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

Hishikawa, Keiichi; Nakaki, Toshio; Marumo, Takeshi; Hayashi, Matsuhiko; Suzuki, Hiromichi; Kato, Ryuichi; Saruta, Takao

doi:10.1172/jci117189

Cited by 117 publications

(71 citation statements)

References 32 publications

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“…Our recent results demonstrated that this dose of NCDC arrested the increase in inositol trisphosphate production (24), suggesting efficient blockade of phospholipase C at the concentration used in this study. 30 min later, arteriolar responses to AngII (0.1-0.3 nM) were assessed.…”

Section: Methodssupporting

confidence: 68%

“…Calcium-free medium contained 2 mM EGTA to decrease calcium concentration adequately (24). AngII (0.3 nM) was then administered (8).…”

Section: Methodsmentioning

confidence: 99%

“…Al/NaF is able to activate all G proteins by substituting for the terminal phosphate in the presence of GDP to mimic GTP (27). NCDC, an inhibitor of phospholipase C (15,24), was then administered to the media in a cumulative manner (from 10 to 200 M).…”

Section: Methodsmentioning

confidence: 99%

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Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Takenaka¹,

Suzuki²,

Fujiwara³

et al. 1997

J. Clin. Invest.

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To assess cellular mechanisms mediating afferent (AA) and efferent arteriolar (EA) constriction by angiotensin II (AngII), experiments were performed using isolated perfused hydronephrotic kidneys. In the first series of studies, AngII (0.3 nM) constricted AAs and EAs by 29 Ϯ 3 ( n ϭ 8, P Ͻ 0.01) and 27 Ϯ 3% ( n ϭ 8, P Ͻ 0.01), respectively. Subsequent addition of nifedipine restored AA but not EA diameter. Manganese (8 mM) reversed EA constriction by 65 Ϯ 9% ( P Ͻ 0.01). In the second group, the addition of N -ethylmaleimide (10 M), a Gi/Go protein antagonist, abolished AngIIinduced EA ( n ϭ 6) but not AA constriction ( n ϭ 6). In the third series of experiments, treatment with 2-nitro-4-carboxyphenyl-N , N -diphenyl-carbamate (200 M), a phospholipase C inhibitor, blocked both AA and EA constriction by AngII ( n ϭ 6 for each). In the fourth group, thapsigargin (1 M) prevented AngII-induced AA constriction ( n ϭ 8) and attenuated EA constriction (8 Ϯ 2% decrease in EA diameter at 0.3 nM AngII, n ϭ 8, P Ͻ 0.05). Subsequent addition of manganese (8 mM) reversed EA constriction. Our data provide evidence that in AAs, AngII stimulates phospholipase C with subsequent calcium mobilization that is required to activate voltage-dependent calcium channels. Our results suggest that AngII constricts EAs by activating phospholipase C via the Gi protein family, thereby eliciting both calcium mobilization and calcium entry. ( J.

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Section: Methodssupporting

confidence: 68%

“…Calcium-free medium contained 2 mM EGTA to decrease calcium concentration adequately (24). AngII (0.3 nM) was then administered (8).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Takenaka¹,

Suzuki²,

Fujiwara³

et al. 1997

J. Clin. Invest.

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“…For example, 40 to 120 mmHg pressure promotes DNA synthesis in cultured rat vascular smooth muscle cells (Hishikawa et al 1994). Therefore, 2 ATA of pressure likely has biological effects in addition to oxygen toxicity.…”

Section: Introductionmentioning

confidence: 99%

Comparison of the effects of 40% oxygen and two atmospheric absolute air pressure conditions on stress-induced premature senescence of normal human diploid fibroblasts

Oh¹,

Lee²,

Lee³

et al. 2008

Cell Stress and Chaperones

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The pressure during hyperbaric oxygen treatment may increase oxygen toxicity via an augmented oxygen pressure in the gas. Nevertheless, only a few reports have been published on the effect of cells grown under 2 atmospheric absolute (ATA) pressure. To evaluate the effect of pressure on oxygen toxicity and to study effects in addition to oxygen toxicity, we designed an experiment to compare the effects of normobaric mild hyperoxia (NMH, 40% oxygen) and hyperbaric air condition (HA, air with 2 ATA) on human diploid fibroblasts (HDF) in a hyperbaric incubator. HDFs in both the NMH and the HA condition had a similar oxidative stress response and exhibited premature senescence. To investigate differences in gene profiling in cells grown in the NMH and HA conditions, samples from cells exposed to each condition were applied to microarrays. We found no expression difference in genes related to aging and deoxyribonucleic acid damage, but the expression of genes including cell adhesion, stress response, and transcription were significantly increased in fibroblasts that were responsive to pressure. Among 26 statistically reliable genes, the expression of apoptosis related genes such as ADAM22, Bax, BCL2L14, and UBD, as well as tumor suppressor-related genes like Axin2 and ATF, and also mitogen-activated protein kinase-related genes like mitogen-activated protein kinase kinase kinase 1, histamine receptor, and RAB24, were significantly changed in cells responsive to pressureinduced oxidative stress.

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“…A pressure-loading apparatus was assembled as previously reported (11), with some modifications. SMCs were seeded in 25-cm 2 flasks.…”

Section: Pressure-loading Apparatusmentioning

confidence: 99%

Carvedilol Inhibits Pressure-Induced Increase in Oxidative Stress in Coronary Smooth Muscle Cells.

et al. 2002

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

Cited by 117 publications

References 32 publications

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Comparison of the effects of 40% oxygen and two atmospheric absolute air pressure conditions on stress-induced premature senescence of normal human diploid fibroblasts

Carvedilol Inhibits Pressure-Induced Increase in Oxidative Stress in Coronary Smooth Muscle Cells.

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