Cellular Hypertrophy in Subcutaneous Small Arteries of Patients With Renovascular Hypertension

Rizzoni, Damiano; Porteri, Enzo; Guefi, Daniele; Piccoli, Alfonso; Castellano, Maurizio; Pasini, Giancarlo; Muiesan, María Lorenza; Mulvany, Michael J.; Rosei, Enrico Agabiti

doi:10.1161/01.hyp.35.4.931

Cited by 103 publications

(70 citation statements)

References 39 publications

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“…16 Our data showing that chronic NE infusion in mice does not evoke any effect on vascular growth could appear to be in conflict with these previous observations. However, Rizzoni et al 17 recently observed eutrophic vascular remodeling in patients with pheochromocytoma similar to that observed in essential hypertensives, with no changes in the vascular smooth muscle cell component, which, in contrast, is significantly increased in patients with renovascular hypertension. Thus, it must be emphasized again that because the vasculature is a highly differentiated organ system composed of multiple cell types, a number of other factors, which are lacking in the cell culture system, can concomitantly participate in vascular remodeling, which confirms the limitations of comparing in vitro and in vivo experiments.…”

Section: Discussionsupporting

confidence: 57%

Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice

et al. 2002

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Background-The ␣ 1 -adrenergic receptors (␣ 1 -ARs) play a key role in cardiovascular homeostasis. However, the functional role of ␣ 1 -AR subtypes in vivo is still unclear. The aim of this study was to evaluate the cardiovascular influences of ␣ 1b -AR. Methods and Results-In transgenic mice lacking ␣ 1 -AR (KO) and their wild-type controls (WT), we evaluated blood pressure profile and cardiovascular remodeling induced by the chronic administration (18 days via osmotic pumps) of norepinephrine, angiotensin II, and subpressor doses of phenylephrine. Our results indicate that norepinephrine induced an increase in blood pressure levels only in WT mice. In contrast, the hypertensive state induced by angiotensin II was comparable between WT and KO mice. Phenylephrine did not modify blood pressure levels in either WT or KO mice. The cardiac hypertrophy and eutrophic vascular remodeling evoked by norepinephrine was observed only in WT mice, and this effect was independent of the hypertensive state because it was similar to that observed during subpressor phenylephrine infusion. Finally, the cardiac hypertrophy induced by thoracic aortic constriction was comparable between WT and KO mice. Conclusions-Our data demonstrate that the lack of ␣ 1b -AR protects from the chronic increase of arterial blood pressure induced by norepinephrine and concomitantly prevents cardiovascular remodeling evoked by adrenergic activation independently of blood pressure levels. (Circulation. 2002;105:1700-1707.)

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Section: Discussionsupporting

confidence: 57%

Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice

et al. 2002

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“…In addition, we could not evaluate the structural alterations of small resistance arteries at cellular levels (vascular smooth muscle cell hypertrophy or hyperplasia), because of the complexity of the techniques needed. 32 In conclusion, the MHS presents cardiac (but not vascular) remodeling, endothelial dysfunction and a peculiar contractile response to NE, compared with the other groups. The increase in systolic blood pressure, together with the observed trend to vascular remodeling observed in the MNA strain support a pathogenic role of a-adducin.…”

Section: Adducin and Small Artery Remodeling D Rizzoni Et Almentioning

confidence: 79%

Functional alterations of mesenteric small resistance arteries in Milan hypertensive and normotensive rats

et al. 2009

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The Milan hypertensive rat strain (MHS) is a genetic strain in which cardiovascular phenotypes seem to be dependent, at least in part, on adducin gene polymorphisms. The aim of our study was to evaluate the structure, contractile responses and endothelium-dependent vasodilation in mesenteric small resistance arteries in 12-week-old MHS, (n¼7), age-matched Milan normotensive rats (MNS, n¼7) and congenic strains in which the DNA segments carrying the a-adducin locus from the MHS have been introgressed into the MNS (MNA, n¼7). Systolic blood pressure (tail cuff) and left ventricular weight to body weight were measured. Mesenteric small arteries were dissected and mounted on a micromyograph; the media:lumen ratio was then calculated. Concentration-response curves to acetylcholine and to norepinephrine (NE) were created. Systolic blood pressure was significantly increased in the MHS and MNA strains compared with the MNS. No significant difference in mesenteric small resistance artery structure was observed among the groups; however, a slightly more elevated media:lumen ratio was observed in MNA compared with the MNS. In contrast, left ventricular weight to body weight was significantly increased and ACH-induced dilatation was significantly impaired in the MHS and in MNA compared with MNS. The concentration-response curve to NE in the MHS showed significantly reduced sensitivity to NE; however, maximum contraction was increased in the MHS vs. the other groups. The MHS presents cardiac (but not vascular) remodeling, endothelial dysfunction and a peculiar contractile response to NE, compared with the other groups. The systolic blood pressure increase and trend to vascular remodeling in MNA support the pathogenic role of a-adducin.

