerular hemodynamics.The goals of the present study were to determine (a) whether pressure-induced constriction of the Af-Art is modulated by flow; (b) whether an intact endothelium is needed in order for flow to modulate pressure-induced constriction; and (c) whether NO and/or Isolation and microperfusion of the renal arterioles. We used a modification of a previously described method to isolate and microperfuse the renal arterioles (27,28). Briefly, young male New Zealand white rabbits (1.5-2.0 kg), fed standard rabbit chow (Ralsto...

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Section: Discussionmentioning

confidence: 99%

Section: Abstract Introductionmentioning

confidence: 99%

Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.

Juncos¹,

Garvin²,

Carretero³

et al. 1995

J. Clin. Invest.

107

View full text Add to dashboard Cite

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“…In some respects PGI2 release parallels that of EDRF, in that it is linked to a pertussis toxin-sensitive Gi protein (Berthiaume & Frangos, 1992) and enhanced by pulsatile flow (Pohl et al 1986). Furthermore, shear-induced PGI2 synthesis requires Ca2+ influx, whereas agonist-induced synthesis is dependent on [Ca2+]i mobilization from intracellular stores (Bhagyalakshmi & Frangos, 1989;MacArthur et al 1993). Changes in the time-dependent profile of the flow wave modulate PGI2 synthesis (Onohara, Okadome, Yamamura, Mii & Sugimachi, 1991), a phenomenon that has not yet been investigated in the context of EDRF. There are complex interactions between the two synthetic pathways.…”

Section: Prostaglandinsmentioning

confidence: 99%

Modulation of blood flow and tissue perfusion by endothelium‐derived relaxing factor

Tm¹

1994

Experimental Physiology

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“…Among these hemodynamic forces, shear stress has been widely and intensely investigated. Changes in shear stress regulate the secretion of several factors, including vasodilators such as NO 1 and prostacyclin, 2 vasoconstrictors such as endothelin-1, 3 and growth factors such as PDGF. 4,5 The role of shear stress on the pathogenesis of vascular disease, especially atherogenesis, has been well characterized.…”

mentioning

confidence: 99%

Cyclic Stretch Upregulates Production of Interleukin-8 and Monocyte Chemotactic and Activating Factor/Monocyte Chemoattractant Protein-1 in Human Endothelial Cells

Okada

Matsumori

Ono

et al. 1998

ATVB

142

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Abstract-In vivo, vascular walls are exposed to mechanical stretch, which may promote atherogenesis. This study was designed to investigate the effect of mechanical stretch on the production and gene expression of cytokines in endothelial cells (ECs) of human umbilical veins. ECs were cultured on flexible silicone membranes and exposed to cyclic mechanical stretch. Although the secretion levels of interleukin (IL)-1␤, tumor necrosis factor-␣, IL-6, granulocyte (G) -colony stimulating factor(CSF), G and macrophage (M) -CSF, and M-CSF were not affected by cyclic stretch over 24 hours, the levels of IL-8 and monocyte chemotactic and activating factor (MCAF)/monocyte chemoattractant protein-1 (MCP-1) were significantly increased by cyclic stretch. Northern blot analysis indicated that the mRNA levels of IL-8 and MCAF/MCP-1 were upregulated by cyclic stretch as a function of its intensity. Cytochalasin D, which disrupts the actin cytoskeleton, abolished the stretch-induced gene expression of IL-8 and MCAF/MCP-1. In contrast, neither inhibition of stretch-activated ion channels nor disruption of microtubules affected the induction of these chemokines by cyclic stretch. Northern blot analysis using enzyme inhibitors showed that phospholipase C, protein kinase C, and tyrosine kinase were involved in the stretch-induced gene expression of IL-8 and MCAF/MCP-1, whereas cAMP-or cGMP-dependent protein kinase was not. Key Words: atherosclerosis Ⅲ interleukin-8 Ⅲ macrophage chemotactic and activating factor Ⅲ monocyte chemoattractant protein-1 Ⅲ hemodynamic forces

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Mechanism of shear-induced prostacyclin production in endothelial cells

Cited by 128 publications

References 13 publications

Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.

Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.

Modulation of blood flow and tissue perfusion by endothelium‐derived relaxing factor

Cyclic Stretch Upregulates Production of Interleukin-8 and Monocyte Chemotactic and Activating Factor/Monocyte Chemoattractant Protein-1 in Human Endothelial Cells

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