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Such efforts recruit fast glycolytic motor units blood pressure chart pdf innopran xl 80 mg generic, as well as slow oxidative motor units blood pressure 300 150 purchase innopran xl toronto. During these efforts, blood supply to the working muscles may be interrupted as tissue pressures rise above intravascular pressure. Regular maximal-strength exercise, such as weightlifting, induces the synthesis of more myofibrils and hence hypertrophy of the active muscle cells. Endurance exercise does not cause fast motor units to become slow, nor does maximal muscular effort produce a shift from slow to fast motor units. Thus any practical exercise regimen, when superimposed on normal daily activities, probably does not alter muscle fiber phenotype. The resultant dull, aching pain develops slowly and reaches its peak within 24 to 48 hours. The pain is associated with reduced range of motion, stiffness, and weakness of the affected muscles. The prime factors that cause the pain are swelling and inflammation from injury to muscle cells, most commonly near the myotendinous junction. Biophysical Properties of Skeletal Muscle the molecular mechanisms of muscle contraction described earlier underlie and are responsible for the biophysical properties of muscle. Historically, these biophysical properties were well described before elucidation of the molecular mechanisms of contraction. Length-Tension Relationship When muscles contract, they generate force (often measured as tension or stress) and decrease in length. In examination of the biophysical properties of muscle, one of these parameters is usually held constant, and the other is measured after an experimental maneuver. Accordingly, an isometric contraction is one in which muscle length is held constant, and the force generated during the contraction is then measured. An isotonic contraction is one in which the force (or tone) is held constant, and the change in length of the muscle is then measured. If the muscle is stimulated to contract at these various lengths, a different relationship is obtained. This length-tension curve is consistent with the sliding filament theory, described previously. C, Plot of active tension as a function of muscle length, with the predicted overlap of thick and thin filamentsatselectedpoints. For construction of the length-tension curves, muscles were maintained at a given length, and then contractile force was measured. Thus the length-tension relationship supports the sliding filament theory of muscle contraction. In the absence of any load, the shortening velocity of the muscle is maximal (denoted as V0). Increasing the load decreases the velocity of muscle shortening until, at maximal load, the muscle cannot lift the load and hence cannot shorten (zero velocity). To calculate the latter curve, the x- and y-coordinates were simply multiplied, and then the product was plotted as a function of the x-coordinate. The appearance of striations in skeletal muscle is due to the highly organized arrangement of thick and thin filaments in the myofibrils of skeletal muscle fibers. Thin filaments, containing actin, extend from the Z line toward the center of the sarcomere. Thick filaments, containing myosin, are positioned in the center of the sarcomere and overlap the actin thin filaments. Muscle contraction results from the Ca++-dependent interaction of myosin and actin, in which myosin pulls the thin filaments toward the center of the sarcomere. Motor centers in the brain control the activity of motor neurons in the ventral horns of the spinal cord. Whereas each skeletal muscle fiber is innervated by only one motor neuron, a motor neuron innervates several muscle fibers within the muscle.

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The hypothalamus regulates the anterior pituitary by secreting releasing hormones blood pressure negative feedback loop discount innopran xl master card. Describe the anatomy and histology of the thyroid gland heart attack damage purchase innopran xl mastercard, including the structure of the thyroid follicle. Explain how thyroid hormones are synthesized within the thyroid gland, including the processes of iodine uptake, iodination of tyrosine residues in thyroglobulin by thyroid peroxidase/dual oxidase, and coupling to form T4 and T3. Describe the process of endocytosis by which thyroglobulin is retrieved from the follicle lumen and processed to yield T3 and T4, which are secreted into the circulation. Discuss the role of thyroid-binding proteins in the transport and stability of thyroid hormones, and the role of peripheral deiodinases in the activation of T4 to T3 or inactivation to reverse T3. Describe the mechanisms of thyroid hormone action, including the nature and location of the thyroid hormone receptor and its ability to either repress or activate target gene transcription. Describe the effects of thyroid hormone on basal metabolic rate and thermogenesis, on the cardiovascular system (heart rate, cardiac output, systemic vascular resistance), and on other organ systems (skin, skeletal muscle, digestive tract). It is drained by three sets of veins on each side: the superior, middle, and inferior thyroid veins. The thyroid gland receives sympathetic innervation that is vasomotor but not secretomotor. The epithelium sits on a basal lamina, the outermost structure of the follicle, and is surrounded by a rich capillary supply. The follicular lumen itself is filled with colloid, which is composed of thyroglobulin. This large (660 kDa) protein is secreted into the lumen