Small Artery Remodeling and Significance in the Development of Hypertension

Mulvany, Michael J.

doi:10.1152/nips.01366.2001

Cited by 91 publications

(92 citation statements)

References 16 publications

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“…Possible pathways through which PM could elevate BP include the elicitation of oxidative stress, systemic proinflammatory responses, and the activation of pulmonary reflexes leading to increased sympathetic tone, potentially causing arterial remodeling (Brook et al 2009; Heagerty et al 2010; Mills et al 2009; Mulvany 2002). Autonomic nervous system imbalance after activation of pulmonary reflexes is most probably the responsible mechanism for acute effects of PM on BP, whereas systemic inflammation and vascular dysfunction involve a longer time of onset (Brook et al 2009).…”

Section: Discussionmentioning

confidence: 99%

“…If this happens repeatedly, hypertrophic remodeling of the resistance vessels results in an increase in the medial thickness, which then leads to an increased total peripheral resistance and a fixation of elevated BP. Similarly, an increase in blood flow may lead to vasodilatation, which increases wall stress, leading to hypertrophic remodeling as well (Heagerty et al 2010; Mulvany 2002). In eutrophic remodeling, neurohumoral activity as affected by PM activation of, for example, pulmonary reflexes leads to vasoconstriction and increased BP, but wall stress remains normal by decreasing the diameter of the vessel and increasing the wall thickness (Heagerty et al 2010; Mulvany 2002).…”

Section: Discussionmentioning

confidence: 99%

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Long-Term Urban Particulate Air Pollution, Traffic Noise, and Arterial Blood Pressure

Fuks

Moebus²,

Hertel³

et al. 2011

Environ Health Perspect

166

168

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Background: Recent studies have shown an association of short-term exposure to fine particulate matter (PM) with transient increases in blood pressure (BP), but it is unclear whether long-term exposure has an effect on arterial BP and hypertension.Objectives: We investigated the cross-sectional association of residential long-term PM exposure with arterial BP and hypertension, taking short-term variations of PM and long-term road traffic noise exposure into account.Methods: We used baseline data (2000–2003) on 4,291 participants, 45–75 years of age, from the Heinz Nixdorf Recall Study, a population-based prospective cohort in Germany. Urban background exposure to PM with aerodynamic diameter ≤ 2.5 μm (PM2.5) and ≤ 10 μm (PM10) was assessed with a dispersion and chemistry transport model. We used generalized additive models, adjusting for short-term PM, meteorology, traffic proximity, and individual risk factors.Results: An interquartile increase in PM2.5 (2.4 μg/m3) was associated with estimated increases in mean systolic and diastolic BP of 1.4 mmHg [95% confidence interval (CI): 0.5, 2.3] and 0.9 mmHg (95% CI: 0.4, 1.4), respectively. The observed relationship was independent of long-term exposure to road traffic noise and robust to the inclusion of many potential confounders. Residential proximity to high traffic and traffic noise exposure showed a tendency toward higher BP and an elevated prevalence of hypertension.Conclusions: We found an association of long-term exposure to PM with increased arterial BP in a population-based sample. This finding supports our hypothesis that long-term PM exposure may promote atherosclerosis, with air-pollution–induced increases in BP being one possible biological pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long-Term Urban Particulate Air Pollution, Traffic Noise, and Arterial Blood Pressure

Fuks

Moebus²,

Hertel³

et al. 2011

Environ Health Perspect

166

168

View full text Add to dashboard Cite

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“…We report that the Bu-Cy regimen specifically affected the microarterial vasculature. The resistance sized arterial vessels are considered to contribute to vascular resistance [51]; their structure and mechanical properties significantly influence systemic blood pressure [52], [53]. The localization of the Bu-Cy induced changes to the resistance arteries might thus be an important component in the late vascular system complications and could potentially affect perfusion and function of some organs.…”

