Remodeling Of Cardiovascular System Research Articles

Sex-Specific Impacts of Exercise on Cardiovascular Remodeling.

Cardiovascular diseases (CVD) remain the leading cause of death in men and women. Biological sex plays a major role in cardiovascular physiology and pathological cardiovascular remodeling. Traditionally, pathological remodeling of cardiovascular system refers to the molecular, cellular, and morphological changes that result from insults, such as myocardial infarction or hypertension. Regular exercise training is known to induce physiological cardiovascular remodeling and beneficial functional adaptation of the cardiovascular apparatus. However, impact of exercise-induced cardiovascular remodeling and functional adaptation varies between males and females. This review aims to compare and contrast sex-specific manifestations of exercise-induced cardiovascular remodeling and functional adaptation. Specifically, we review (1) sex disparities in cardiovascular function, (2) influence of biological sex on exercise-induced cardiovascular remodeling and functional adaptation, and (3) sex-specific impacts of various types, intensities, and durations of exercise training on cardiovascular apparatus. The review highlights both animal and human studies in order to give an all-encompassing view of the exercise-induced sex differences in cardiovascular system and addresses the gaps in knowledge in the field.

The impact of various antihypertensive medications on vascular aging

The review summarizes the data of past two decades on the effect of hypertension on vascular aging and considers the effect of chronic inflammation and oxidative stress patterns on the remodeling of cardiovascular system. Clinical studies on the effect of various classes of antihypertensive drugs on age-associated parameters of vascular aging are discussed. These include endothelial dysfunction and arterial assessed by endothelium-dependent vasodilation, pulse wave velocity, augmentation index, cardiovascular index, thickness of the intima-media complex, and so on.

Influence of losartan on structural and functional remodelling of cardiovascular system in comorbidity of chronic obstructive lung disease and arterial hypertension

Aim. To assess the influence of losartan treatment for comorbid chronic obstructive lung disease (COPD) and arterial hypertension (AH) on arterial pressure variability (BP), diastolic function and remodelling of the left ventricle myocardium (LV). Material and methods . Totally, 50 patients with AH and COPD included, mean age 59,8±7,9 y. Depending on the level of mean-daily BP variability (BPV) patients were selected to subgroups with normal (n=15) and increased (n=35) BPV. Results. Patients with normal BPV had concentric hypertrophy type of LV and moderate diastolic dysfunction of LV mostly with relaxation disorder, but in COPD+AH with higher BPV patients there were more prominent structural and geometric LV disorders with tendency to eccentric LV hypertrophy, as more significant diastolic function disorders with the part of patients having pseudonormal diastolic dysfunction type. Conclusion . With inclusion of losartan to the protocol of patients’ treatment, there is decrease of structural impairment of the LV that is the lowering of end diastolic LV size, LV myocardial mass, increase of ejection fraction, increase of the number of patients having normal LV geometry, decrease of signs of diastolic dysfunction. In losartan prescription, there is better adherence of patients to treatment.

Prognostic significance of endothelial dysfunctional markers of the first stage of chronic kidney disease

Non-adaptive remodeling of cardiovascular system and progressive kidney damage at chronic kidney disease (CKD) is associated with the development of endothelial dysfunction (ED) and apoptosis. The aim of this research was to study the changes of indicators of apoptosis and ED in patients with CKD 1 stage throughout 12 months. Complex biochemical, immunoferment and tool methods were applied at patient examinations. Arterial pressure of all observed patients was resolved on target values in 12 months. However, the indicators of endothelium-dependent vasodilation (EDV) increased in 55 patients (1st group), and the peak of circulating blood volume in skin microvessels in 22 patients (2nd group) wasn't changed: 134±4 % и 136±4 %, p>0.1. The level of the annexin A5 reduced from 3.5±0.47 to 1.27±0.31 ng/ml (p 0.1 in 2nd group. Diurnal excretion of sodium chloride decreased from 6.8±0.57 g/d to 2.8±0.39 g/d (p<0.05) in patients of 1st group. Dynamics of these indicators was not marked in patients of 2nd group: accordingly from 7.39±0.63 g/d to 7.01±0.65 g/d. Diurnal excretion of sodium chloride reflected the salt intake in patients with CKD 1 stage is associated with disturbance of endothelial-dependent vasodilation and apoptosis.

