Nitric oxide and the proliferation of vascular smooth muscle cells

Jeremy, Jamie Y.; Rowe, Daniel C.; Emsley, Alison M; Newby, Andrew C.

doi:10.1016/s0008-6363(99)00171-6

Cited by 260 publications

(184 citation statements)

References 189 publications

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“…This stimulated growth of SMCs leads to the adverse narrowing of the lumen of the blood vessel, fibrous and ultimately restenosis. The endothelium in the blood vessel is the principal source of nitric oxide (NO), which is vital to suppressing SMC migration and proliferation [1,2].…”

Section: Introductionmentioning

confidence: 99%

Endothelial nitric oxide synthase induces heat shock protein HSPA6 (HSP70B′) in human arterial smooth muscle cells

2016

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Section: Introductionmentioning

confidence: 99%

Endothelial nitric oxide synthase induces heat shock protein HSPA6 (HSP70B′) in human arterial smooth muscle cells

2016

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“…Intracellular cGMP decreases the concentration of intracellular calcium, thereby relaxing vascular smooth muscle cells [7]. Endothelial nitric oxide may also inhibit smooth muscle cell proliferation through cGMP-dependent mechanisms [8]. In the lung, cGMP is metabolised primarily by the action of phosphodiesterase (PDE)5.…”

Section: Introductionmentioning

confidence: 99%

Sildenafil in a cigarette smoke-induced model of COPD in the guinea-pig

et al. 2015

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Sildenafil, a phosphodiesterase-5 inhibitor used to treat pulmonary hypertension, may have effects on pulmonary vessel structure and function. We evaluated the effects of sildenafil in a cigarette smoke (CS)-exposed model of chronic obstructive pulmonary disease (COPD).42 guinea-pigs were exposed to cigarette smoke or sham-exposed and treated with sildenafil or vehicle for 12 weeks, divided into four groups. Assessments included respiratory resistance, pulmonary artery pressure (PAP), right ventricle (RV) hypertrophy, endothelial function of the pulmonary artery and lung vessel and parenchymal morphometry. CS-exposed animals showed increased PAP, RV hypertrophy, raised respiratory resistance, airspace enlargement and intrapulmonary vessel remodelling. CS exposure also produced wall thickening, increased contractility and endothelial dysfunction in the main pulmonary artery. CS-exposed animals treated with sildenafil showed lower PAP and a trend to less RV hypertrophy than CS-exposed only animals. Furthermore, sildenafil preserved the intrapulmonary vessel density and attenuated the airspace enlargement induced by CS. No differences in gas exchange, respiratory resistance, endothelial function and vessel remodelling were observed.We conclude that in this experimental model of COPD, sildenafil prevents the development of pulmonary hypertension and contributes to preserve the parenchymal and vascular integrity, reinforcing the notion that the nitric oxide-cyclic guanosine monophosphate axis is perturbed by CS exposure.

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“…15,16 Apart from its vasodilator activity, endothelium-derived NO also modifies inflammatory responses, 17,18 platelet aggregation, 19 and smooth muscle cell proliferation. 20 Animal studies have demonstrated that the short-term withdrawal of statin therapy leads to a profound rebound phenomenon with impaired NO bioavailability. 21 Consistently, a recent study in patients with stable coronary heart disease showed a 3-fold increase in thrombotic vascular events after simvastatin treatment was stopped and continued with relatively lower doses of fluvastatin.…”

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confidence: 99%

Withdrawal of Statins Increases Event Rates in Patients With Acute Coronary Syndromes

et al. 2002

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.15). This was related to an increased event rate during the first week after onset of symptoms and was independent of cholesterol levels. In a multivariate model, troponin T elevation (Pϭ0.005), ST changes (Pϭ0.02), and continuation of statin therapy (Pϭ0.008) were the only independent predictors of patient outcome. Conclusions-Statin pretreatment in patients with acute coronary syndromes is associated with improved clinical outcome.However, discontinuation of statins after onset of symptoms completely abrogates this beneficial effect. (Circulation.

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Nitric oxide and the proliferation of vascular smooth muscle cells

Cited by 260 publications

References 189 publications

Endothelial nitric oxide synthase induces heat shock protein HSPA6 (HSP70B′) in human arterial smooth muscle cells

Endothelial nitric oxide synthase induces heat shock protein HSPA6 (HSP70B′) in human arterial smooth muscle cells

Sildenafil in a cigarette smoke-induced model of COPD in the guinea-pig

Withdrawal of Statins Increases Event Rates in Patients With Acute Coronary Syndromes

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