Smooth muscle is comparable to skeletal muscle in terms of length-tension relationships, hyperbolic velocity-load relationships, power output curves, and ability to resist imposed loads. However, smooth muscle has lower shortening velocities and ATP consumption rates due to the expression of a myosin isoform with low activity. One unique characteristic of smooth muscle is its ability to alter velocity-stress relationships, which is regulated by both the number of active cross-bridges (determining force) and their average cycling rates for a given load (determining velocity).

Smooth muscle also plays a role in the formation of the extracellular matrix that surrounds and connects the cells. It can undergo cellular hypertrophy in response to physiological needs and retains the potential to divide. 

Various studies have focused on the regulation and signaling pathways of smooth muscle. These include purinergic signaling and blood vessels, the regulation of increased blood flow during exercise, ion channel networks in cerebral blood flow control, G q-mediated activation of smooth muscle, cAMP signaling in the vasculature, and the role of Epac (exchange protein directly activated by cAMP). Additionally, factors such as IRAG and novel PKG targeting, RhoA/Rho-Kinase in the cardiovascular system, Ca2+ sensitivity of smooth muscle and nonmuscle myosin II, ORAI channel-mediated Ca2+ signals in vascular and airway smooth muscle, and ATP-sensitive potassium channels in the cardiovascular system have been studied.

In terms of circulation regulation and the cardiovascular system, the arrangement of the heart and vessels enables the unidirectional flow of well-oxygenated blood to the body. The reciprocal relation between blood flow velocity and vascular cross-sectional area is advantageous for efficient circulation. The differing compositions of blood vessels, including smooth muscle, fibrous tissue, and elastic tissue, contribute to their respective functions.
The length-tension relationships, hyperbolic velocity-load relationships, power output curves, and ability to resist imposed loads are comparable to those of skeletal muscle. Shortening velocities and ATP consumption rates are very low in smooth muscle, in keeping with expression of a myosin isoform with low activity. Smooth muscles also have the unusual ability to alter velocity-stress relationships, which reflects regulation of both the number of active cross-bridges (determining force) and their average cycling rates for a given load (determining velocity).
Burnstock G, Ralevic V. Purinergic signaling and blood vessels in health and disease. Pharmacol Rev. 2014;66:102-192.
Joyner MJ, Casey DP. Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiol Rev. 2015;95:549-601.
Longden TA, et al. Ion channel networks in the control of cerebral blood flow. J Cereb Blood Flow Metab. 2016;36:492-512.
Momotani K, Somlyo AV. p63RhoGEF: a new switch for G q-mediated activation of smooth muscle. Trends Cardiovasc Med. 2012;22:122-127.
Roberts OL, Dart C. cAMP signalling in the vasculature: the role of Epac (exchange protein directly activated by cAMP). Biochem Soc Trans. 2014;42:89-97.
8. Smooth muscle is also a synthetic and secretory cell with a major role in formation of the extensive extracellular matrix that surrounds and links the cells. Cellular hypertrophy occurs in response to physiological needs, and smooth muscle cells retain the potential to divide.
Schlossmann J, Desch M. IRAG and novel PKG targeting in the cardiovascular system. Am J Physiol Heart Circ Physiol. 2011;301: H672-H682.
Shimokawa H, et al. RhoA/Rho-Kinase in the Cardiovascular System. Circ Res. 2016;118:352-366.
Somlyo AP, Somlyo AV. Ca2+ sensitivity of smooth muscle and nonmuscle myosin II: modulated by G proteins, kinases, and myosin phosphatase. Physiol Rev. 2003;83:1325-1358.
Spinelli AM, Trebak M. ORAI channel-mediated Ca2+ signals in vascular and airway smooth muscle. Am J Physiol Cell Physiol. 2016;310:C402-C413.
Tinker A, et al. The role of ATP-sensitive potassium channels in cellular function and protection in the cardiovascular system. Br J Pharmacol. 2014;171:12-23.
SECTION 4The Cardiovascular System ACHILLES J. PAPPANO AND WITHROW GIL WIER
Overview of Circulation Regulation of the Heart and Vasculature
Chapter 16 Elements of Cardiac Function Chapter 19 Integrated Control of the Chapter 17 Cardiovascular System Properties of the Vasculature
Upon completion of this chapter, the student should be able to answer the following questions: 1.
How does the arrangement of heart and vessels enable unidirectional flow of well-oxygenated blood to the body?
2.
What is the advantage of the reciprocal relation between blood flow velocity and vascular cross-sectional area?
3.
How do the differing compositions (smooth muscle, fibrous and elastic tissue) of blood vessels contribute to their respective functions?