Cell Physiology Notes Pdf

[Marilu Mandez]

Cellphysiology is the biological study of the activities that take place in a cell to keep it alive. The term physiology refers to normal functions in a living organism.[1] Animal cells, plant cells and microorganism cells show similarities in their functions even though they vary in structure.[2][page needed]

There are two types of cells: prokaryotes and eukaryotes. Prokaryotes were the first of the two to develop and do not have a self-contained nucleus. Their mechanisms are simpler than later-evolved eukaryotes, which contain a nucleus that envelops the cell's DNA and some organelles.[3]

Prokaryotes have DNA located in an area called the nucleoid, which is not separated from other parts of the cell by a membrane. There are two domains of prokaryotes: bacteria and archaea. Prokaryotes have fewer organelles than eukaryotes. Both have plasma membranes and ribosomes (structures that synthesize proteins[clarification needed] and float free in cytoplasm). Two unique characteristics of prokaryotes are fimbriae (finger-like projections on the surface of a cell) and flagella (threadlike structures that aid movement).[2]

Eukaryotes have a nucleus where DNA is contained. They are usually larger than prokaryotes and contain many more organelles. The nucleus, the feature of a eukaryote that distinguishes it from a prokaryote, contains a nuclear envelope, nucleolus and chromatin. In cytoplasm, endoplasmic reticulum (ER) synthesizes[clarification needed] membranes and performs other metabolic activities. There are two types, rough ER (containing ribosomes) and smooth ER (lacking ribosomes). The Golgi apparatus consists of multiple membranous sacs, responsible for manufacturing and shipping out materials such as proteins. Lysosomes are structures that use enzymes to break down substances through phagocytosis, a process that comprises endocytosis and exocytosis. In the mitochondria, metabolic processes such as cellular respiration occur. The cytoskeleton is made of fibers that support the structure of the cell and help the cell move.[2]

There are different ways through which cells can transport substances across the cell membrane. The two main pathways are passive transport and active transport. Passive transport is more direct and does not require the use of the cell's energy. It relies on an area that maintains a high-to-low concentration gradient. Active transport uses adenosine triphosphate (ATP) to transport a substance that moves against its concentration gradient.[4][page needed]

The pathway for proteins to move in cells starts at the ER. Lipids and proteins are synthesized[clarification needed] in the ER, and carbohydrates are added to make glycoproteins. Glycoproteins undergo further synthesis[clarification needed] in the Golgi apparatus, becoming glycolipids. Both glycoproteins and glycolipids are transported into vesicles to the plasma membrane. The cell releases secretory proteins known as exocytosis.[2]

Ions travel across cell membranes through channels, pumps or transporters. In channels, they move down an electrochemical gradient to produce electrical signals. Pumps maintain electrochemical gradients. The main type of pump is the Na/K pump. It moves 3 sodium ions out of a cell and 2 potassium ions into a cell. The process converts one ATP molecule to adenosine diphosphate (ADP) and Phosphate.[clarification needed] In a transporter, ions use more than one gradient to produce electrical signals.[3]

Cardiac muscle also called the myocardium, is one of three major categories of muscles found within the human body, along with smooth muscle and skeletal muscle. Cardiac muscle, like skeletal muscle, is made up of sarcomeres that allow for contractility. However, unlike skeletal muscle, cardiac muscle is under involuntary control.

The cardiac muscle is responsible for the contractility of the heart and, therefore, the pumping action. The cardiac muscle must contract with enough force and enough blood to supply the metabolic demands of the entire body. This concept is termed cardiac output and is defined as heart rate x stroke volume, which is determined by the contractile forces of the cardiac muscle and the frequency at which they are activated. With a change in metabolic demand comes a change in the contractility of the heart.

Cardiac muscle cells (cardiomyocytes) are striated, branched, contain many mitochondria, and are under involuntary control. Each myocyte contains a single, centrally located nucleus surrounded by a cell membrane known as the sarcolemma. The sarcolemma of cardiac muscle cells contains voltage-gated calcium channels, specialized ion channels that skeletal muscle does not possess.