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“…Paper [37], which is also based on the biopsy-test data, studies the enlargement of VSMCs in the small arteries as well. It deals with the arteries in the inner layer of the skin, i.e., the layer of subcutaneous fat.…”

Section: Appendix Main Vibration Injuries In An Slt Thementioning

confidence: 99%

Propagation of Acoustic Waves Caused by the Accelerations of Vibrating Hand-Held Tools in Viscoelastic Soft Tissues of Human Hands and a Mechanobiological Picture for the Related Injuries

Mamontov¹,

Berbyuk²

2017

JAMP

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As is well known, hand-arm vibration syndrome (HAVS), or vibration-induced white finger (VWF), which is a secondary form of Raynaud's syndrome, is an industrial injury triggered by regular use of vibrating hand-held tools. According to the related biopsy tests, the main vibration-caused lesion is an increase in the thickness of the artery walls of the small arteries and arterioles resulted from enlarged vascular smooth muscle cells (VSMCs) in the wall layer known as tunica media. The present work develops a mechanobiological picture for the cell enlargement. The work deals with acoustic variables in solid materials, i.e., the non-equilibrium components of mechanical variables in the materials in the case where these components are weakly non-equilibrium. The work derives an explicit expression for the infinite-time cell-volume relative enlargement. This enlargement is directly affected by the acoustic pressure in the soft living tissue (SLT). In order to reduce the enlargement, one can reduce either the ratio of the acoustic pressure in the SLT to the cell bulk modulus or the relaxation time induced by the cell osmosis, or both the characteristics. Also, a mechanoprotective role of the above relaxation time in the cell-volume maintenance is noted. The above mechanobiological picture focuses attention on the pressure in an SLT and, thus, modeling of propagation of acoustic waves caused by the acceleration of a vibrating hand-held tool. The present work analyzes the propagation along the thickness of an infinite planar layer of an SLT. The work considers acoustic modeling. As a general viscoelastic acoustic model, the work suggests linear non-stationary partial integro-differential equation (PIDE) for the weakly non-equilibrium component of the average normal stress (ANS) or, briefly, the acoustic ANS. The PIDE is, in the exponential approximation for the normalized stress-relaxation function (NSRF) reduced to the third-order linear non-stationary partial differential equation (PDE), which is of the Zener type. The unique advantage of the PIDE is that it presents a compact model for the acoustic ANS in an SLT, which explicitly includes the NSRF, thereby enabling a consistent description of the lossy-propagation effects inherent in SLTs. The one-spatial-coordinate version of this PDE in the planar SLT layer with the corresponding boundary conditions is considered. The relevance of these settings is motivated by a conclusion of other authors, which is based on the results of the frequency-domain simulation in three spatial coordinates. The boundary-value problem at arbitrary value of the stress-relaxation time (SRT) and arbitrary but sufficiently regular shape of the external acceleration is analytically solved by means of the Fourier method. The obtained solution is the steady-state acoustic ANS and allows calculation of the corresponding steady-state acoustic pressure as well. The derived analytical representations are computationally implemented. Propagation of the pressure waves in the SLT layer at zero ...

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Cellular Hypertrophy in Subcutaneous Small Arteries of Patients With Renovascular Hypertension

Cited by 103 publications

References 39 publications

Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice

Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice

Functional alterations of mesenteric small resistance arteries in Milan hypertensive and normotensive rats

Propagation of Acoustic Waves Caused by the Accelerations of Vibrating Hand-Held Tools in Viscoelastic Soft Tissues of Human Hands and a Mechanobiological Picture for the Related Injuries

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Cellular Hypertrophy in Subcutaneous Small Arteries of Patients With Renovascular Hypertension

Cited by 103 publications

References 39 publications

Cardiovascular Influences of α 1b -Adrenergic Receptor Defect in Mice

Cardiovascular Influences of α 1b -Adrenergic Receptor Defect in Mice

Functional alterations of mesenteric small resistance arteries in Milan hypertensive and normotensive rats

Propagation of Acoustic Waves Caused by the Accelerations of Vibrating Hand-Held Tools in Viscoelastic Soft Tissues of Human Hands and a Mechanobiological Picture for the Related Injuries

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Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice

Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice