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      Tunica intima compensation for reduced stiffness of the tunica media in aging renal arteries as measured with scanning acoustic microscopy

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      Journal: PLoS ONE
      Publisher: Public Library of Science

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          Abstract

          Objectives

          Aging causes stiffness and decreased function of the renal artery (RA). Histological study with light microscopy can reveal microscopic structural remodeling but no functional changes. The present study aimed to clarify the association between structural and functional aging of the RA through the use of scanning acoustic microscopy.

          Methods

          Formalin-fixed, paraffin-embedded cross-sections of renal arteries from 64 autopsy cases were examined. Speed-of-sound (SOS) values of three layers, which correspond to the stiffness, were compared among different age groups. SOS of the tunica media was examined in terms of blood pressure (BP) and SOS of the ascending aorta. Vulnerability to proteases was assessed by SOS reduction after collagenase treatment.

          Results

          The tunica intima presented inward hypertrophy with luminal narrowing, and the tunica media showed outward hypertrophic remodeling with aging. SOS of the tunica media and internal and external elastic laminae showed a reverse correlation with age. SOS of the tunica media was negatively correlated with BP and strongly associated with that of the aorta. The tunica media of young RAs were more sensitive to collagenase compared with the old ones.

          Conclusions

          Scanning acoustic microscopy is useful for observing the aging process of the RA. This technique simultaneously shows structural and mechanical information from each portion of the RA. In the process of aging, the RA loses contractile function and elasticity as a result of protease digestion. The tunica media and the internal and external elastic laminae exhibit reduced stiffness, but the tunica intima stiffens with atherosclerosis. As a consequence, the RA’s outer shape changes from round to oval with inward and outward hypertrophy. This indicates that the inner resistant intima supports the mechanical weakness of the tunica media to compensate for an increase in BP with aging.

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          Most cited references22

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          Structural and Functional Changes With the Aging Kidney.

          Aleksandar Denic, Richard Glassock, Andrew D Rule (2016)
          Senescence or normal physiologic aging portrays the expected age-related changes in the kidney as compared to a disease that occurs in some but not all individuals. The microanatomical structural changes of the kidney with older age include a decreased number of functional glomeruli from an increased prevalence of nephrosclerosis (arteriosclerosis, glomerulosclerosis, and tubular atrophy with interstitial fibrosis), and to some extent, compensatory hypertrophy of remaining nephrons. Among the macroanatomical structural changes, older age associates with smaller cortical volume, larger medullary volume until middle age, and larger and more numerous kidney cysts. Among carefully screened healthy kidney donors, glomerular filtration rate (GFR) declines at a rate of 6.3 mL/min/1.73 m(2) per decade. There is reason to be concerned that the elderly are being misdiagnosed with CKD. Besides this expected kidney function decline, the lowest risk of mortality is at a GFR of ≥75 mL/min/1.73 m(2) for age <55 years but at a lower GFR of 45 to 104 mL/min/1.73 m(2) for age ≥65 years. Changes with normal aging are still of clinical significance. The elderly have less kidney functional reserve when they do actually develop CKD, and they are at higher risk for acute kidney injury.
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            Clinical applications of arterial stiffness; definitions and reference values.

            Michael F O'Rourke, Jan Staessen, Charalambos Vlachopoulos … (2002)
            Arterial stiffening is the most important cause of increasing systolic and pulse pressure, and for decreasing diastolic pressure beyond 40 years of age. Stiffening affects predominantly the aorta and proximal elastic arteries, and to a lesser degree the peripheral muscular arteries. While conceptually a Windkessel model is the simplest way to visualize the cushioning function of arteries, this is not useful clinically under changing conditions when effects of wave reflection become prominent. Many measures have been applied to quantify stiffness, but all are approximations only, on account of the nonhomogeneous structure of the arterial wall, its variability in different locations, at different levels of distending pressure, and with changes in smooth muscle tone. This article summarizes the methods and indices used to estimate arterial stiffness, and provides values from a survey of the literature, followed by recommendations of an international group of workers in the field who attended the First Consensus Conference on Arterial Stiffness, which was held in Paris during 2000, under the chairmanship of M.E. Safar and E.D. Frohlich.
            Article 0 comments Cited 201 times – based on 0 reviews     Review now
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              Vascular Smooth Muscle Cells and Arterial Stiffening: Relevance in Development, Aging, and Disease.

