Mechanotransduction by Vascular Smooth Muscle

Osol, George

doi:10.1159/000159102

Cited by 190 publications

(144 citation statements)

References 62 publications

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“…The mechanism triggering activation of contractile protein is different in cardiac and smooth muscle cells (Stern & Lakatta, 1992;Osol, 1995 However, we cannot exclude the possibility that the large amounts of NO produced by iNOS activation after LPS treatment (see Moncada & Higgs, 1993) can activate another system through a cyclic GMP-independent mechanism (Bolotina et al, 1994). In addition, LPS could release other mediators which produce more complex effects on vascular responsiveness than those mediated by NO (Beutler & Kruys, 1995).…”

Section: Discussionmentioning

confidence: 98%

Alteration by lipopolysaccharide of the relationship between intracellular calcium levels and contraction in rat mesenteric artery

Martínez

Müller

Stoclet

et al. 1996

British J Pharmacology

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1 The aim of this work was to investigate the effect of lipopolysaccharide (LPS) treatment on the relationship between the cytosolic Ca2+ ion concentration ([Ca2]i) and contraction in rat resistance arteries, and the involvement of the L-arginine-nitric oxide (NO)-guanosine 3'-5' cyclic monophosphate (cyclic GMP) pathway in these effects. 2 [Ca2+]i and tension were simultaneously recorded in small mesenteric arteries removed from rats 4 h after intraperitoneal injection of E. coUi LPS (30 mg kg-') or solvent. Cyclic GMP was assayed in vessels submitted to identical treatments.3 Basal [Ca21], was higher in vessels from LPS-treated rats compared to controls. LPS did not modify the concentration-contraction curve of noradrenaline. However, the increase in basal [Ca2+], produced by LPS resulted in a shift of the noradrenaline [Ca2+]i-contraction curve to higher [Ca2+], concentrations.4 L-Arginine (300 gM) relaxed noradrenaline (10 gM) pre-contracted arteries from LPS-treated but not from control rats. This effect of L-arginine was reversed by two inhibitors of NO synthase: Nw-nitro-Larginine-methyl-ester (L-NAME, 1 mM) and S-methyl-isothiourea (SMT, 0.1 mM). Both the relaxing effect of L-arginine and its reversal by L-NAME or SMT occurred without any change in [Ca21],.5 LPS treatment did not modify the cyclic GMP content of the small mesenteric arteries. In arteries removed from LPS-treated rats but not from controls, addition of L-arginine (300 gM) was associated with a significant increase in cyclic GMP content, an effect which was prevented by both L-NAME (1 mM) and SMT (0.1 mM). 6 L-NAME (1 mM) produced a greater reduction in cyclic GMP content than SMT (0.1 mM) in control vessels exposed to L-arginine (300 giM). Under the same conditions, SMT produced a larger decrease in cyclic GMP level than L-NAME in arteries taken from LPS-treated rats, consistent with selective inhibition by SMT of the inducible NO-synthase after LPS. 7 These results show that LPS produced two effects in small mesenteric arteries: (i) alterations in Ca21 handling and a decreased sensitivity of myofflaments to Ca2 , (ii) induction of NO-synthase activity resulting in exogenous L-arginine-dependent production of NO and cyclic GMP accumulation. Both effects are likely to be involved in the hyporeactivity induced by LPS in resistance arteries. Keywords: Calcium; endotoxin shock; resistance arteries Introduction Lipopolysaccharide (LPS)-administration decreases vascular resistance, produces vascular hyporeactivity to different vasoconstrictors and promotes the overproduction of nitric oxide (NO) through activation of the inducible isoform of NO synthase (iNOS) (see Stoclet et al., 1993). The effect of LPS on vascular reactivity and the involvement of NO in this effect have been well documented in large conductance arteries such as the aorta (Julou-Schaeffer et al., 1990). However, the sensitivity to noradrenaline was only slightly decreased in the femoral artery (Schneider et al., 1994) and was not significantly impaired in small mesenteric ...

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Section: Discussionmentioning

confidence: 98%

Alteration by lipopolysaccharide of the relationship between intracellular calcium levels and contraction in rat mesenteric artery

Martínez

Müller

Stoclet

et al. 1996

British J Pharmacology

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“…In a study by O'Rourke et al (11), calculations based on the rubber method indicated that if elastin was repeatedly stretched by 10% of its length, it would fracture after 800 10 6 cyclic stretches, while it would fracture after 3,000 10 6 cycles if stretched by 5% of its length per cycle. The increase of PP contributed to hypertrophy and/or hyperplasia of smooth muscle in the arterial wall, and intraarterial pulsatile flow was the major stimulant of the structure and function of vessel smooth muscle cells (12). On the other hand, with the increase of PWV, wave re-PP, pulse pressure; PWV, pulse wave velocity.…”

Section: Discussionmentioning

confidence: 99%

The Relationship between Pulse Wave Velocity and Pulse Pressure in Chinese Patients with Essential Hypertension

Wang

et al. 2003

Hypertens Res

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“…Interpreting our data in the light of the in vitro findings suggests that birth is followed by transient smooth muscle cell dedifferentiation in conduit pulmonary arteries. The physical environment of the vessel wall changes abruptly at birth and cell cycle progression can be influenced by signals from the extracellular matrix which transmit mechanical information via focal adhesion integrins to the cytoskeleton (Osol, 1995 ;Ingber, 1997 ;Mills et al 1997).…”

Section: mentioning

confidence: 99%

Neonatal pulmonary hypertension prevents reorganisation of the pulmonary arterial smooth muscle cytoskeleton after birth

Hall¹,

Gorenflo

Reader³

et al. 2000

Journal of Anatomy

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The pulmonary arterial smooth muscle cell (SMC) cytoskeleton was studied in tissue from 36 piglets aged from within 5 min of birth to 21 d of age, and in 8 adults. An additional 16 piglets were made pulmonary hypertensive by exposure to hypobaric hypoxia (50n8 kPa) for 3 d. In conduit intrapulmonary elastic arteries α, β and γ actin, the 204, 200 and 196 kDa myosin heavy chain (MHC) isoforms and vinculin were localised by immunohistochemistry. The total actin content, the proportion of monomeric to filamentous α and γ actin and changes in the proportions of the MHC isoforms were determined biochemically. Dividing SMCs were localised and quantified using Ki-67. We found a transient reduction in immunohistochemical expression of γ actin, 204 kDa MHC isoform and vinculin at 3 and 6 d in the inner media, associated with a transient increase in Ki-67 labelling. The actin content also decreased at 3 and 6 d (P 0n05), but there was a postnatal, permanent increase in monomeric actin, first the α then the γ isoform. The relative proportions of the MHC isoforms did not change between birth and adulthood in elastic pulmonary arteries but in muscular arteries the 200 kDa isoform increased between 14 d and adulthood. Pulmonary hypertension prevented both the immunohistochemical changes and the postnatal burst of SMC replication and prevented the transient postnatal reduction in actin content. These findings suggest that rapid remodelling of the actin cytoskeleton is an essential prerequisite of a normal postnatal fall in pulmonary vascular resistance.

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Mechanotransduction by Vascular Smooth Muscle

Cited by 190 publications

References 62 publications

Alteration by lipopolysaccharide of the relationship between intracellular calcium levels and contraction in rat mesenteric artery

Alteration by lipopolysaccharide of the relationship between intracellular calcium levels and contraction in rat mesenteric artery

The Relationship between Pulse Wave Velocity and Pulse Pressure in Chinese Patients with Essential Hypertension

Neonatal pulmonary hypertension prevents reorganisation of the pulmonary arterial smooth muscle cytoskeleton after birth

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