Neurofibromatosis type 1 (NF1) and pheochromocytoma: prevalence, clinical and cardiovascular aspects

The aim of the study was to evaluate the prevalence of pheochromocytoma (PHEO) in patients with neurofibromatosis type 1 (NF1), and to analyze the behavior of some anthropometric and cardiovascular parameters. In 48 consecutive NF1 patients, urinary metanephrines and vanillylmandelic acid excretion were assessed. The body mass index (BMI), waist circumference (WC), ambulatory blood pressure monitoring (ABPM), echocardiography and ultrasound carotid arterial wall evaluation were performed. In NF1 patients, 11 (29.3%) had arterial hypertension, 7 (14.6%) had a PHEO. Four (57%) NF1 patients with PHEO were symptomatic at the diagnosis. In PHEO-NF1 patients, we revealed a lower BMI and WC values with respect to NF1 patients without PHEO and normal subjects (NSs) (p<0.05), respectively. The nocturnal non-dipping pattern at the ABPM was present in 40.4% of NF1 patients, and in particular this phenomenon was present in PHEO-NF1 patients (71.4%). Left ventricular mass index and intima media thickness were significantly higher in NF1 patients as compared to NS (p<0.05), particularly in NF1-PHEO patients (p<0.05). In conclusions, these findings revealed high prevalence of PHEO in NF1 patients and suggest that, in addition to blood pressure, humoral factors (increased sympathetic activity or neurofibromin), influence the pathogenesis of remodeling of cardiovascular system.

Remodeling of cardiovascular system and function of parathyroid glands in patients with arterial hypertension

Features of structural and functional remodeling of the left ventricular and brachial artery and parathyroid hormone blood levels are studied in 95 patients with arterial hypertension. It was shown that increased parathyroid hormone blood levels correlate with increased frequency and evidence of remodeling of left ventricular and brachial artery, also significant decrease in diastolic function and endothelium-dependent vasodilatation. 21.6 % of hypertensive patients have asymptomic of parathyroid hormone hyper secretion. Pathological type of circadian blood pressure profile was observed in these patients.

740. Delivery of Recombinant Adeno-Associated Virus Mediated Human Kallikrein Gene Reduces Permanently Blood Pressure, Attenuates the Remodeling of Cardiovascular System and Prevents Stroke in Spontaneously Hypertensive Rats

740. Delivery of Recombinant Adeno-Associated Virus Mediated Human Kallikrein Gene Reduces Permanently Blood Pressure, Attenuates the Remodeling of Cardiovascular System and Prevents Stroke in Spontaneously Hypertensive Rats

Proadrenomedullin-derived peptides as autocrine-paracrine regulators of cell growth.

Proadrenomedullin (pADM)-derived peptides, adrenomedullin (ADM) and pADM N-terminal 20 peptide (PAMP), are hypotensive peptides, which are expressed, along with their receptors, in several tissues and organs, the function of which they regulate by acting in an autocrine-paracrine manner. Apart from their involvement in the regulation of blood pressure and fluid and electrolyte homeostasis, pADM-derived peptides appear to play a role in the modulation of cell and tissue growth. Evidence has been provided that ADM: 1) favors the remodeling of cardiovascular system under pathological conditions, by exerting an antiapoptotic effect on endothelial cells and an antiproliferogenic and antimigratory action on vascular smooth-muscle cells during neointimal hyperplasia, and by decreasing proliferation and protein synthesis of cardiac myocytes and fibroblasts. These last two effects are mediated by calcitonin gene-related peptide type 1 (CGRP1) receptors coupled to the adenylate cyclase (AC)/protein kinase (PK) A-dependent cascade; 2) inhibits proliferation and enhances apoptosis of kidney mesangial cells, through the modulation of mitogen-activated PK (MAPK) cascades; 3) stimulates proliferation of adrenal zona glomerulosa cells, acting via CGRP1 receptor coupled to the tyrosine kinase-dependent MAPK cascade, thereby possibly being involved in the maintenance and stimulation of adrenal growth; 4) enhances proliferation of skin and mucosa epithelial cells and fibroblasts, by activating CGRP1 receptor coupled to the AC/PKA signaling pathway; and 5) enhances proliferation of several tumor-cell lines through the activation of the AC/PKA cascade, which suggests a potential role for ADM as promoter of neoplastic growth. The growth effects of PAMP have been far less investigated: findings indicate that this peptide, like ADM, enhances adrenal zona glomerulosa-cell proliferation, and, in contrast with ADM, depresses DNA synthesis in some cancer-cell lines. Both pADM-derived peptides are thought to be involved in embryogenesis, such a contention being based on the demonstration of high pADM-gene expression during the crucial phases of organ growth and differentiation.

