As parturition (birth) approaches, the smooth muscle component of the uterus, known as the myometrium, undergoes hypertrophy. Hormones play a crucial role in this response. During pregnancy, when progesterone is dominant, the smooth muscle remains inactive, and only a few gap junctions that connect the smooth muscle cells electrically are present. However, at term, estrogen becomes dominant and leads to significant hypertrophy of the myometrium. Just before birth, a large number of gap junctions form, transforming the myometrium into a single-unit tissue to coordinate contractions during parturition.

The growth and development of tissues containing smooth muscle are associated with increased connective tissue. Smooth muscle cells carry out various activities, such as division during normal growth or in response to certain pathological conditions like the formation of atherosclerotic plaques. Additionally, cells may hypertrophy in response to increased loads. Chromosomal replication without cell division results in cells with a higher content of contractile proteins. Smooth muscle cells also synthesize and secrete the components of the extracellular matrix.

While smooth muscle is involved in physiological adjustments to exercise, sustained changes in mechanical loading usually occur due to pathological conditions, such as hypertension. A common example is urinary bladder hypertrophy in men caused by the benign or cancerous enlargement of the prostate gland, which obstructs the bladder outlet. This condition leads to difficulty urinating due to the distention of the bladder and impaired emptying. The smooth muscle of the bladder loses its ability to contract and develop stress, potentially due to phenotypic modulation of the smooth muscle cells, altered expression of contractile protein isoforms, and gross anatomical distortion of the bladder wall. Neuromuscular changes also affect the mobilization of myoplasmic calcium ions and cross-bridge phosphorylation. Fortunately, normal structure and function are typically restored after relieving the obstruction.

Smooth muscle cells have the capacity to synthesize and secrete the materials that make up the extracellular matrix, including collagen, elastin, and proteoglycans. This synthetic and secretory capacity becomes evident when smooth muscle cells are isolated and placed in tissue culture. These cells rapidly lose thick myosin filaments and a significant portion of the thin-filament lattice. Additionally, there is an expansion of the rough endoplasmic reticulum and Golgi apparatus. The phenotypically altered cells undergo multiplication and deposit connective tissue. However, this process is reversible, and some degree of redifferentiation with the formation of thick filaments can occur once cell replication ceases. The determinants of the smooth muscle cell phenotype are largely unknown, although hormones, growth factors in the blood, and mechanical loads on cells have been implicated in the control of phenotypic modulation.
The myometrium, which is the smooth muscle component of the uterus, undergoes hypertrophy as parturition (birth) approaches. Hormones play an important role in this response. The smooth muscle is quiescent during pregnancy when the hormone progesterone predominates, and few gap junctions that electrically couple the smooth muscle cells are present. At term, under the dominant influence of estrogen, the myometrium undergoes marked hypertrophy. Large numbers of gap junctions form just before birth and convert the myometrium to a single-unit tissue to coordinate contraction during parturition.
The growth and development of tissues that contain smooth muscle are associated with increases in the connective tissue 1.4 1.2 1.0 0.8 0.6 0.0 •Fig. 14.14 Smoothmusclecellscarryoutmanyactivities.A,Theyretainthecapacitytodivideduringnormalgrowthorincertainpatho logicalresponsessuchasformationofatheroscleroticplaque.B,Cellsmayalsohypertrophyinresponsetoincreasedloads.Chromosomalreplicationnotfollowedbycelldivisionyieldscellswithagreatercontentofcontractileproteins.C,Smoothmusclecellsalsosynthesizeandsecretetheconstituentsoftheextracellularmatrix.
Althoughsmoothmuscleisinvolvedinphysiologicaladjustmentstoexercise,sustainedchangesinthe mechanicalloadingthatinducecellularadaptationsareusuallytheresultofapathologicalcondition(e.g.,hypertension).Afairlycommonexampleinmenisurinary bladder hypertrophy causedbybenignorcancerous enlargementoftheprostategland,whichobstructsthebladderoutlet.Theclinicalresultisdifficultyurinating, •Fig. 14.13 Myogenicresponseinvascularsmoothmuscleisanautoregulatoryresponsetomaintainconstantflowtoatissue.Anincreaseintransmuralpressure(TMP; top panel) elevatesintracellular[Ca++](middle panel), resultinginavasoconstriction(bottom panel). Notethattheincreaseintransmuralpressureinitiallystretchestheskeletalmuscleresistanceartery(bottom panel), butthisisquicklyfollowedbyvasoconstriction.(FromSchubertRetal.Cardiovasc Res 2008;77:8-18.) matrix. Smooth muscle cells can synthesize and secrete the materials that make up this matrix, including collagen, elastin, and proteoglycans (see
Fig. 14.14 ). The synthetic and secretory capacities are evident when smooth muscle cells are isolated and placed in tissue culture. The cells rapidly distentionofthebladder,andimpairedemptying.Inthissituationtheabilityofthebladdersmoothmuscletocontractanddevelopstressisdiminished.Thereasonsforthisremainunexplained,butphenotypicmodulationofthesmoothmusclecellswithalteredcontractileproteinisoformexpressionandgrossanatomicdistortionofthebladderwalloccurs.NeuromuscularchangesalsoaffectmyoplasmicCa++ mobilizationandcross-bridgephosphorylation.Fortunately,normalstructureandfunctionareusuallyrestoredaftertheobstructionisalleviated.
lose thick myosin filaments and much of the thin-filament lattice, and there is expansion of the rough endoplasmic reticulum and Golgi apparatus. The phenotypically altered cells multiply and lay down connective tissue. This process is reversible, and some degree of redifferentiation with the formation of thick filaments occurs after cell replication ceases. Determinants of the smooth muscle cell phenotype are largely unknown, but hormones and growth factors in blood, as well as mechanical loads on cells, have been implicated in the control of phenotypic modulation.