PMD 08. Endocr. physiol.doc

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D’YOUVILLE COLLEGE
PMD 604 - ANATOMY, PHYSIOLOGY, PATHOLOGY II
Lecture 8: Endocrine system physiology
G & H chapters 74 - 77
1.
Chemical Messengers in the Body: substances that alter activity of cells
bearing receptors to bind them; messenger molecules (ligands) cannot affect activity
of cells that lack receptors for them
• neurotransmitters: messengers at synapses
• cytokines: e.g., lymphokines (interleukins) facilitate interactions of immune
system cells, also tumor necrosis factor & other growth factors
• autocrines & paracrines: substances produced by a cell to stimulate itself
(autocrine) or to stimulate nearby cells (paracrine), e.g., prostaglandins, histamine
• endocrines & neuroendocrines: products of cells (hormones or
neurohormones) that travel in bloodstream to act at distant targets
• chemistry of hormones (table 74 - 1):
- proteins & polypeptides, e.g., parathormone from parathyroid glands,
tropic hormones from anterior pituitary, antidiuretic hormone & oxytocin from
posterior pituitary; stored in vesicles & released by exocytosis (ppts. 1 & 2)
- steroids, e.g., cortisol & aldosterone from adrenal cortex, androgens,
estrogens & progestins from gonads (fig. 74 - 3 & ppt. 3); synthesized ad hoc from
stored cholesterol esters & secreted by diffusion through plasma membrane
- amino acid derivatives, e.g. thyroid hormones, adrenal medullary
hormones (catechol amines) (ppt. 4)
- synthesized from tyrosine, stored in vesicles & released by exocytosis
• mechanisms of hormone action (figs. 74 - 4 to 74 - 8 & ppts. 5 to 9):
- must bind to specific receptor in target cell to achieve 'hormonal effect'
- receptors may be located in plasma membrane (for polar hormones - proteins,
peptides & most tyrosine derivatives), in the cytoplasm (for steroids) and in the nucleus
(for thyroid hormone)
- hormone-receptor complex triggers intracellular events that may involve:
- G-protein-mediated enzyme activation
- direct activation of enzyme (on inner end of receptor) that synthesizes
'second messenger' (cyclic AMP or phospholipid ) formation
- interaction with promoter site of nuclear DNA (to control
transcription of RNA and the ensuing protein synthesis)
PMD 604, lec 8
- p. 2 -
- the result of most actions is a shift in target cell's enzyme activity
(often a cascade effect that amplifies the 'hormonal effect') (ppt. 10)
PMD 604, lec 8
2.
- p. 3 -
Endocrine System:
• exocrine glands secrete to an external surface via ducts
• endocrine glands are ductless and secrete directly into the bloodstream;
their products are called hormones
• anatomy (fig. 74 - 1 & ppt. 11):
- hypothalamus: special areas of grey matter in this brain region regulate or
produce the secretions of the posterior pituitary gland
- pituitary or hypophysis: suspended from infundibulum of hypothalamus
(floor of diencephalon), divided into two major parts, a glandular anterior lobe
(adenohypophysis) that maintains vascular link to hypothalamus and a neural
posterior lobe (neurohypophysis) that maintains neural link with hypothalamus
- anterior lobe secretes several tropic hormones that influence activity of
other endocrine glands, also secretes growth hormone & prolactin
- posterior lobe is site of secretion for neurohormones synthesized by
hypothalamus (ADH & oxytocin)
- thyroid gland: produces thyroid hormones (T3 & T4) that are stored in
follicles; also produces a peptide (calcitonin) that regulates blood calcium
- parathyroid glands: embedded in posterior surface of each lobe of the
thyroid gland; secrete parathormone (PTH) that regulates blood calcium
- adrenal cortex: outer layer of adrenal (aka suprarenal) glands, located at
superior pole of each kidney; secretes steroids regulating blood sugar (glucocorticoids)
and regulating blood sodium & potassium (mineralocorticoids)
- adrenal medulla: interior of each adrenal gland, derived from embryonic
neural tissue; secretes epinephrine (major product) & norepinephrine (catecholamines)
- pancreatic islets: endocrine clumps of cells nested amongst acini (exocrine
components) of pancreas
- secrete insulin & glucagon that regulate blood glucose
- ovaries: female reproductive organs, located at posterolateral edge of brim
of pelvis
- secrete estrogens, which govern female secondary sex characteristics &
progesterone, which prepares uterine endometrium for implantation of conceptus
- testes: male reproductive organs, located within scrotum; secrete
testosterone, which governs male secondary sex characteristics
- other endocrine tissues: located within various organs, e.g., stomach
mucosa, intestinal mucosa, kidney parenchyma, heart, adipose tissue & placenta
3.
