Skeletal muscle arteries

Pernow, J. (1989) Actions of constrictor (NPY and endothelin) and dilator (substance P, GGRP and VIP) peptides on pig splenic and human skeletal muscle arteries involvement of the endothelium. Br.J. Pharmacol. 97, 983-989. 

Pernow, J. Lundberg,J.M. (1986) Neuropeptide Y constricts human skeletal muscle arteries via a nifedipine-sensitive mechanism independent of extracellular calcium Acta Physiol. Scand. 128, 655-656. 

Expression (Human) Tissues Leukocytes, thymus, spleen, liver, ovary Cells PBLs, neutrophils,T-cells, dendritic cells, mast cells, eosinophils, macrophages, leukocytes Tissues spleen, small intestine, placenta, lung smooth muscle, Cells bronchial smooth muscle, CD34+ hemapoietic progenitor cells, monocytes, macrophages, mast cells, eosinophils, neutrophils, PBLs, human umbilical vein endothelial cells Tissues, heart, skeletal muscle, spleen, brain, lymp node, adrenal medulla, lung, human pumonary/ saphenous vein Cells monocytes, macrophages, mast cells, eosinophils, cardiac muscle, coronary artery, PBLs... 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

Stimulation of the motoneuron releases acetylcholine onto the muscle endplate and results in contraction of the muscle fiber. Contraction and associated electrical events can be produced by intra-arterial injection of ACh close to the muscle. Since skeletal muscle does not possess inherent myogenic tone, the tone of apparently resting muscle is maintained by spontaneous and intermittent release of ACh. The consequences of spontaneous release at the motor endplate of skeletal muscle are small depolarizations from the quantized release of ACh, termed miniature endplate potentials (MEPPs) [15] (seeCh. 10). Decay times for the MEPPs range between l and 2 ms, a duration similar to the mean channel open time seen with ACh stimulation of individual receptor molecules. Stimulation of the motoneuron results in the release of several hundred quanta of ACh. The summation of MEPPs gives rise to a postsynaptic excitatory potential (PSEP),... 

Cardiac index and blood pressure must be sufficient to ensure adequate organ perfusion, as assessed by alert mental status, creatinine clearance sufficient to prevent metabolic azotemic complications, hepatic function adequate to maintain synthetic and excretory functions, a stable heart rate and rhythm, absence of ongoing myocardial ischemia or infarction, skeletal muscle and skin blood flow sufficient to prevent ischemic injury, and normal arterial pH (7.34 to 7.47) with a normal serum lactate concentration. These goals are most often achieved with a cardiac index greater than 2.2 L/min/m2, a mean arterial blood pressure greater than 60 mm Hg, and PAOP of 25 mm Hg or greater. 

What we commonly call movement depends on mnscle cells. There are several types of muscle in the hnman body heart mnscle striated skeletal muscle, which includes the large muscles of the body and smooth mnscle of the stomach, intestines, arteries and veins, and nterns. There is a fnndamental difference between striated and smooth muscle. You can control the former bnt not the latter. Yon can pretty mnch will what yon do with yonr arms and legs, for example. The activities of your stomach, veins and arteries, and intestines are pretty mnch beyond yonr ability to control by force of will. Heart is an exception heart mnscle is basically a striated muscle but we are at a loss to willfully control the rate or force of its contractions. 

The concentration difference is that between blood in the femoral artery and that in the femoral vein. The minus sign indicates release from the muscle. Data taken from Felig (1975). It is estimated that about 80 g of glutamine is released each day from skeletal muscle. 

Isoxsuprine is a vasodilator that also stimulates p-adrenergic receptors. It causes relaxation of vascular and uterine smooth muscles, and its vasodilating action is greater on the arteries supplying skeletal muscles than on those supplying skin. The drug also produces positive inotropic and chronotropic effects [39]. 

Systemic arterial blood pressure decreases progressively with increasing depth of anaesthesia with isoflurane. It also increases heart rate but arrhythmias are not precipitated. Isoflurane depresses respiration as concentration is increased. Uterine and skeletal muscle relaxation is similar to enflurane. 

Isoprenaline stimulates pi and 32 adrenoceptors (pi>32) resulting in increased myocardial contractility and reduced peripheral vascular resistance. It does not act on a adrenoceptors. Cardiac output increases partly due to reduced afterload and an increase in heart rate. There is a diversion of blood to non-essential tissues, e.g. skeletal muscle and skin. Because of the decrease in peripheral vascular resistance arterial blood pressure and coronary perfusion pressure may decrease, which may predispose to myocardial ischaemia. 

