Macro- and microvascular disorders currently represent the principal causes of morbidity and mortality in patients with diseases involving the cardiovascular system, such as atherosclerosis, hypertension, stroke, and diabetes. Abnormal vasomotor responses and impaired endothelium-dependent vasodilation have been demonstrated in a number of vessels in a variety of animal models and in humans with such diseases. Endothelial dysfunction plays a key role in the development of these diseases, yet the genesis of this endothelial dysfunction and its associated vasomotor abnormalities remain poorly understood. Peroxisome proliferator-activated receptor (PPAR)γ is a nuclear receptor and transcription factor in the steroid superfamily, and PPARγ agonists (the thiazolidinediones) are used clinically to treat type 2 diabetes. Recent studies have revealed that as well as being involved in adipogenesis and in increased sensitivity to insulin, PPARγ plays critical roles in the vasculature. In the present review, we discuss the beneficial effects of PPARγ agonists on vasomotor activities, focusing in particular on endothelium-dependent relaxation in vessels affected by cardiovascular diseases.
After major abdominal surgery, postoperative ileus is inevitable, and it has always been a challenge for the surgical team to shorten the duration of this period. Based on many clinical and basic reports that affirm the effect on the recovery of gastrointestinal motility, epidural analgesia has been used widely to promote recovery from postoperative ileus. Different techniques have been used to measure gastrointestinal motility in laboratory and clinical investigations. Many of the techniques used in clinical investigations of gastrointestinal motility are controversial because they are subjective. In the laboratory strain gauge force transducer (SGT) can provide objective data on gastrointestinal motility. Nevertheless the significance of SGT in the clinical setting is yet to be confirmed. Therefore in this review we examine both clinical and laboratory outcomes of epidural analgesia on gastrointestinal motility to present the possibility for the development of gastrointestinal motility research with SGTs. We suggest that further investigation using SGTs may lead to the development of objective methods that allow objective assessment of post-surgical gastrointestinal function.
In this review, we present the basic properties, physiological functions, regulation, and pathological alterations of four major classes of K+ channels that have been detected in vascular smooth muscle cells. Voltage-dependent K+ (Kv) channels open upon depolarization of the plasma membrane in vascular smooth muscle cells. The subsequent efflux of K+ through the channels induces repolarization to the resting membrane potential. Changes in the intracellular Ca2+ concentration and membrane depolarization stimulate large-conductance Ca2+-activated K+ (BKCa) channels, which are thought to play an important role in maintaining the membrane potential. ATP-sensitive K+ (KATP) channels underscore the functional bond between cellular metabolism and membrane excitability. The blockade of KATP channel function results in vasoconstriction and depolarization in various types of vascular smooth muscle. Inward rectifier K+ (Kir) channels, which are expressed in smooth muscle of the small-diameter arteries, contribute to the resting membrane potential and basal tone. Kir channel activation has been shown to raise the extracellular K+ concentration to 10-15 mM, resulting in vasodilation. Each of K+ channels listed above is responsive to a number of vasoconstrictors and vasodilators, which act through protein kinase C (PKC) and protein kinase A (PKA), respectively. Impaired Kv, KATP, and Kir channel functions has been linked to a number of pathological conditions, which may lead to vasoconstriction.
Mast cells are a native composer of connective tissue of the skin dermis and intestinal and respiratory mucosa. Independent lines of accumulated evidence indicate the existence of an intensive bidirectional crosstalk between mast cells and sensory nerves and suggest that mast cells and sensory nerves may be viewed as a functional unit, which could be of crucial importance in neuroimmunological pathways. Mast cells appear to have a property of influencing smooth muscle function via not only such nerve-mast cell effects, but also direct pathways. In bronchial asthma, mast cells infiltrate the airway smooth muscle layer, and interact directly with smooth muscle cells, suggesting pathogenic roles for mast cells in airway obstruction. Current studies on mast cell biology identified a novel adhesion molecule of mast cells, namely cell adhesion molecule-1, CADM1. This molecule is unique, because it serves as not only simple glue but also appears to promote functional communication between nerve and mast cells and between smooth muscle and mast cells.
In the present study, the change in Gq protein level in bronchial smooth muscle of mice with antigen-induced airway hyperresponsiveness (AHR) was determined. BALB/c mice were actively sensitized and repeatedly challenged with ovalbumin antigen to induce bronchial smooth muscle hyperresponsiveness. The contraction induced by 10 μM AlF4- (generated by 10 μM AlCl3 plus 10 mM NaF) of bronchial smooth muscles isolated from the antigen-challenged mice was significantly augmented as compared with that from the control animals. The G αq protein level determined by immunoblotting was also significantly increased in bronchial smooth muscles of the antigen-challenged group. Thus, an upregulation of Gαq protein may be involved in the pathogenesis of bronchial smooth muscle hyperresponsiveness, one of the causes of AHR in asthmatics.
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