The Na/K/2Cl cotransporter is increased in hypertrophied vascular smooth muscle cells.

Tseng, Hennessey; Berk, Bradford C.

doi:10.1016/s0021-9258(18)42421-0

Cited by 20 publications

(2 citation statements)

References 36 publications

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“…Importantly, in all these tissues, AR, ion channels and transporters, and aquaporins have been explored in many other papers [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ], suggesting their involvement in ion/water compartment changes.…”

Section: Resultsmentioning

confidence: 99%

“…The cell nucleus appears affected as well by edema that may be severe enough to induce focal chromatolysis ( Figure 1 panel E). Accordingly, several previous papers [ 13 , 14 , 17 ] have demonstrated that vacuoles and cytosol swelling with electron-clear material are produced by massive movements of ions and water accumulating both in the cytosol (cloudy swelling) and/or segregated into vacuoles (vacuolar degeneration), strictly associated with alterations of cell volume control mechanisms—not in the myocardium, but in several other tissues, such as in kidney [ 17 ], liver [ 13 , 14 , 15 ], smooth muscle [ 18 , 19 , 20 ], and lung [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

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Myocardial Aldosterone Receptor and Aquaporin 1 Up-Regulation Is Associated with Cardiomyocyte Remodeling in Human Heart Failure

Frustaci

Letizia

Chimenti

et al. 2021

JCM

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Background: Abnormal aldosterone signaling is a recognized source of cardiovascular damage. Its influence on cardiomyocyte structure, function, and hormonal receptors when associated with heart failure is still unreported. Methods: Twenty-six consecutive patients with heart failure (LVEF < 40%) and normal coronaries and valves underwent left ventricular endomyocardial biopsy (EMB) for evaluation of myocardial substrate. Biopsy samples were processed for histology, electron microscopy, immunohistochemistry, and Western blot analysis of myocardial aldosterone receptor and aquaporin-1 correlated with plasma aldosterone (AD) and renin activity (PRA). Eight patients with virus-negative inflammatory cardiomyopathy (ICM) had a control EMB after 6 months of immunosuppressive therapy and recovery of cardiac function with re-evaluation of cardiomyocyte structure and receptor expression. Results: EMB in addition to the diagnosis of myocarditis (15 cases), dilated cardiomyopathy CM (6), alcohol CM (2), and diabetic CM (3) showed vacuolar degeneration and cloudy swelling of cardiomyocytes corresponding at electron microscopy to ions and water accumulation into cytosol, membrane-bound vesicles, nucleus, and other organelles, and was associated with an increased AD, PRA, and myocardial expression of aldosterone receptor (2.6 fold) and aquaporin 1 (2.7 fold). In the 8 patients recovered from ICM, cardiomyocyte diameter reduced with disappearance of intracellular vacuoles and normalization of cytosol, nucleus, and cell organelles’ electron-density, along with down-regulation of aldosterone receptor and aquaporin-1. Conclusion: Human heart failure is associated with overexpression of myocardial aldosterone receptor and aquaporin-1. These molecular changes are paralleled by intracellular water overloading and cardiomyocyte swelling and dysfunction. Cardiac recovery is accompanied by down-regulation of hormonal receptors and normalization of cell structure and composition.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Myocardial Aldosterone Receptor and Aquaporin 1 Up-Regulation Is Associated with Cardiomyocyte Remodeling in Human Heart Failure

Frustaci

Letizia

Chimenti

et al. 2021

JCM

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Smooth Muscle Cell Hypertrophy, Proliferation, Migration and Apoptosis in Pulmonary Hypertension

Tajsic

Morrell

2010

Comprehensive Physiology

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Pulmonary hypertension is a multifactorial disease characterized by sustained elevation of pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP). Central to the pathobiology of this disease is the process of vascular remodelling. This process involves structural and functional changes to the normal architecture of the walls of pulmonary arteries (PAs) that lead to increased muscularization of the muscular PAs, muscularization of the peripheral, previously nonmuscular, arteries of the respiratory acinus, formation of neointima, and formation of plexiform lesions. Underlying or contributing to the development of these lesions is hypertrophy, proliferation, migration, and resistance to apoptosis of medial cells and this article is concerned with the cellular and molecular mechanisms of these processes. In the first part of the article we focus on the concept of smooth muscle cell phenotype and the difficulties surrounding the identification and characterization of the cell/cells involved in the remodelling of the vessel media and we review the general mechanisms of cell hypertrophy, proliferation, migration and apoptosis. Then, in the larger part of the article, we review the factors identified thus far to be involved in PH intiation and/or progression and review and discuss their effects on pulmonary artery smooth muscle cells (PASMCs) the predominant cells in the tunica media of PAs.

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Angiotensin II‐induced vascular smooth muscle cell hypertrophy: PDGF A‐chain mediates the increase in cell size

Berk

Rao

1993

Journal Cellular Physiology

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We report here that angiotensin II-mediated hypertrophy of vascular smooth muscle cells (VSMC) exhibits PDGF A-chain-dependent and -independent pathways. Secretion of PDGF A-chain is required for the increase in cell size, but not for the increase in protein synthesis. Angiotensin II stimulates a hypertrophic growth response in VSMC characterized by increases in cell size and protein synthesis, but not cell number. Because angiotensin II-stimulated VSMC hypertrophy has been associated with increased PDGF A-chain expression, we studied its role in the hypertrophic response by inhibiting PDGF A-chain expression with hydrocortisone or anti-PDGF antibody. Hydrocortisone (1 microM for 48 h) inhibited basal protein synthesis by 47%, but angiotensin II-stimulated protein synthesis was enhanced (111% increase after hydrocortisone treatment vs. 25% increase in control). In contrast, hypertrophy, as measured by cell size, was completely inhibited. Although hydrocortisone had no effect on early growth signals stimulated by angiotensin II (e.g., activation of protein kinase C, stimulation of Na+/H+ exchange, and c-fos and c-myc expression), it significantly decreased angiotensin II-stimulated secretion of PDGF-like material into the medium from 0.4 to 0.1 ng/ml/24 h (p < 0.01). However, the time course for PDGF secretion (maximal at 16-24 h) was significantly slower than the time course for angiotensin II-stimulated protein synthesis (maximal at 4-12 h). To block the action of PDGF A-chain selectively, VSMC were treated with anti-PDGF A-chain antibody. The antibody completely inhibited the angiotensin II-stimulated increase in cell size, but it had no significant effect on protein synthesis at early times (< 8 h). These findings demonstrate two pathways involved in angiotensin II-stimulated VSMC hypertrophy: an increase in cell size dependent on PDGF A-chain and an increase in protein synthesis independent of PDGF A-chain.

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The Na/K/2Cl cotransporter is increased in hypertrophied vascular smooth muscle cells.

Cited by 20 publications

References 36 publications

Myocardial Aldosterone Receptor and Aquaporin 1 Up-Regulation Is Associated with Cardiomyocyte Remodeling in Human Heart Failure

Myocardial Aldosterone Receptor and Aquaporin 1 Up-Regulation Is Associated with Cardiomyocyte Remodeling in Human Heart Failure

Smooth Muscle Cell Hypertrophy, Proliferation, Migration and Apoptosis in Pulmonary Hypertension

Angiotensin II‐induced vascular smooth muscle cell hypertrophy: PDGF A‐chain mediates the increase in cell size

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