and iodinated by the thyroid epithelial cells, serving as a scaffold for production of thyroid hormones. The size of the epithelial cells and the amount of colloid are dynamic features that change with activity of the gland. Scattered within the gland are parafollicular cells, or C cells, which are the source of the polypeptide hormone calcitonin (see Chapter 40). Approximately 90% of the thyroid output is 3,5,3,5-tetraiodothyronine (thyroxine, or T4). About 10% is 3,5,3-triiodothyronine (T3), which is the active form of thyroid hormone. Less than 1% of thyroid output is 3,3,5-triiodothyronine (reverse T3, or rT3), which is inactive. Normally these three products are secreted in the same proportions at which they are stored in the gland. Most 753 The thyroid gland produces the prohormone tetraiodothyronine (T4, also called thyroxine) and the active hormone triiodothyronine (T3). Synthesis of T4 and T3 requires iodine, which can be a limiting factor in some parts of the world. Thyroid hormone acts primarily through a nuclear receptor that regulates gene transcription. T3 is critical for normal brain and bone development and has broad effects on metabolism and cardiovascular function in adults. This process supplies basal circulating T3 for uptake by other tissues in which local T3 generation is low or absent. D1 is also expressed in the thyroid (again, where T4 is abundant) and has relatively low affinity. Levels of D1 are paradoxically increased in hyperthyroidism and contribute to the elevated circulating T3 levels in this disease. D2 has a Km of 1 nM and maintains intracellular concentrations of T3 even when circulating T4 falls to low levels. Expression of D2 is increased during hypothyroidism, which helps maintain constant T3 levels in the brain. Type 3 deiodinase is increased during hyperthyroidism, which helps blunt overproduction of T4.

Renin-Angiotensin-Aldosterone System Cells in the afferent arterioles (juxtaglomerular cells heart attack in the style of demi lovato ameritz top tracks purchase generic innopran xl, also known as granular cells) are the site of synthesis hypertension 16080 discount generic innopran xl canada, storage, and release of the proteolytic enzyme renin. Activation of the sympathetic nerve fibers that innervate the afferent arterioles increases renin secretion (mediated by -adrenergic receptors). Renin alone does not have a physiological function; it functions solely as a proteolytic enzyme. Its substrate is a circulating protein, angiotensinogen, which is produced by the liver. Activation of this system results in a decrease in excretion of Na+ and water by the kidneys. As shown, the endothelial cells within the lungs play a significant role in this conversion process. An increase in plasma K+ concentration is the other important stimulus for aldosterone secretion (see Chapter 36). Aldosterone is a steroid hormone produced by the glomerulosa cells of the adrenal cortex and acts in a number of ways on the kidneys (see also Chapters 34, 36, and 37). Thus aldosterone increases reabsorption of NaCl from the tubular fluid by distal nephron segments, whereas reduced levels of aldosterone decreases the amount of NaCl reabsorbed by these segments. With decreased secretion of aldosterone (hypoaldosteronism), the reabsorption of NaCl, mainly by the aldosterone-sensitive distal nephron, is reduced and NaCl is lost in the urine. With increased aldosterone secretion (hyperaldosteronism) the effects are the opposite; NaCl reabsorption by the aldosterone-sensitive distal nephron is enhanced and excretion of NaCl is reduced. These effects decrease water reabsorption by the collecting duct and thus increase excretion of water in the urine. The net effect of natriuretic peptides is to increase excretion of NaCl and water by the kidneys. Hypothetically a reduction in circulating levels of these peptides would be expected to decrease NaCl and water excretion, but convincing evidence for this has not been reported. Control of NaCl Excretion During Euvolemia Maintenance of Na+ balance and therefore euvolemia requires precise matching of the amount of NaCl ingested with the amount excreted from the body. Accordingly, in a euvolemic individual we can equate daily urine NaCl excretion with daily NaCl intake. Conversely, in individuals who ingest large quantities of NaCl, renal NaCl excretion can exceed 1000 mEq/day. The time course for adjustment of renal NaCl excretion varies (hours to days) and depends on the magnitude of the change in NaCl intake. Acclimation to large changes in NaCl intake requires a longer time than acclimation to small changes in intake. Most (67%) of the Na+ filtered by the glomerulus is reabsorbed by the proximal tubule. An additional 25% is reabsorbed by the thick ascending limb of the loop of Henle, and the remainder by the distal tubule and collecting duct. In a normal adult the filtered amount (load) of Na+ is approximately 25,000 mEq/day: Equation 35. Natriuretic Peptides the body produces a number of substances that act on the kidneys to increase NaCl excretion (see Chapter 34). Of these, natriuretic peptides produced by the heart and kidneys are best understood and will be the focus of the following discussion. Vasodilation of the afferent and vasoconstriction of the efferent arterioles of the glomerulus. Inhibition of aldosterone secretion by the glomerulosa cells of the adrenal cortex. Inhibition of NaCl reabsorption by the collecting duct, which is also caused in part by reduced levels of aldosterone. The percentage of the filtered load excreted in urine is termed fractional excretion.

