Chap11 Part1 Human Phys
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Chap11 Part1 Human Phys
1. What are the three general chemical classes of hormones?
amines, peptides, and steroids
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. What are the major hormones produced by the adrenal cortex? By the testes? By the ovaries?
: cortisol, corticosterone, aldosterone, dehydroepiandrosterone (DHEA),
: androgen (testosterone and dihydrotestosterone), inhibin, Müllerian-inhibiting substance
: estrogen (estradiol), progesterone, inhibin, relaxin
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. 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. Which organs are the major sites of hormone excretion and metabolic transformation?
the liver and kidneys
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. 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. 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. 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. Describe the sequence of events when peptide or catecholamine hormones bind to their
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. 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. 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. 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. 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. 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. 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.