              Patrick Lacolley, Véronique Regnault, Patrick Segers … (2017)
              The cushioning function of large arteries encompasses distension during systole and recoil during diastole which transforms pulsatile flow into a steady flow in the microcirculation. Arterial stiffness, the inverse of distensibility, has been implicated in various etiologies of chronic common and monogenic cardiovascular diseases and is a major cause of morbidity and mortality globally. The first components that contribute to arterial stiffening are extracellular matrix (ECM) proteins that support the mechanical load, while the second important components are vascular smooth muscle cells (VSMCs), which not only regulate actomyosin interactions for contraction but mediate also mechanotransduction in cell-ECM homeostasis. Eventually, VSMC plasticity and signaling in both conductance and resistance arteries are highly relevant to the physiology of normal and early vascular aging. This review summarizes current concepts of central pressure and tensile pulsatile circumferential stress as key mechanical determinants of arterial wall remodeling, cell-ECM interactions depending mainly on the architecture of cytoskeletal proteins and focal adhesion, the large/small arteries cross-talk that gives rise to target organ damage, and inflammatory pathways leading to calcification or atherosclerosis. We further speculate on the contribution of cellular stiffness along the arterial tree to vascular wall stiffness. In addition, this review provides the latest advances in the identification of gene variants affecting arterial stiffening. Now that important hemodynamic and molecular mechanisms of arterial stiffness have been elucidated, and the complex interplay between ECM, cells, and sensors identified, further research should study their potential to halt or to reverse the development of arterial stiffness.
              Article 0 comments Cited 176 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Katsutoshi Miura:
                ORCID: https://orcid.org/0000-0002-9262-7702
                Role: ConceptualizationRole: Data curationRole: Funding acquisitionRole: InvestigationRole: MethodologyRole: ResourcesRole: Writing – original draftRole: Writing – review & editing
                Jun Yu: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS One
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 4 November 2020
                Publication date Collection: 2020
                Volume: 15
                Issue: 11
                Electronic Location Identifier: e0234759
                Affiliations
                [001]Department of Health Science, Pathology and Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Japan
                Temple University School of Medicine, UNITED STATES
                Author notes

                Competing Interests: The author has declared that no competing interests exist.

                Author information
                https://orcid.org/0000-0002-9262-7702
                Article
                Publisher ID: PONE-D-20-16504
                DOI: 10.1371/journal.pone.0234759
                PMC ID: 7641345
                PubMed ID: 33147291
                SO-VID: ec8af734-1614-4c64-bf51-1bcab0def9ba
                Copyright © © 2020 Katsutoshi Miura
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 1 June 2020
                Date accepted : 29 September 2020
                Page count
                Figures: 10, Tables: 0, Pages: 18
                Funding
                Funded by: Japan Society for the Promotion of Science KAKENHI
                Award ID: 17K1088901 and 15K08375
                Award Recipient :
                ORCID: https://orcid.org/0000-0002-9262-7702
                Funded by: Toukai Foundation for Technology
                Award Recipient :
                ORCID: https://orcid.org/0000-0002-9262-7702
                This study was funded by the Japan Society for the Promotion of Science KAKENHI (grant no. 17K1088901 and 15K08375), and by the Toukai Foundation for Technology. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology and Life Sciences
                Subject: Developmental Biology
                Subject: Organism Development
                Subject: Aging
                Subject: Biology and Life Sciences
                Subject: Physiology
                Subject: Physiological Processes
                Subject: Aging
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Cardiovascular Anatomy
                Subject: Blood Vessels
                Subject: Arteries
                Subject: Renal Arteries
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Cardiovascular Anatomy
                Subject: Blood Vessels
                Subject: Arteries
                Subject: Renal Arteries
                Subject: Physical Sciences
                Subject: Materials Science
                Subject: Material Properties
                Subject: Mechanical Properties
                Subject: Stiffness
                Subject: Medicine and Health Sciences
                Subject: Vascular Medicine
                Subject: Blood Pressure
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Cardiovascular Anatomy
                Subject: Blood Vessels
                Subject: Aorta
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Cardiovascular Anatomy
                Subject: Blood Vessels
                Subject: Aorta
                Subject: Biology and Life Sciences
                Subject: Organisms
                Subject: Eukaryota
                Subject: Animals
                Subject: Vertebrates
                Subject: Fish
                Subject: Osteichthyes
                Subject: Eels
                Subject: Biology and Life Sciences
                Subject: Zoology
                Subject: Animals
                Subject: Vertebrates
                Subject: Fish
                Subject: Osteichthyes
                Subject: Eels
                Subject: Medicine and Health Sciences
                Subject: Vascular Medicine
                Subject: Atherosclerosis
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Musculoskeletal System
                Subject: Muscles
                Subject: Smooth Muscles
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Musculoskeletal System
                Subject: Muscles
                Subject: Smooth Muscles
                Custom metadata
                Data Availability All relevant data are within the paper and its Supporting Information files.

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