The most common configuration is 1 blood pressure medication nifedipine purchase 40 mg innopran xl visa, 2 blood pressure 00 order innopran xl 40 mg on-line, 2 in a 2: 2: 1 stoichiometry, which may account for 80% of the receptors; however, many other heteromers are found in the brain. The sedative and anticonvulsant actions of benzodiazepines appear to be mediated by receptors with the 1 subunit, whereas the anxiolytic effects reflect binding to receptors with the 2 subunit. Excitatory Amino Acid Receptors: Glutamate Glutamate has both ionotropic and metabotropic receptors. Overall, there are 18 known genes that code for glutamate subunits for the ionotropic glutamate receptors. Thus, there is a certain correspondence between the genes and the receptor types that are formed. As was mentioned for the other receptors, the receptor properties vary with subunit composition. Ionotropic glutamate receptors are excitatory and contain a cationic-selective channel. Thus, all the channels are permeable to Na+ and K+, but only a subset allow Ca++ to pass. Second, they display voltage sensitivity as a result of Mg++ blockade of the channel. That is, at resting (or more negative) membrane potentials, a Mg++ ion blocks the entrance to the channel so that even when glutamate and glycine are bound, no current flows through the channel. Eight genes coding for metabotropic glutamate receptors have been identified and classified into three groups. An interesting localization distinction between P2X and P2Y receptors is that although both are present on neurons, the latter dominates on astrocytes. These receptors are located presynaptically and act to inhibit synaptic transmission by inhibiting influx of Ca++. Thus, these neurotransmitters tend to act on relatively long time scales by generating slow synaptic potentials and by initiating second messenger cascades. Agonists and blockers of many of these receptors are important clinical tools for treating various neurological and psychiatric disorders. The role of different dopamine receptors in basal ganglia disorders will be covered in the motor systems (see Chapter 9). Neuropeptide Receptors As is the case with the biogenic amines, receptors for the various peptides are essentially all of the metabotropic type and are coupled to G proteins that mediate effects via second messenger cascades. It is worth mentioning again that studies consistently show a mismatch between the locations of terminals containing a particular peptide and the receptors for it. Thus, these receptors are often activated by neurotransmitter diffusing through the extracellular space rather than at synapses. This implies that these receptors will experience much lower concentrations of agonist, and indeed, they are very sensitive to their agonists. There are seven identified P2X subunit types that form channels, and they represent their own superfamily of ligand-gated channels. In general, these receptors form a cationic channel that is permeable to Na+, K+, and Ca++. One way they do affect cell activity is to activate enzymes involved in second messenger cascades, such as guanylyl cyclase. Both electrical and chemical synapses are important means of cellular communication in the mammalian nervous system. Electrical synapses directly connect the cytosol of two neurons and allow rapid bidirectional current flow between neurons. Standard chemical synaptic transmission involves the release of transmitter from a presynaptic terminal, diffusion of transmitter across a synaptic cleft, and binding of the transmitter to receptors on the apposed postsynaptic membrane. Entry of calcium into the presynaptic terminal triggers the release of neurotransmitter. Excitatory and inhibitory synapses increase or decrease, respectively, the probability that the postsynaptic neuron will spike. The reversal potential is the membrane potential at which net current flow through a ligand-gated channel reverses. Inhibitory synapses can decrease spike probability by two mechanisms: hyperpolarization of the membrane and a decrease in the input resistance of the neuron, leading to a shunt of synaptic currents. The process by which a neuron decides to fire an action potential as a result of its inputs is referred to as synaptic integration. The efficacy of synaptic transmission depends on the timing and frequency of action potentials in the presynaptic neuron.