Smooth muscle resting tension

The contractile elements in smooth muscle are not organized into sarcomeres. Furthermore, the resting length of smooth muscle is much shorter than its optimal length. In other words, this muscle can be significantly stretched and the amount of tension developed may actually increase because the muscle is closer to its optimal length. Finally, thick filaments are longer in smooth muscle than they are in skeletal muscle. As a result, overlap... 

The pleura and peritoneum are composed of a thin mesothelial cell lining that rests on a basement membrane and a thin layer of connective tissue that contains endothelium and smooth muscle cells (peritoneum) and fibroblasts (Figure 3.6). These cell linings are continuous with internal tissues that he beneath and also contract when the tension is released but not as much as cornea or skin. 

Stimulation or inhibition of autonomic effector cells by ACh results from interaction of ACh with muscarinic ACh receptors. In this case, the effector is coupled to the receptor by a G protein (see Chapter 1). In contrast to skeletal muscle and neurons, smooth muscle and the cardiac conduction system (sinoatrial [SA] node, atrium, atrioventricular [AV] node, and the His-Purkinje system) normally exhibit intrinsic activity, both electrical and mechanical, that is modulated but not initiated by nerve impulses. At some smooth muscle, ACh causes a decrease in the resting potential (i.e., the membrane potential becomes less negative) and an increase in the frequency of spike production, accompanied by a rise in tension. A primary action of ACh in initiating these effects through muscarinic receptors is probably partial depolarization of the cell membrane brought about by an increase in Na and, in some instances, Ca conductance activation of muscarinic receptors can also activate the G -PLC-IP pathway leading to the mobilization of stored Ccf. Hence, ACh stimulates ion fluxes across membranes and/or mobilizes intracellular Ca to cause contraction. 

Chronic hypoxia causes pulmonary arterial smooth muscle cell depolarisation, elevated endothelin-1, and vasoconstriction. Resting [Ca li in smooth muscle cells from intrapulmonary arteries of rats exposed to 10 % O2 for 21 days was 293.9 25.2 nM (vs. 153.6 28.7nM in normoxia) (Shimoda et al. 2000). Resting [Ca " ] was decreased after extracellular Ca removed but not with nifedipine (10" M), an L-type Ca " channel antagonist. After chronic hypoxia, the endothelin-1-induced increase in [Ca ]i was reduced and was aboHshed after extracellular Ca removal or nifedipine. Removal of extracellular Ca " reduced endothehn-1-induced tension however, nifedipine had only a slight effect. 

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