Effects of long-term treatment with nonselective endothelin receptor antagonist, TAK-044, on remodeling of cardiovascular system with sustained volume overload.

To assess the role of endothelin-1 (ET-1) on cardiovascular remodeling, nonselective endothelin-receptor antagonist TAK-044 was administered for the long term to rabbits with or without arteriovenous (A-V) shunt formation. Six weeks after sham operation (n = 12) or carotid-jugular shunt formation (n = 21), TAK-044 (30 mg/day) or saline was infused subcutaneously using osmotic mini pumps for another 6 weeks. Twelve weeks after operation, left ventricular (LV) diameter was enlarged with the presence of an A-V shunt; however, the levels of LV diameter and arterial pressure or the postmortem weight of LVs of shunt rabbits were similar between saline and TAK-044 groups. A linear relation of the luminal diameter and the medial cross-sectional area of the left and right carotid arteries was similar between shunt + saline and shunt + TAK-044 groups. In saline groups, myocardial ET-1 levels were higher in shunt than in sham rabbits (217+/-22 vs. 136+/-19 pg/g tissue; p < 0.01 between rabbit groups) without changes in plasma ET-1 concentrations during saline infusion for 6 weeks. Differences in plasma ET-1 levels before and 6 weeks after the administration of TAK-044 were 0.32+/-0.78 and 0.16+/-0.28 pg/ml (NS between periods) in shunt and sham groups, respectively. In TAK-044 groups, myocardial ET-I levels 12 weeks after operation were similarly lower in both sham (105+/-7.4 pg/g tissue) and shunt rabbits (126+/-9.2 pg/g tissue) than in those with saline administration; however, the plasma ET-1 concentrations were increased significantly 6 weeks after TAK-044 administration by 5.0+/-0.6-fold and 3.5 +/-0.3-fold (p < 0.01) of the levels 6 weeks after operation in shunt and sham groups (NS between groups), respectively. Accordingly, myocardial but not plasma ET-1 levels were increased by a long-term burden of volume overload and were attenuated by a long-term administration of TAK-044 without altering drastically the hemodynamics or vascular remodeling. These results suggest that endogenous ET-1 does not play a major role in the compensatory stage of cardiovascular remodeling in the present volume-overload model.

Physiological functions of prostanoid receptors and their subtypes

Prostaglandins exert a wide variety of biological actions through specific receptors. The prostaglandins PGE2 and PGF2 alpha have been suggested to affect many physiological processes. There have been four pharmacologically identified receptor subtypes, EP1 through EP4 for PGE2 and a single receptor type, FP for PGF2 alpha. However, it is yet unknown as to which receptor is involved in each process. To make this clear, we investigated the distribution of these receptors in various systems and established mice deficient in each receptor and examined their physiology. Finally, we found that these receptors are involved in several processes associated with reproduction physiology. FP-deficient mice are able to become pregnant, but cannot deliver their pups because of the lack of parturition; luteolysis does not occur normally. EP2-deficient mice are able to become pregnant, but their litter sizes are much reduced, which is due to defects in ovulation and fertilization; cumulus cell function is impaired. EP4-deficient mice die within a few days after birth because of patency of the ductus arteriosus; remodeling of cardiovascular system during birth is impaired. Thus, the E- and F-types of prostaglandins play roles in cumulus function, luteolysis and ductus closure through EP2, FP and EP4, respectively.

Effects of chronic treatment with non-selective endothelin receptor antagonist, TAK-044, on remodeling of cardiovascular system with sustained volume-overload

Effects of chronic treatment with non-selective endothelin receptor antagonist, TAK-044, on remodeling of cardiovascular system with sustained volume-overload