Which of the following events do not occur during smooth muscle contraction
The active contraction of vascular smooth muscle regulates precapillary resistance, which controls capillary blood flowSmooth-muscle tone in arterioles, metarterioles, and precapillary sphincters (seepp. 459–460) determines the access resistance to the capillary beds. This resistance upstream of the capillary bed is also known as the afferent orprecapillary resistance (Rpre). The overall resistance of a microcirculatory bed is the sum ofRpre, the resistance of the capillary bed itself (Rcap), and the efferent orpostcapillary resistance (Rpost). Show
How do these resistances influence the flow of blood (Fcap) through a capillary bed? We can answer this question by rearranging the Ohm's law–like expression that we introduced asEquation 17-1: (20-12). Pa is the pressure just before the beginning of the precapillary resistance, andPv is the pressure just after the end of the postcapillary resistance. Because the aggregateRcap is small, andRpost/Rpre is usually ~0.3,Rpre is usually much greater thanRcap +Rpost. BecauseRpre is the principal determinant of total resistance, capillary flow is roughly inversely proportional toRpre. Thus, modulating the contractility of VSMCs inprecapillary vessels is the main mechanism for adjusting perfusion of a particular tissue. Smooth-muscle cells can function as a syncytium when they are coupled through gap junctions (unitary smooth muscle), or they can function independently of one another as do skeletal muscle fibers (multiunit smooth muscle; seep. 243). Most vascular smooth muscle has a multiunit organization. In contrast to skeletal muscle, VSMCs receive multiple excitatory as well as inhibitory inputs (seep. 251). Moreover, these inputs come not only from chemical synapses (i.e., neural control) but also from circulating chemicals (i.e., humoral control). The actual contraction of VSMCs may follow smooth-muscle electrical activity in the form of action potentials, slow waves of depolarization, or graded depolarizations without spikes. VSMCs can show spontaneous rhythmic variations in tension leading to periodic changes in vascular resistance and microcirculatory flow in a process calledvasomotion. These spontaneous, rhythmic smooth-muscle contractions result either from pacemaker currents or from slow waves of depolarization and associated [Ca2+]i increases in the VSMCs (seep. 244). Humoral agents can also directly trigger contraction of VSMCs via increases in [Ca2+]i without measurable fluctuations in membrane potential (pharmacomechanical coupling; seep. 247). Cyclic Nucleotides and Protein Phosphorylation in Vascular Smooth Muscle RelaxationGIOVANNI M. PITARI, ... SCOTT A. WALDMAN, in Heart Physiology and Pathophysiology (Fourth Edition), 2001 I. INTRODUCTIONVascular smooth muscle contractility is regulated by a complex balance between a variety of antagonistic and synergistic signal transduction pathways and intracellular second messenger molecules. Contraction is initiated by increases in the concentration of intracellular calcium ([Ca2+]i), which is regulated by the interplay of a variety of systems, including receptor- and voltage-operated Ca2+ channels, other ion channels, and receptor-mediated increases in the metabolism of signal-transducing phospholipids. Calcium interacts with a number of receptor proteins, particularly calmodulin, which alters the activity of other enzymes, ultimately resulting in increases in the activity of actin-activated myosin ATPase and smooth muscle contraction. Relaxation of vascular smooth muscle involves reducing [Ca2+]i by increasing the efflux of this cation out of the cell, decreasing its influx, or increasing its intracellular sequestration. Additionally, the sensitivity of the contractile apparatus to Ca2+ may be decreased so that there is a decreased contractile response at any given intracellular concentration of Ca2+. Smooth muscle relaxation is mediated by the intracellular second messengers cyclic AMP and cyclic GMP. The production and metabolism of these cyclic nucleotides and the regulation of intracellular concentrations of Ca2+ are highly interdependent. Experimental evidence suggests that each of these messenger molecules exerts regulatory influences on the intracellular concentration of the others. However, which of the several possible interacting mechanisms predominates in mediating vascular smooth muscle relaxation in a variety of physiological or pathophysiological conditions remains to be better defined. This chapter concentrates on defining the mechanisms by which cyclic AMP and cyclic GMP regulate vascular tone. These mechanisms are defined by available experimental evidence, focusing on their relationships to the regulation of [Ca2+]i and on the Ca2+ sensitivity of the contractile apparatus. Although vascular smooth muscle function is the focus of this chapter, evidence obtained with other types of smooth muscle and, in some cases, with tissues other than smooth muscle is evaluated. It is hoped that this review permits the reader to appreciate the complexity of vascular smooth muscle function at the molecular level and the gaps in understanding that remain to be filled. What are the events of smooth muscle contraction?Steps involved in smooth muscle cell contraction: Depolarization of membrane or hormone/neurotransmitter activation. L-type voltage-gated calcium channels open. Calcium-induced calcium release from the SR.
Which of the following is not a result of muscular contraction?So, the correct option is 'production of antibody'.
Which of the following is not a function of smooth muscle?Answer and Explanation: The correct answer is option C . Option C is not a function of smooth muscle because forcing blood from the heart to the major arteries is accomplished by cardiac muscles, which is the only muscle type found in the heart.
Which one of the following about smooth muscle is not true?Which one of the following is NOT true about smooth muscle? Both actin and myosin are found in the smooth muscle cell cytoplasm, but these are not arranged in sarcomere units.
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