Vascular remodeling in experimental hypertension.

The basic hemodynamic abnormality in hypertension is an increased peripheral resistance that is due mainly to a decreased vascular lumen derived from structural changes in the small arteries wall, named (as a whole) vascular remodeling. The vascular wall is an active, flexible, and integrated organ made up of cellular (endothelial cells, smooth muscle cells, adventitia cells, and fibroblasts) and noncellular (extracellular matrix) components, which in a dynamic way change shape or number, or reorganize in response to physiological and pathological stimuli, maintaining the integrity of the vessel wall in physiological conditions or participating in the vascular changes in cardiovascular diseases such as hypertension. Research focused on new signaling pathways and molecules that can participate in the mechanisms of vascular remodeling has provided evidence showing that vascular structure is not only affected by blood pressure, but also by mechanisms that are independent of the increased pressure.

Effect of nebivolol on cardiovascular changes associated with a rat model of insulin-resistance.

Nebivolol is a vasodilator that combines beta-adrenergic blocking activity with a relaxant effect on vascular smooth muscle cells (VSMC) mediated by the endothelial nitric oxide (NO) pathway. FFR provide a model of dietary-induced insulin-resistance syndrome, which has been used to study the pathophysiological mechanisms associated with this syndrome. Our main objective was to examine the effect of long-term administration of nebivolol on metabolic and cardiovascular variables in fructose-fed rats (FFR), a model in which an altered bioavailability of NO has been already described.

Chronic administration of resveratrol prevents biochemical cardiovascular changes in fructose-fed rats.

Background: There seems to be a link between the cluster of risk factors known as insulin resistance syndrome with endothelial dysfunction. Resveratrol (3,4,5-trihydroxyestilbene) (RV), an antioxidant found in many components of the human diet, has been proposed as an effective agent in the prevention of several pathologic processes. This study examined the effect of chronic administration of RV on endothelial nitric oxide synthase (eNOS) activity in cardiovascular tissues and on plasma lipid peroxidation in fructose-fed rats (FFR), an experimental model of this syndrome.

Vascular smooth muscle cell NAD(P)H oxidase activity during the development of hypertension: Effect of angiotensin II and role of insulinlike growth factor-1 receptor transactivation.

Objective: We investigated whether angiotensin II (Ang II)-induced reactive oxygen species (ROS) generation is altered in vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHR) during the phases of prehypertension, developing hypertension, and established hypertension and assessed the putative role of insulinlike growth factor-1 receptor (IGF-1R) in Ang II-mediated actions.

Methods: The VSMCs from SHR and Wistar-Kyoto rats (WKY) aged 4 (prehypertensive), 9 (developing hypertension), and 16 (established hypertension) weeks were studied. The ROS production and NAD(P)H oxidase activation were determined by fluorescence and chemiluminescence, respectively.

Mechanisms of cardiovascular changes in an experimental model of syndrome X and pharmacological intervention on the renin-angiotensin-system.

Various cardiovascular risk factors and disease states similar to those present in type 2 diabetic patients also seem to be present in non-diabetic individuals. This cluster of risk factors has been called syndrome X, also known as metabolic cardiovascular syndrome or insulin resistance syndrome. Vascular wall components changes, including endothelial dysfunction and vascular smooth muscle cell (VSMC) migration and proliferation, could be involved in the cardiovascular alterations associated with this state.

Chronic administration of losartan reverses cardiovascular changes in hypertensive fructose-fed rats.

The cluster of risk factors including hyperinsulinemia, insulin resistance, hypertriglyceridemia and hypertension has been called syndrome X. Several evidences link the insulin resistance syndrome with endothelial dysfunction. Since the participation of the renin-angiotensin system (RAS) in this pathology is still unclear, the present study examined the effect of chronic administration of an angiotensin AT1 receptor antagonist, losartan (L), on endothelial nitric oxide synthase (eNOS) activity in aortic endothelium and cardiac tissue, and on the proliferation of primary cultured aortic smooth muscle cells (SMC), obtained from fructose-fed rats (FFR), an experimental model of syndrome X Male Wistar rats were used: Control, FFR and FFR+L (n = 8 in each group).

Proteoglycans production by aortic vascular smooth muscle cells from hypertensive rats.

Remodeling of large and small arteries contributes to the development and complications of hypertension. Artery structural changes in chronic sustained hypertension include vascular smooth muscle cells (VSMC) proliferation and extracellular matrix (ECM) modifications. Extracellular constituents such as proteoglycans (PGs), may modulate vascular stiffness and VSMC growth and differentiation.

Effects of enalapril on the vascular wall in an experimental model of syndrome X.

