Chap11 Part1 Human Phys

  1. 1. What are the three general chemical classes of hormones?
    amines, peptides, and steroids
  2. 2. Which catecholamine is secreted in the largest amount by the adrenal medulla, and why?
    • epinephrine, because the adrenal medulla has high activity levels of the enzyme phenyl-Nmethyltransferase
    • (PNMT) which converts norepinephrine into epinephrine
  3. 3. What are the major hormones produced by the adrenal cortex? By the testes? By the ovaries?
    • Adrenal cortex: cortisol, corticosterone, aldosterone, dehydroepiandrosterone (DHEA),
    • androstenedione
    • Testes: androgen (testosterone and dihydrotestosterone), inhibin, Müllerian-inhibiting substance
    • Ovaries: estrogen (estradiol), progesterone, inhibin, relaxin
  4. 4. Which classes of hormones are carried in the blood mainly as unbound, dissolved hormone?
    • Mainly bound to plasma proteins?
    • Most peptide and catecholamine hormones are carried in the blood mainly as unbound, dissolved
    • hormone. Steroid and thyroid hormones are carried in the blood mainly bound to plasma proteins.
  5. 5. Do protein-bound hormones diffuse out of capillaries?
    • No. The binding proteins are too large to cross, and so only the free form of the hormone diffuses across
    • the capillary membrane to encounter the target cells.
  6. 6. Which organs are the major sites of hormone excretion and metabolic transformation?
    the liver and kidneys
  7. 7. How do the rates of metabolism and excretion differ for the various classes of hormones?
    • The rates of metabolism and excretion of most peptide hormones and the catecholamines are fast—
    • minutes to an hour—because they are freely dissolved in the plasma and are thus more susceptible to
    • enzymatic attack. The rates for steroid and thyroid hormones are slower—hours to days. This
    • difference reflects the fact that binding proteins serve a “protective” function for hormones and slow
    • the rate of their removal from the blood.
  8. 8. List some metabolic transformations that prohormones and some hormones must undergo
    • before they become biologically active.
    • Some hormones must be changed by metabolism to become physiologically active. An example is
    • thyroxine (T4) which can be converted to a more active form, triiodothyronine (T3), in its target cells
    • before binding to its receptors. Another example is renin, a hormone that acts as an enzyme to convert
    • biologically inactive angiotensinogen to angiotensin I. This is the first step in the formation of
    • angiotensin II. A third example is testosterone, which is converted either to estradiol or
    • dihydrotestosterone in certain of its target cells. These molecules, rather than testosterone itself, then
    • bind to receptors inside the target cells and elicit the cell's response.
  9. 9. Contrast the locations of receptors for the various classes of hormones.
    • The receptors for water-soluble chemical messengers like peptide and catecholamine hormones are in
    • the plasma membrane of their target cells, while those for the lipid-soluble, nonpolar steroid and
    • thyroid hormones are (primarily) inside the target cells, generally in the nucleus.
  10. 10. How do hormones influence the concentrations of their own receptors and those of other
    • hormones? How does this explain permissiveness in hormone action?
    • Hormones can up-regulate (increase the number of) their own receptors, and down-regulate (decrease
    • the number of) them. In general, high concentrations of the hormone over time lead to down-regulation
    • and low concentrations over time lead to up-regulation.
    • Some hormones may, by a different mechanism, increase or decrease the number of receptors for a
    • different hormone. In some cases, such as epinephrine receptors in fat cells, receptor numbers are very
    • low unless they are up-regulated by a low concentration of thyroid hormones. Thyroid hormone,
    • therefore, causes the adipose tissue to become much more sensitive to epinephrine; this effect of thyroid
    • hormones is called permissiveness.
  11. 11. Describe the sequence of events when peptide or catecholamine hormones bind to their
    • receptors.
    • Binding of a peptide or catecholamine hormone to its plasma membrane receptor activates the receptor.
    • When activated, the receptor triggers one or more of the signal transduction pathways described in
    • Chapter 5. That is, the activated receptors directly influence: (1) enzyme activity that is part of the
    • receptor; (2) activity of cytoplasmic janus kinases associated with the receptor; or (3) G proteins
    • coupled in the plasma membrane to effector proteins—ion channels and enzymes that generate second
    • messengers such as cAMP and Ca2+. The opening or closing of ion channels causes a change in the
    • electrical potential across the membrane, and when a Ca2+ channel is involved, a change in the
    • cytosolic concentration of this important ionic second messenger. The changes in enzyme activity
    • rapidly produce—most commonly by phosphorylation catalyzed by protein kinase enzymes—changes
    • in the conformation and hence the activity of various cellular proteins. In some cases the signal
    • transduction pathways also lead to the activation or the inhibition of particular genes, causing a
    • change in the rate of synthesis of the proteins coded for by these genes.
