Stretch increases inositol trisphosphate and inositol tetrakisphosphate in cultured pulmonary vascular smooth muscle cells

Kulik, Thomas J.; Bialecki, Russell; Colucci, Wilson S.; Rothman, Abraham; Glennon, Eileen T.; Underwood, Richard H.

doi:10.1016/s0006-291x(05)81162-3

Cited by 53 publications

(26 citation statements)

References 15 publications

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“…Although there was no significant inhibition ofpressure-induced DNA synthesis at 3 ,M ofeither W-5 or W-7 (Fig. 4 a), 30 ,uM of W-7 significantly inhibited pressure-induced DNA synthesis at 40 and 120 mmHg, as compared with equimolar amounts of W-5 (Fig. 4 b).…”

Section: Resultsmentioning

confidence: 90%

“…Kulik et al (30) reported that stretch-induced IP3 production in vascular smooth muscle cells was increased after 25 s of a 20% stretch and returned to the control level within 45 s, and that stretchinduced 1P3 production was not inhibited by 20 ng/ml pertussis toxin. We have also found that 20 ng/ml of pertussis toxin did not inhibit pressure-induced 1P3 production at 80 mmHg (data not shown), but the difference in response time to stimuli between pressure and stretch-induced IP3 production may distinguish pressure from stretch stimuli.…”

Section: Discussionmentioning

confidence: 99%

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Pressure promotes DNA synthesis in rat cultured vascular smooth muscle cells.

Hishikawa¹,

Nakaki²,

Marumo³

et al. 1994

J. Clin. Invest.

117

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High blood pressure is one of the major risk factors for atherosclerosis. In this study, we examined the effects of pressure on cell proliferation and DNA synthesis in cultured rat vascular smooth muscle cells. Pressure without shear stress and stretch promotes cell proliferation and DNA synthesis in a pressuredependent manner. Pressure-induced DNA synthesis was inhibited significantly by the phospholipase C (PLC) inhibitor 2-nitro4-carboxyphenyl-N,N-diphenylcarbamate, the protein kinase C inhibitor H-7, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, staurosporine, and the tyrosine kinase inhibitor (l3,4,5-trihydroxyphenyljmethylene) propanedinitrile. Toclarify whether activation of PLC and calcium mobilization are involved in pressure-induced DNA synthesis, production of 1,4,5-inositol trisphosphate (IP3) and intracellular Ca2" was measured. Pure pressure increased IP3 and intracellular Ca2"

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Section: Resultsmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Pressure promotes DNA synthesis in rat cultured vascular smooth muscle cells.

Hishikawa¹,

Nakaki²,

Marumo³

et al. 1994

J. Clin. Invest.

117

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“…In fact, studies of cultured vascular cells have shown that mechanical stimulation is able to activate intracellular signaling systems that were followed by specific cellular responses. 17,[20][21][22] Other possible explanations for our results include increased production of vasoconstrictor prostaglandins and/or endothelial contractile factors from vascular endothelial cells stimulated by elevated transmural pressure. [22][23][24] We also assessed the endothelium-independent dilation of SMA by using SNP: dilation responses to increasing doses of SNP were significantly reduced at high pressures and hence the sensitivity to SNP (ie, EC50) was also reduced.…”

Section: Discussionmentioning

confidence: 99%

High Intravascular Pressure Attenuates Vascular Dilation Responses of Small Mesenteric Arteries in the Rat

