prehypertension/phosphatase

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Induction of mitogen-activated protein kinase phosphatase-1 during acute hypertension.

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Recently, we demonstrated that elevated blood pressure activates mitogen-activated protein (MAP) kinases in rat aorta. Here we provide evidence that the vascular response to acute hypertension also includes induction of MAP kinase phosphatase-1 (MKP-1), which has been shown to function in the

Transgenic Overexpression of Tissue-Nonspecific Alkaline Phosphatase (TNAP) in Vascular Endothelium Results in Generalized Arterial Calcification.

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BACKGROUND Ectopic vascular calcification is a common condition associated with aging, atherosclerosis, diabetes, and/or chronic kidney disease. Smooth muscle cells are the best characterized source of osteogenic progenitors in the vasculature; however, recent studies suggest that cells of

Metabolic intermediates, enzymes and lysosomal activity in aortas of spontaneously hypertensive rats.

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Metabolic intermediate levels, glycolytic and Krebs cycle enzyme activities and lysosomal acid hydrolase activities were measured in aortas of spontaneously hypertensive (SHR) versus normotensive (WKY) rats. In the hypertensive aortas the level of lactate, the ratio of lactate to glucose and of

High-Sensitivity CRP (C-Reactive Protein) Is Associated With Incident Carotid Artery Plaque in Chinese Aged Adults.

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Background and Purpose- CRP (C-reactive protein) is an inflammatory biomarker which predicts the risk of cardiovascular diseases. However, whether CRP is associated with carotid artery plaque (CAP) remains unclear. Methods- The current retrospective study was performed in 8229 Chinese aged adults

Off-Target Vascular Effects of Cholesteryl Ester Transfer Protein Inhibitors Involve Redox-Sensitive and Signal Transducer and Activator of Transcription 3-Dependent Pathways.

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Elevated blood pressure was an unexpected outcome in some cholesteryl ester transfer protein (CETP) inhibitor trials, possibly due to vascular effects of these drugs. We investigated whether CETP inhibitors (torcetrapib, dalcetrapib, anacetrapib) influence vascular function and explored the putative

Effect of repeated fasting/refeeding on obesity development and health complications in rats arising from reduced nest.

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BACKGROUND Overnutrition during postnatal life represents a risk factor for later obesity and associated metabolic disorders. OBJECTIVE We investigated the interaction between postnatal and later-life nutrition on body composition, blood pressure and the jejunal enzyme activities in male

Chronic PARP-1 inhibition reduces carotid vessel remodeling and oxidative damage of the dorsal hippocampus in spontaneously hypertensive rats.

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Vascular remodeling during chronic hypertension may impair the supply of tissues with oxygen, glucose and other compounds, potentially unleashing deleterious effects. In this study, we used Spontaneously Hypertensive Rats and normotensive Wistar-Kyoto rats with or without pharmacological inhibition

Biochemical abnormalities of venous plasma membrane fraction isolated from spontaneously hypertensive rats.

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Alkaline phosphatase activity and Ca2+ accumulation were examined in the isolated plasma membrane fractions from small arteries and veins of spontaneously hypertensive (SHR) and normotensive (WKY). Increased Ca2+ binding by plasma membrane fractions from veins, decreased ATP-dependent Ca2+

Rap1b in smooth muscle and endothelium is required for maintenance of vascular tone and normal blood pressure.

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OBJECTIVE Small GTPase Ras-related protein 1 (Rap1b) controls several basic cellular phenomena, and its deletion in mice leads to several cardiovascular defects, including impaired adhesion of blood cells and defective angiogenesis. We found that Rap1b(-/-) mice develop cardiac hypertrophy and

Pharmacological characterization of SAR407899, a novel rho-kinase inhibitor.

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Recent advances in basic and clinical research have identified Rho kinase as an important target potentially implicated in a variety of cardiovascular diseases. Rho kinase is a downstream mediator of RhoA that leads to stress fiber formation, membrane ruffling, smooth muscle contraction, and cell

ERK signaling mediates enhanced angiotensin II-induced rat aortic constriction following chronic intermittent hypoxia.

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BACKGROUND Obstructive sleep apnea (OSA) has been recognized as an independent risk factor for systemic hypertension. The study investigated the functional consequences of chronic intermittent hypoxia (CIH) on aortic constriction induced by angiotensin II (Ang II) and the possible signaling

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