Cardiac muscle cells contain branched fibers connected via intercalated discs that contain gap junctions and desmosomes. These interconnections allow the cardiomyocytes to contract together synchronously to enable the heart to work as a pump.[2]

Gap junctions between adjacent cardiomyocytes allow for the propagation of coordinated action potentials from one cell to the next in a phenomenon known as electrical coupling.[3] Cardiac desmosomes are intercellular structures that anchor cardiac muscle fibers together and are vital in maintaining the structural integrity of the heart.[4]

The functional unit of cardiomyocyte contraction is the sarcomere, which consists of thick (myosin) and thin (actin) filaments, the interactions between which form the basis of the sliding filament theory.[5]

The sarcolemma is the cardiomyocyte plasma membrane containing transverse tubules (t-tubules). These t-tubules are highly branched invaginations of the cardiomyocyte sarcolemma that function in excitation-contraction coupling (ECC), action potential initiation and regulation, maintaining the resting membrane potential, and signal transduction. T-tubules regulate the cardiac ECC by concentrating voltage-gated L-type calcium channels and positioning them in close proximity to calcium sense and release channels, ryanodine receptors (RyRs), at the junctional membrane of the sarcoplasmic reticulum.[6]

The development of the heart occurs in various stages. During embryogenesis, the formation of the primitive streak follows the invagination of epiblast cells, indicating the start of gastrulation. Gastrulation divides the embryonic plate, which originally contained two layers between the yolk sac and amniotic cavity, into three germ layers; ecto-, meso-, and endoderm. The mesoderm is situated between the ectoderm and endoderm layers and, during development, spreads laterally and cranially, forming different structures, particularly the heart.[7]

The myocardium begins developing during the second week of gestation in the dorsal mesocardium. After three weeks post-fertilization, the primitive heart begins to develop as a straight tube changing its configuration as time proceeds. This entails folding of the tube, giving rise to bulges that become analogous to the adult heart; truncus arteriosus develops into the aorta and pulmonary artery, bulbus cordis develops into smooth left and right ventricles, primitive ventricle into trabeculated LV/RV, primitive atrium into trabeculated atria and the sinus venosus which develops into the right atrium (sinus venarum) and coronary sinus.[8]

Around the fourth week of development, the heart undergoes a cardiac looping process that establishes the heart's left-sided orientation. This is performed with the help of cilia, a motile structure, and dynein, a protein.[9] If these factors fail to function correctly, dextrocardia will occur, which places the heart on the right side of the chest. This cardiac anomaly is typically seen in Kartagener Syndrome and primary ciliary dyskinesia (PCD).[10]

Further developmental changes occur as the heart is shaped into its proper configuration. The heart begins as a single chamber, but four separate chambers are created through the growth of various septa. The muscular ventricular septum originates from the bottom of the ventricle, with a membranous septum forming shortly after, joining with the aortic-pulmonary septum as its twists down and fuses. The endocardial cushions also appear at this time and separate the left and right atria and ventricles. Any structural changes or defects in these processes can lead to congenital heart disorders.

The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force. The mechanism behind each coordinated contraction involves the cardiac muscle and electrical impulses. These contractile functions of the heart require ATP, which can be obtained through various substrates, including fatty acids, carbohydrates, proteins, and ketones. Aerobic production is the core utilization process; however, the heart may use anaerobic processes in a limited capacity.[11]

The generation of a cardiac action potential is involuntary and proceeds via a process known as excitation-contraction coupling (ECC). Action potentials travel along the sarcolemma and into the t-tubules to depolarize the membrane. Voltage-sensitive dihydropyridine (DHP) receptors on t-tubules allow calcium influx into the cell via L-type (long-lasting) calcium channels during the plateau phase (phase 2) of the action potential. This increased intracellular calcium concentration triggers the sarcoplasmic reticulum to release more calcium through the ryanodine receptor, known as calcium-induced calcium-released.[12]

The released calcium attaches to troponin C, causing tropomyosin to detach from the myosin-binding sites on actin. Actin and myosin then form a cross-bridge, and contraction occurs. Cross bridges last as long as calcium is attached to troponin.[13]

Lusitropy is the term used to define the relaxation of the myocardium following ECC. Lusitropy is mediated by the SERCA (sarco-endoplasmic reticulum calcium-ATPase) pump, which sequesters calcium into the sarcoplasmic reticulum, allowing calcium to be removed from troponin-C and returning the myocardium to its relaxed state.[14]

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