Autonomic nerves can regulate coronary arteriolar tone. Acetylcholine released from postganglionic parasympathetic nerves relaxes coronary arteriolar smooth muscle via the NO/cGMP pathway in humans as described above. Damage to the endothelium, as occurs with atherosclerosis, eliminates this action, and acetylcholine is able to contract arterial smooth muscle and produce vasoconstriction. Skeletal muscle receives sympathetic cholinergic vasodilator nerves, but the view that acetylcholine caused vasodilation in this vascular bed has not been verified experimentally. Moreover, NO, rather than acetylcholine, may be released from neurons. However, this vascular bed responds to exogenous choline esters because of the presence of M3 receptors on endothelial and smooth muscle cells. 

Most blood vessels receive no direct innervation from the parasympathetic system. However, parasympathetic nerve stimulation dilates coronary arteries, and sympathetic cholinergic nerves cause vasodilation in the skeletal muscle vascular bed (see Chapter 6). Atropine can block this vasodilation. Furthermore, almost all vessels contain endothelial muscarinic receptors that mediate vasodilation (see Chapter 7). These receptors are readily blocked by antimuscarinic drugs. At toxic doses, and in some individuals at normal doses, antimuscarinic agents cause cutaneous vasodilation, especially in the upper portion of the body. The mechanism is unknown. 

Atherosclerosis can result in ischemia of peripheral muscles just as coronary artery disease causes cardiac ischemia. Pain (claudication) occurs in skeletal muscles, especially in the legs, during exercise and disappears with rest. Although claudication is not immediately life-threatening, peripheral artery disease is associated with increased mortality, can severely limit exercise tolerance, and may be associated with chronic ischemic ulcers and susceptibility to infection. 

The constitutive isoforms of NOS are mainly, but not only, localized in the tissues where they were originally identified. In some brain regions, eNOS and nNOS occur in the same cell populations (Dinerman et al., 1994). In mice it was shown that hippocampal neurons express eNOS, and nNOS was found in human bronchi as well as in human skeletal muscle (Hobbs et al., 1999). In coronary arteries of eNOS knock-out mice, nNOS-derived NO, via activation of cGMP, takes over the role of eNOS and maintains blood flow-induced vessel dilation (Huang et al., 2002). 

Vascular smooth muscle tone is regulated by adrenoceptors consequently, catecholamines are important in controlling peripheral vascular resistance and venous capacitance. Alpha receptors increase arterial resistance, whereas 2 receptors promote smooth muscle relaxation. There are major differences in receptor types in the various vascular beds (Table 9-4). The skin vessels have predominantly receptors and constrict in the presence of epinephrine and norepinephrine, as do the splanchnic vessels. Vessels in skeletal muscle may constrict or dilate depending on whether ffor 13 receptors are activated. Consequently, the overall effects of a sympathomimetic drug on blood vessels depend on the relative activities of that drug at and 8receptors and the anatomic sites of the vessels affected. In addition, Di receptors promote vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels. Activation of the Di receptors in the renal vasculature may play a major role in the natriuresis induced by pharmacologic administration of dopamine. 

In vitro, urotensin II is a potent constrictor of vascular smooth muscle its activity depends on the type of blood vessel and the species from which it was obtained. Vasoconstriction occurs primarily in arterial vessels, where urotensin II can be more potent than endothelin 1, making it the most potent known vasoconstrictor. In vivo, urotensin II has complex hemodynamic effects, the most prominent being regional vasoconstriction and cardiac depression. The extent to which the peptide is involved in the regulation of vascular tone and blood pressure in humans is not clear recent studies have produced conflicting results. The actions of urotensin II are mediated by G protein-coupled receptors that are widely distributed in the brain, spinal cord, heart, vascular smooth muscle, skeletal muscle, and pancreas. Some effects of the peptide including vasoconstriction are mediated by the phospholipase C/IP3/DAG signal transduction pathway. 

Transfection efficacy of naked DNA can be increased by physical methods such as electroporation and sonication. Electroporation employs electric pulses to punch holes in the cell membrane, usually smaller than 10 nm but larger than oligonucleotides. With the use of electroporation, DNA was delivered into the cytosol of cells by diffusion. Since its introduction in 1982, in vivo transfection has been achieved in skeletal muscle, fiver, skin, tumors, testis, and the kidney. Tsujie et al. (2001) developed a method to target glomeruli using electroporation in vivo wherein injection of plasmid DNA via the renal artery was followed by application of electric fields. The kidney was electroporated by sandwiching the organ... 

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