Endocrine Glands and Their Hormones:
Hypothalamus & Pituitary Gland (fig. 75 - 1 & ppts. 12 & 13):
• control of secretion:
- hypothalamus controls adenohypophysis (anterior pituitary) via
neurohormones (releasing hormones, or inhibiting hormones)
- neurosecretion: modified nerve cells (neurosecretory cells) release
neurohormones (instead of neurotransmitter) to hypophyseal portal system (fig. 75 4 & ppt. 14)
PMD 604, lec 8
- p. 4 -
- adenohypophysis: releases tropic hormones that control target glands;
this constitutes a neuroendocrine axis, e.g., hypothalamo-hypophysio-adrenal
cortical axis or hypothalamo-hypophysio-thyroid axis
- negative feedback: elevated level of target tissue product has inhibitory
influence upon hormone source, e.g., on hypothalamic activity (long loop negative
feedback) or hypophysial activity (short loop negative feedback) (ppts. 15 & 16)
• hormones of adenohypophysis (table 74 – 1, fig. 75 - 2 & ppts. 17 & 18)
- growth hormone (GH) promotes growth (protein buildup in muscle, &
cell proliferation in epiphysial discs of long bones) and stimulates metabolism:
- a) by increasing fat mobilization from adipose
- b) by stimulating glucose release from liver, while impeding its uptake
by other tissues (anti-insulin or diabetogenic effect)
- GH release is stimulated by growth hormone RH and inhibited by
GHIH (somatostatin) from the hypothalamus
- prolactin stimulates milk production in mammary glands of the female; its
release is controlled by prolactin inhibiting hormone from the hypothalamus
- ACTH (adrenocorticotropic hormone or corticotropin) stimulates
glucocorticoid release from the adrenal cortex; it’s controlled by corticotropin RH
from the hypothalamus
- TSH (thyroid stimulating hormone/thyrotropin) stimulates thyroid
hormone release; it’s controlled by thyrotropin RH from hypothalamus
- GTH (Gonadotropic Hormones):
-1) FSH (Follicle Stimulating Hormone) stimulates proliferation of
follicles in the ovary and of spermatogonia in the testis
-2) LH (Luteinizing Hormone) promotes maturation of follicles &
estrogen release in the ovary; a high concentration (spike) causes ovulation; LH also
promotes formation and maintenance of the corpus luteum of the ovary (following
ovulation)
- in males, LH promotes maturation of spermatozoa and release of
testosterone by interstitial cells of the testis
- GnRH from the hypothalamus controls gonadotropin release
• hormones of neurohypophysis (table 74 – 1 & ppt. 19)
- oxytocin causes smooth muscle contraction in uterine wall to promote
parturition, and in ducts of mammary glands to promote milk ejection
- antidiuretic hormone (ADH) promotes water retention by the kidney
- neurohypophysis is composed of pituicytes (like neuroglia), and is
technically not an endocrine tissue, but a site for release of neurohormones of
hypothalamus via hypothalamo-hypophysial tract (fig 75 - 9 & ppt. 20)
Thyroid Gland:
PMD 604, lec 8
- p. 5 -
• thyroid hormone (T3 or T4) stimulates metabolic rate (action is slow to
develop but prolonged); many widespread effects on various tissues relate to
elevated metabolic rate
- synthesized from tyrosine (combined with 3 or 4 iodine atoms) (fig. 76 - 3
& ppt. 21) & stored inside follicles as colloid (fig. 76 – 1 & ppt. 22)
- secretion is regulated by TSH from anterior pituitary (fig. 76 - 7 & ppt. 23)
• calcitonin is a weak hypocalcemic hormone, from parafollicular C cells; it
inhibits osteoclasts that mobilize calcium from bone, and promotes calcium uptake and
incorporation into bone (bone sparing effect)
Parathyroid Glands (figs. 79 – 10 & ppt. 24):
• parathormone (PTH) is a strong hypercalcemic hormone
- it raises blood calcium by causing bone resorption by osteoclasts, by
promoting kidney retention of calcium and by promoting activation of vitamin D,
which facilitates intestinal absorption (fig. 79 - 13 & ppt. 25)
- secretion is stimulated by low blood level of Ca2+
PMD 604, lec 8
- p. 6 -
Adrenal Glands (fig. 77 – 1 & ppt. 26):
a. cortex: produces steroids from cholesterol (fig. 77 - 2 & ppt. 27):
• glucocorticoids (cortisol) have a glucose sparing effect on carbohydrate
metabolism: promotion of gluconeogenesis & mild inhibition of glucose utilization
- they are also anti-inflammatory
- secretion is controlled by ACTH from the anterior pituitary (fig. 77 - 7 &
ppt. 28)
• mineralocorticoids (aldosterone) promote sodium retention and potassium
excretion in the kidney; effect is achieved by increasing synthesis of Na+/K+ pump in
renal cells
- aldosterone secretion is controlled by the renin-angiotensin system (in
kidney), and by elevated blood level of potassium
• gonadocorticoids (mostly androgens produced in small amounts) may be
responsible for onset of puberty (preceding gonadal output of sex steroids); excess
produces adrenogenital syndrome
b. medulla: produces catecholamines: (ppt. 29)
• epinephrine produces cardioaccelerator activity (alpha receptor mediated);
it also stimulates muscle metabolism, hyperglycemia, and blood flow (beta receptor
mediated); stronger beta receptor action than norepinephrine
• norepinephrine produces vasoconstrictor and cardioaccelerator activity
(alpha receptor mediated)
Pancreatic Islets: (fig. 78 - 1 & ppt. 30)
• insulin (insula = island) is a hypoglycemic hormone, also known as the
“feasting hormone” (fig. 78 - 2 & ppt. 31); secreted by islet  cells
- essential for glucose uptake (especially liver & muscle, but not brain) and
storage (glycogenesis - mainly by liver)
- promotes fat synthesis, inhibits fat breakdown (adipose tissue)
- promotes protein synthesis, inhibits protein catabolism & gluconeogenesis
- secretion triggered by elevation of blood glucose
- a deficiency causes diabetes mellitus
• glucagon is a hyperglycemic hormone; secreted by islet  cells
- stimulates glycogenolysis and gluconeogenesis by liver, both causing an
elevation of blood glucose (ppt. 32)
Gonads: to be discussed with reproductive physiology
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