  12. 12. Describe the sequence of events when steroid or thyroid hormones bind to their receptors.
    • These hormones have intracellular receptors. Binding of such a hormone to its receptor, generally in
    • the nucleus, leads to the activation or inhibition of transcription of particular genes, causing a change
    • in the rate of synthesis of the proteins coded for by those genes. The ultimate result of changes in the
    • concentration of these proteins is an enhancement or inhibition of particular processes carried out by
    • the cell, or a change in the rate of protein secretion by the cell.
    • In some cases, target cells for certain steroid hormones also have plasma membrane receptors for
    • the hormone. In these cases, binding of the hormone to its plasma membrane receptor initiates
    • activation of signal transduction pathways that elicit fast, nongenomic cell responses, while the
    • intracellular receptor mediates a delayed response to the hormone.
  13. 13. What are the direct inputs to endocrine glands controlling hormone secretion?
    • Most hormone secretion by endocrine glands is controlled by changes in the plasma concentrations of
    • mineral ions or organic nutrients, by neurotransmitters released from neurons ending on the
    • endocrine cell, or by another hormone (or paracrine substance) acting on the endocrine cell.
  14. 14. How does control of hormone secretion by plasma mineral ions and nutrients achieve
    • negative feedback control of these substances?
    • In the case of hormones whose secretion is affected by plasma concentrations of mineral ions or
    • nutrients, a major function of the hormone is to regulate the plasma concentration of that ion or
    • nutrient. For example, insulin-secreting cells in the pancreas respond to increased plasma
    • concentration of glucose by increasing their secretion of insulin. One of the major functions of insulin
    • is to increase the uptake of glucose into skeletal muscle and adipose tissue cells. This action causes the
    • concentration of plasma glucose to be decreased. In this example, the receptors in the negative feedback
    • loop are glucose receptors in the pancreatic cell’s plasma membrane; the afferent pathway and the
    • integrative center are both contained within the same pancreatic cell; the efferent pathway is insulin
    • circulating in the blood; and the effectors are the cells that respond to insulin by increasing their
    • uptake of glucose.
  15. 15. What roles does the autonomic nervous system play in controlling hormone secretion?
    • The adrenal medulla is functionally a part of the sympathetic division of the autonomic nervous
    • system, and adrenal medullary hormone secretion is stimulated by sympathetic preganglionic fibers. In
    • addition, both sympathetic and parasympathetic postganglionic fibers innervate other endocrine gland
    • cells, such as in the endocrine pancreas, and inhibit or stimulate hormone secretion.
  16. 16. What groups of hormone-secreting cells receive input from neurons located in the brain
    • rather than in the autonomic nervous system?
    • The hormones secreted by the hypothalamus and by the anterior and posterior pituitary glands.
  17. 17. How would you distinguish between primary and secondary hyposecretion of a hormone?
    • Between hyposecretion and hyporesponsiveness?
    • Primary hyposecretion of a hormone is caused by a defect in the gland that secretes the hormone.
    • Secondary hyposecretion of a hormone is caused by too little stimulation of the gland by its tropic
    • hormone. One way to diagnose hyposecretion is to administer the tropic hormone. In primary
    • hyposecretion, the target gland for the tropic hormone is damaged leading to its failure to respond
    • normally. In secondary hyposecretion, the target gland was initially normal, but has atrophied due to
    • lack of tropic hormone stimulation, so it does not respond normally to stimulation. The latter condition
    • can be reversed over time with normalization of tropic hormone input. Another way to distinguish
    • between primary and secondary hyposecretion is to measure the level of the tropic hormone in the
    • blood. If elevated, the cause is primary; if not elevated, the cause is secondary.
    • If a person has primary hypothyroidism, for example, such analysis would show low levels of TH
    • and high levels of TSH in plasma, because the pituitary would be functioning normally and secreting
    • increased amounts of TSH due to too little negative-feedback signal from TH. If the pituitary were at
    • fault, the concentrations of both TH and TSH would be low. However, this last finding would not rule
    • out a problem at the hypothalamic level, in which case there would be secondary hyposecretion of TSH
    • and tertiary hyposecretion of TH, ultimately due to lower than normal levels of TRH release from the
    • hypothalamus. Unfortunately, the concentration of the hypophysiotropic hormones in the peripheral
    • plasma is too low to measure. However, one could rule out the pituitary as the cause of the defect if the
    • administration of TRH produced an increase in TSH secretion.
    • Hyporesponsiveness occurs when target cells of a hormone do not respond normally to the
    • hormone. To differentiate this condition from hyposecretion, one would measure the concentration of
    • the hormone in plasma. If hyporesponsiveness is the problem, the hormone concentration would be
    • normal or elevated, but the response of target cells to administered hormone would be diminished.
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Chap11 Part1 Human Phys