Disease relevance of Muscle, Smooth, Vascular

• Fgf2 knockout mice are morphologically normal and display decreased vascular smooth muscle contractility, low blood pressure and thrombocytosis [1].
• PDGF has been shown to contribute to hypertrophy in vascular smooth muscle cells (VSMC) [2].
• The migration of vascular smooth muscle cells (VSMCs) is thought to play a key role in the pathogenesis of many vascular diseases and is regulated by soluble growth factors/ chemoattractants as well as interactions with the extracellular matrix [3].
• Endothelin receptor is coupled to phospholipase C via a pertussis toxin-insensitive guanine nucleotide-binding regulatory protein in vascular smooth muscle cells [4].
• These findings suggest that the ACH-induced coronary vasospasm in patients with variant angina results from hyperreactivity of vascular smooth muscle to ACH but not from endothelial dysfunction [5].

Psychiatry related information on Muscle, Smooth, Vascular

• Expression of scavenger receptor class B, type I, by astrocytes and vascular smooth muscle cells in normal adult mouse and human brain and in Alzheimer's disease brain [6].
• Mutations in the human Notch 3 gene cause the vascular stroke and dementia syndrome CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) characterized by degeneration of vascular smooth muscle cells and multiple small infarcts in the white and deep gray matter of the brain [7].
• We conclude that maternal marijuana smoking in late ovine pregnancy has a direct relaxant effect on both maternal and fetal placental vascular smooth muscles that decreases the normal heterogeneity of flow and improves macroscopic placental perfusion balance [8].

High impact information on Muscle, Smooth, Vascular

• Loss of vascular smooth muscle SG-SSPN complex was only detected in Sgcd null mice and associated with irregularities of the coronary vasculature [9].
• Administration of a vascular smooth muscle relaxant prevented onset of myocardial necrosis [9].
• The antidiuretic hormone arginine vasopressin interacts with two types of receptors: V1, which mediates the effects of vasopressin on vascular smooth muscle, and V2, which mediates the antidiuretic effects on renal tubules [10].
• Salt-sensitive hypertension is triggered by Ca2+ entry via Na+/Ca2+ exchanger type-1 in vascular smooth muscle [11].
• Nitric oxide (NO) physiologically stimulates the sarco/endoplasmic reticulum calcium (Ca(2+)) ATPase (SERCA) to decrease intracellular Ca(2+) concentration and relax cardiac, skeletal and vascular smooth muscle [12].

Chemical compound and disease context of Muscle, Smooth, Vascular

• The antifungal antibiotic clotrimazole (CLT) blocks directly and with high potency the Ca2+-activated K+ channels of human erythrocytes, erythroleukemia cells, and ferret vascular smooth muscle cells [13].
• BACKGROUND & AIMS: In cirrhosis, increased amounts of circulating hormones such as angiotensin II may induce vascular tone changes and alter vascular smooth muscle cell (VSMC) function and growth [14].
• These cells, derived from a nitrosourea-induced mouse brain neoplasm, have some of the morphological characteristics of smooth muscle and have been shown to express the vascular smooth muscle isoform of alpha-actin [15].
• BACKGROUND: Angiotensin II may contribute to hypoxic pulmonary hypertension via its vasoconstrictor and growth-stimulatory effects on vascular smooth muscle cells (VSMCs) [16].
• Vein graft stenosis and the heparin responsiveness of human vascular smooth muscle cells [17].

Biological context of Muscle, Smooth, Vascular

• These chemokines, and a specific set of other pro-inflammatory genes, are also upregulated in human vascular smooth muscle cells during Fas-induced apoptosis, in part through a process that requires interleukin-1alpha activation [18].
• The unexpected effects of HO-1 on vascular smooth muscle cell growth were mediated by cell-cycle arrest involving p21Cip1 [19].
• Other notable effects of vasopressin on peripheral tissues include contraction of vascular smooth muscle, leading to elevation of blood pressure, and activation of glycogenolysis in liver [20].
• Signal transduction mechanisms mediating the physiological and pathophysiological actions of angiotensin II in vascular smooth muscle cells [21].
• Mineralocorticoids, the most prominent of which is aldosterone, also influence the activity of nonepithelial target cells, including vascular smooth muscle cells, by altering intracellular ion transport and content [22].