Gündüz

Meiselman

Başkurt

2008

Circ J

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revious studies have demonstrated that hypertension and cardiovascular diseases are associated with functional and morphological changes in arteries. [1][2][3] In hypertension, the small arteries and arterioles that determine peripheral resistance undergo changes such as increased reactivity to contractile agents, impaired endothelial function, and vascular smooth muscle growth. 4,5 Although it is unclear whether these are primary or secondary abnormalities, it is plausible that the increased intravascular pressure itself has some deleterious effect on vascular functional and/or morphological properties, and it has been proposed that such functional and morphological changes in arteries could be prevented by normalizing intravascular pressure. 6 Thus, independent of origin, high intravascular pressure can directly induce structural and functional modifications of the arterial wall.Blood vessels are continuously exposed to biomechanical forces, such as consist of shear stress induced by the movement of blood through the vessel lumen and stretch determined by luminal pressure and compliance. Chronic alterations in these forces could be important in vascular remodeling induced by both physiological (ie, exercise training) and pathological (ie, hypertension) conditions. 7 However, the variations in these mechanical forces can occur acutely and transiently in vivo. It is well documented that stretching of the arterial wall by increased transmural pressure alters the mechanical properties of vessels, as well as triggering various intracellular signaling pathways. [8][9][10] Thus it is possible that the vascular responsiveness of arteries also changes under conditions of high intraluminal pressure.However, to our knowledge, the vascular responses of vessels from normotensive subjects under high intraluminal pressure conditions have not yet been investigated. Rather, in previous studies, vascular responses to shear stress or agonists have been assessed at basal intraluminal pressures after a defined period of high intraluminal pressure. 11,12 Those myography studies using pre-pressurized vessels from normotensive subjects have demonstrated that endothelium-dependent dilation responses are directly attenuated by transient elevations in intravascular pressure, 11,12 while endothelium-independent vasorelaxation was found to be unaffected. 12 Because the vessel responses were examined after decreasing pressure to the original basal conditions, the mechanical effect of sustained high intravascular pressure on the vascular responses was not explored. Thus, the aim of this study was to investigate the vascular dilation responses of small mesenteric arteries (SMA) in rats at high intra-arterial pressure conditions. For this purpose, we examined the endothelium-dependent and -independent dilation responses under 3 different intravascular pressure conditions (ie, 50, 80 and 120 mmHg) using a pressure myography method. Methods AnimalsThirty adult male Wistar rats, 14 weeks old and weighing 300-320 g, were used in the present study...

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“…Total RNA was isolated from each well and pooled to yield one RNA sample for each 6-well plate. Total RNA was hybridized with 32 muscle cells and monocytes suggests that VEGF could be important in the development of atherosclerotic lesions (8,22). Increased expression of VEGF in pulmonary artery smooth muscle cells in patients with congenital heart disease with increased pulmonary blood flow suggests a role for VEGF as a mediator of pulmonary arteriopathy (20).…”

Section: Discussionmentioning

confidence: 99%

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

Quinn

Schlueter

Soifer

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Vascular endothelial growth factor (VEGF) and basic (b) fibroblast growth factor (FGF-2/bFGF) are involved in vascular development and angiogenesis. Pulmonary artery smooth muscle cells express VEGF and FGF-2 and are subjected to mechanical forces during pulsatile blood flow. The effect of stretch on growth factor expression in these cells is not well characterized. We investigated the effect of cyclic stretch on the expression of VEGF and FGF-2 in ovine pulmonary artery smooth muscle cells. Primary confluent cells from 6-wk-old lambs were cultured on flexible silicon membranes and subjected to cyclic biaxial stretch (1 Hz; 5–25% stretch; 4–48 h). Nonstretched cells served as controls. Expression of VEGF and FGF-2 was determined by Northern blot analysis. Cyclic stretch induced expression of both VEGF and FGF-2 mRNA in a time- and amplitude-dependent manner. Maximum expression was found at 24 h and 15% stretch (VEGF: 1.8-fold; FGF-2: 1.9-fold). These results demonstrate that mechanical stretch regulates VEGF and FGF-2 gene expression, which could play a role in pulmonary vascular development or in postnatal pulmonary artery function or disease.

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Stretch increases inositol trisphosphate and inositol tetrakisphosphate in cultured pulmonary vascular smooth muscle cells

Cited by 53 publications

References 15 publications

Pressure promotes DNA synthesis in rat cultured vascular smooth muscle cells.

Pressure promotes DNA synthesis in rat cultured vascular smooth muscle cells.

High Intravascular Pressure Attenuates Vascular Dilation Responses of Small Mesenteric Arteries in the Rat

Cyclic mechanical stretch induces VEGF and FGF-2 expression in pulmonary vascular smooth muscle cells

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