Section: Discussionmentioning

confidence: 99%

Busulphan-Cyclophosphamide Cause Endothelial Injury, Remodeling of Resistance Arteries and Enhanced Expression of Endothelial Nitric Oxide Synthase

et al. 2012

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Stem cell transplantation (SCT) is a curative treatment for malignant and non malignant diseases. However, transplantation-related complications including cardiovascular disease deteriorate the clinical outcome and quality of life. We have investigated the acute effects of conditioning regimen on the pharmacology, physiology and structure of large elastic arteries and small resistance-sized arteries in a SCT mouse model. Mesenteric resistance arteries and aorta were dissected from Balb/c mice conditioned with busulphan (Bu) and cyclophosphamide (Cy). In vitro isometric force development and pharmacology, in combination with RT-PCR, Western blotting and electron microscopy were used to study vascular properties. Compared with controls, mesenteric resistance arteries from the Bu-Cy group had larger internal circumference, showed enhanced endothelium mediated relaxation and increased expression of endothelial nitric oxide synthase (eNOS). Bu-Cy treated animals had lower mean blood pressure and signs of endothelial injury. Aortas of treated animals had a higher reactivity to noradrenaline. We conclude that short-term consequences of Bu-Cy treatment divergently affect large and small arteries of the cardiovascular system. The increased noradrenaline reactivity of large elastic arteries was not associated with increased blood pressure at rest. Instead, Bu-Cy treatment lowered blood pressure via augmented microvascular endothelial dependent relaxation, increased expression of vascular eNOS and remodeling toward a larger lumen. The changes in the properties of resistance arteries can be associated with direct effects of the compounds on vascular wall or possibly indirectly induced via altered translational activity associated with the reduced hematocrit and shear stress. This study contributes to understanding the mechanisms that underlie the early effects of conditioning regimen on resistance arteries and may help in designing further investigations to understand the late effects on vascular system.

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“…Dissociation between changes in vascular wall area and in wall thickness is a common finding with established explanations. Elegant studies by Baumbach and Heistad (5, 6) and by Mulvany (35, 36) have made it clear that an increase in the ratio of the vascular wall to lumen may be achieved by at least two very different situations. For instance, the ratio may be increased by a reduction in lumenal diameter without a change in medial volume.…”

Section: Discussionmentioning

confidence: 99%

Long-term exposure to high-altitude chronic hypoxia during gestation induces neonatal pulmonary hypertension at sea level

Herrera

Riquelme

Ebensperger³

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

107

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We determined whether postnatal pulmonary hypertension induced by 70% of pregnancy at high altitude (HA) persists once the offspring return to sea level and investigated pulmonary vascular mechanisms operating under these circumstances. Pregnant ewes were divided into two groups: conception, pregnancy, and delivery at low altitude (580 m, LLL) and conception at low altitude, pregnancy at HA (3,600 m) from 30% of gestation until delivery, and return to lowland (LHL). Pulmonary arterial pressure (PAP) was measured in vivo. Vascular reactivity and morphometry were assessed in small pulmonary arteries (SPA). Protein expression of vascular mediators was determined. LHL lambs had higher basal PAP and a greater increment in PAP after NG-nitro-l-arginine methyl ester (20.9 ± 1.1 vs. 13.7 ± 0.5 mmHg; 39.9 ± 5.0 vs. 18.3 ± 1.3 mmHg, respectively). SPA from LHL had a greater maximal contraction to K+ (1.34 ± 0.05 vs. 1.16 ± 0.05 N/m), higher sensitivity to endothelin-1 and nitroprusside, and persistence of dilatation following blockade of soluble guanylate cyclase. The heart ratio of the right ventricle-to-left ventricle plus septum was higher in the LHL relative to LLL. The muscle area of SPA (29.3 ± 2.9 vs. 21.1 ± 1.7%) and the protein expression of endothelial nitric oxide synthase (1.7 ± 0.1 vs. 1.1 ± 0.2), phosphodiesterase (1.4 ± 0.1 vs. 0.7 ± 0.1), and Ca2+-activated K+ channel (0.76 ± 0.16 vs. 0.30 ± 0.01) were greater in LHL compared with LLL lambs. In contrast, LHL had decreased heme oxygenase-1 expression (0.82 ± 0.26 vs. 2.22 ± 0.44) and carbon monoxide production (all P < 0.05). Postnatal pulmonary hypertension induced by 70% of pregnancy at HA promotes cardiopulmonary remodeling that persists at sea level.

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Small Artery Remodeling and Significance in the Development of Hypertension

Cited by 91 publications

References 16 publications

Long-Term Urban Particulate Air Pollution, Traffic Noise, and Arterial Blood Pressure

Long-Term Urban Particulate Air Pollution, Traffic Noise, and Arterial Blood Pressure

Busulphan-Cyclophosphamide Cause Endothelial Injury, Remodeling of Resistance Arteries and Enhanced Expression of Endothelial Nitric Oxide Synthase

Long-term exposure to high-altitude chronic hypoxia during gestation induces neonatal pulmonary hypertension at sea level

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