Evidence links the insulin resistance syndrome with endothelial dysfunction. Previously, we have described a decreased endothelial nitric oxide synthase (eNOS) activity in both aortic endothelium and cardiac tissue, and an increased proliferation of aortic primary cultured vascular smooth muscle cells (pC-VSMCs), obtained from fructose-fed rats (FFR), an experimental model of syndrome X. Because the participation of the renin-angiotensin system (RAS) in this model is still unclear, the present study examined the effect of chronic administration of an angiotensin converting enzyme (ACE) inhibitor enalapril (E) on pC-VSMCs proliferation and eNOS activity in a conduit artery (aorta) and in resistance vessels (mesenteric vascular bed) from fructose-fed rats.

Changes of inducible nitric oxide synthase in aortic cells during the development of hypertension: effect of angiotensin II.

Nitric oxide (NO) generation by inducible nitric oxide synthase (iNOS) in the vascular smooth muscle cells (VSMC), may play a role in blood vessel tone regulation. Lipopolysaccharide (LPS) induced iNOS activity and subsequent nitrite production by cultured aortic VSMC, from SHR with an established chronic blood pressure elevation (adult SHR) or during the period preceding the development of hypertension (young SHR) and from age-matched normotensive Wistar (W) rats were compared. Angiotensin II (Ang II) effect was also evaluated.

Early changes in proteoglycans production by resistance arteries smooth muscle cells of hypertensive rats.

Several functional and structural modifications at the vascular level have been described in spontaneously hypertensive rats (SHR) during the early development of hypertension. In this study, we hypothesize that changes in the extracellular matrix (ECM) could precede the development of hypertension. Synthesis of secreted and membrane-bound sulfated proteoglycans (S-PG) by cultured vascular smooth muscle cells (VSMC) obtained from young spontaneously hypertensive rats (pSHR) mesenteric resistance arteries, during the period preceding the elevation of blood pressure (BP) was tested.

Aortic smooth muscle cell proliferation and endothelial nitric oxide synthase activity in fructose-fed rats.

The aim of this study was to evaluate the proliferative behavior of vascular smooth muscle cells in primary culture (pC-SMC) and the endothelial nitric oxide synthase (eNOS) activity in the endothelial lining of the aorta of fructose-fed rats (FFR). This is an experimental model of syndrome X, a cluster of cardiovascular risk factors including hyperinsulinemia, insulin resistance, and hypertension that has been suggested to be of pathophysiologic importance for the development of atherosclerosis. Male Wistar rats were used: Control (n = 12) and FFR (n = 12).

Proteoglycan production by vascular smooth muscle cells from resistance arteries of hypertensive rats.

Extracellular matrix (ECM) modifications in the vascular wall contribute to the narrowing of arteries in hypertension. Because direct evidence for the role of proteoglycans (PGs) in the pathological process of resistance-sized arteries has not already been demonstrated, we examined the effect of growth factors on secreted and membrane-bound PG synthesis by cultured mesenteric vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and Wistar rats. After 48 hours of stimulation with angiotensin II (Ang II), platelet-derived growth factor (PDGF-BB), and 10% fetal calf serum (FCS) or 0.

[Accumulation of actin and adhesion to HEp-2 cells of strains of Escherichia coli isolated from children with diarrhea in Mendoza, Argentina].

E. coli strains are the major bacterial cause of diarrhea among children under 2 years of age residing in Mendoza, Argentina. Detection of diarrheogenic E.

Proliferative effect of insulin on cultured smooth muscle cells from rat mesenteric resistance vessels.

The present study evaluates the growth promoting effect of insulin on the proliferative activity of cells from rat mesenteric arteries in culture in order to test the hypothesis that insulin may play a pathogenetic role in the hypertrophy of resistance vessels. The proliferative effect of insulin was studied in cultured vascular smooth muscle cells (SMC) obtained from two functionally different rat vessels: mesenteric arteries and aorta. Growth characteristics (cell number and growth rate) of mesenteric and aortic cells were determined after a quiescent period and followed-up for 24, 72, and 120 h after the addition of insulin.

Magnesium: effects on reperfusion arrhythmias and membrane potential in isolated rat hearts.

The effects of Mg2+ concentration (Mg2+o, 0, 1.2, 2.4, and 4.

Effect of beta adrenoreceptor blocking drugs on the responses of isolated rat mesenteric arteries.

The effect of several beta-blockers on the vasoactive effect of several substances was studied on the perfused isolated rat mesenteric vessels. The agonists were tested while the beta-blocker was infused; the effects were compared in the same experiment with those observed in a control period in which the agonists were injected without simultaneous infusion of beta-blocker. l-propranolol, infused at three different doses, did not modify the vascular effect of either angiotensin II (AII) or vasopressin (VP).