Anatomical context of Muscle, Smooth, Vascular

• Stimulation of alpha2b receptors in vascular smooth muscle produced hypertension and counteracted the clinically beneficial hypotensive effect of stimulating alpha2a receptors in the central nervous system [23].
• Smooth muscle relaxation by acetylcholine and a number of other agonists was found to be dependent on the presence of endothelial cells, which, when stimulated by the agonist, released a diffusable, very labile, nonprostanoid substance, termed EDRF, that acted on vascular smooth muscle cells to activate relaxation [24].
• Angiotensin II type 2 (AT2) receptor is abundantly expressed in vascular smooth muscle cells (VSMC) of the fetal vasculature during late gestation (embryonic day 15-20), during which the blood vessels undergo remodeling [25].
• The present study demonstrates an enhanced vasoreactivity of atherosclerotic coronary arteries to cocaine in vivo, the mechanism of which appears to be mediated by endogenous vasoactive substances rather than by a direct action of cocaine on vascular smooth muscle [26].
• Dietary intake of sodium chloride in the rat influences [3H]nitrendipine binding to adrenal glomerulosa cell membranes but does not alter binding to vascular smooth muscle membranes [27].

Associations of Muscle, Smooth, Vascular with chemical compounds

• Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle [28].
• Functionally, 1,4-dihydropyridines such as nifedipine and nitrendipine block Ca channels; this effect is believed to form the basis for their clinical importance as Ca antagonists in relaxing vascular smooth muscle [29].
• Finally, nitroprusside, thought to generate NO in vascular smooth muscle, relaxes rat aorta without increasing rubidium efflux [30].
• Recently, small modifications to the nifedipine molecule produced a derivative, BAY-K-8644 (methyl-1,4-dihydro-2, 6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine-5-carboxylate), that in contrast to the Ca2+-channel blocking agents, stimulated cardiac and vascular smooth muscle contractility [31].
• In view of its potent effects on salt metabolism in the kidney and on vascular smooth muscle, ANF is considered to play an important part in the control of fluid volume and vascular function [32].

Gene context of Muscle, Smooth, Vascular

• Notch3 is required for arterial identity and maturation of vascular smooth muscle cells [33].
• Here we show that the basic helix-loop-helix transcription factor, dHAND/Hand2, is expressed in the developing vascular mesenchyme and its derivative, vascular smooth muscle cells (VSMCs) [34].
• To clarify the role of K(ATP) channels in vascular smooth muscle, we studied Sur2 gene-targeted mice (Sur2(-/-)) and found significantly elevated resting blood pressures and sudden death [35].
• Urokinase-induced signaling in human vascular smooth muscle cells is mediated by PDGFR-beta [36].
• CONCLUSIONS: Vascular smooth muscle cells of human IMA, IMV, and PCA contain both ETA and ETB receptors, whereas the endothelium of IMA and PCA does not express functional ETB receptors linked to nitric oxide and/or prostacyclin production [37].

Analytical, diagnostic and therapeutic context of Muscle, Smooth, Vascular

• By measurements of NO2-/NO3- (NOx) production and Northern blot analysis, we studied the effects of a membrane-permeable cAMP derivative, 8-bromo-cAMP, on the expression of inducible nitric oxide synthase (iNOS) gene and the synthesis of NOx in cultured rat vascular smooth muscle cells (VSMCs) [38].
• These observations indicate that carvedilol may also be effective in the treatment of pathological disorders principally associated with abnormal vascular smooth muscle growth, such as atherosclerosis and acute vascular wall injury induced by angioplasty or coronary artery bypass grafting [39].
• CONCLUSIONS: Time-zero hearts (n = 68) and 34 of 38 stable allografts contained immunocytochemically detectable TPA only in vascular smooth muscle cells [40].
• Potentially therapeutic levels of human adenosine deaminase activity were detected over 6 months of observation, indicating the utility of vascular smooth muscle cells for gene therapy in humans [41].
• Gel retardation assays also documented the presence of functional estrogen receptors in extracts from human vascular smooth muscle cells [42].

References