Autoregulation is a process that maintains a relatively constant blood flow to tissues like the brain, even when blood pressure varies. This is achieved through the myogenic response, where an increase in distending pressure causes vasoconstriction in the artery, while a decrease in transmural pressure causes vasodilation within a specific pressure range. Fig. 14.13 shows that when the resistance artery is distended, there is an immediate rise in intracellular calcium concentration ([Ca++]), leading to vasoconstriction in order to maintain a consistent flow. The mechanism behind this increase in intracellular [Ca++] and subsequent vasoconstriction is intricate and involves stretch-activated channels, InsP3-signaling, and voltage-gated Ca++ channels.

During development and growth, the number of smooth muscle cells increases, as depicted in Fig. 14.14. Additionally, if an organ experiences a sustained increase in mechanical work, the mass of smooth muscle tissue also increases. This increase in mass is known as compensatory hypertrophy. For instance, hypertensive patients often exhibit arterial smooth muscle cell hypertrophy in the tunica media of the artery, which is caused by the increased mechanical load on the muscle cells. This hypertrophy can result in the replication of chromosomes and the presence of polyploid muscle cells containing multiple sets of chromosomes. These polyploid cells synthesize more contractile proteins, thereby increasing the size of the cell (see Fig. 14.14).
Cat.Cat.Ca2˜Ca2˜IP3RICa2˜Ca2˜K˜CaV1.2BKCaCaMMLCK PDE5 RGS2 MYPT1 MLCP GMP pGC cGMP Hyper-polarization NucleuscGMP-A/B cGMP-A/B LZ LZ ˜˜˜°PKG1 NO sGC GTPGPCR IRAG ER Actin/myosin °˛G˜q IP3 PLC°12354 •Fig. 14.12 Signalingmechanismsbywhichnitricoxide(NO)andnitroprusside(NP)promoterelaxationofvascularsmoothmuscle.Nitricoxidestimulatessolubleguanylcyclase(sGC)inthevascularsmoothmusclecell,resultinginproductionofcGMP,activationofproteinkinaseG(PKG1),whichinturnphosphorylatesvarioussubstratesthat(1)inhibitInP3production,(2)inhibitInsP3-inducedCa++ release, (3)activatemyosinlight-chainphosphatase,(4)activatethelargeconductanceCa++-activatedK+ channel(BKCa),whichhyperpolarizesthecellandthusinhibitsthevoltage-gatedCa++ channel(Cav1.2)(5).BKCa,calcium-activatedmaxi-Kchannel;CaM,calmodulin;Cat,catalyticdomain;Cav1.2,L-typecalciumchannel;ER,endoplasmicreticulum;GPCR,Gprotein–coupledreceptor;IP3RI,inositol1,4,5-trisphosphate(IP3)receptorI;IRAG,inositoltrisphosphatereceptor-associatedcGMP-kinasesubstrate;LZ,leucine/isoleucinezipper;MLCK,myosinlight-chainkinase;MLCP,myosinlight-chainphosphatase;MYPT,regulatorymyosinphosphatasetargetingsubunit1;PDE5,phosphodiesterase5;pGC,particulateguanylylcyclase;PLCβ,phospholipaseCbeta;RGS2,regulatorofG-proteinsignaling2;sGC,solubleguanylylcyclase.(ModifiedfromSchlossmannJ,DeschM.Am J Physiol Heart Circ Physiol 2011;301:H672–H682.)
Blood flow to tissues such as the brain is maintained at a relatively constant flow over a wide range of blood pressures through a process called autoregulation. The mechanism underlying autoregulation of blood flow involves the myogenic response, wherein an increase in distending pressure in an artery results in vasoconstriction, whereas a decrease in transmural pressure results in a vasodilation (over a given range of pressures). As shown in
Fig. 14.13 , distention of the resistance artery resulted in an immediate elevation of intracellular [Ca++], followed by vasoconstriction in an effort to maintain relatively constant flow. The mechanism underlying this elevation of intracellular [Ca++] and subsequent vasoconstriction is complex. The rise in intracellular [Ca++] in response to stretch been reported to involve stretch-activated channels, InsP3-signaling, and voltage-gated Ca++ channels.
During development and growth, the number of smooth muscle cells increases (
Fig. 14.14 ). Smooth muscle tissue mass also increases if an organ is subjected to a sustained increase in mechanical work. This increase in mass is called compensatory hypertrophy. A striking example occurs with arterial smooth muscle cells (i.e., in the tunica media of the artery) in hypertensive patients. The increased mechanical load on the muscle cells appears to be the common factor that induces this hypertrophy. Chromosomal replication can result in significant numbers of polyploid muscle cells. The polyploid cells contain multiple sets of the normal number of chromosomes. They synthesize more contractile proteins and thus increase the size of the cell (see
Fig. 14.14