Hormones And Receptors

Front 1

Receptors

Back 1

are proteins that bind to induce biological effects:
-hormones
-drugs
-paracrine messengers
-neurotransmitters

Front 2

Binding properties

Back 2

-stereospecific
-saturable
-selectivly inhibited
-trigger intracellular cascades

Front 3

Cascade targets

Back 3

-enzymes
-membrane transporters
-ion channels
-transcription factors

Front 4

Transcription factors

Back 4

retinoic acid,steroids,thyroid hor,vit D:
-diffuse across cell memb.
-bind to receptor in cytoplasm or nucleus
-complex moves to nucleus
-binds to promoters/enchancers
-inhibits/stimulates synthesis of proteins

Front 5

Neurotransmitters

Back 5

-in PM of cell (excitable)
-fast
-channels close until NT binds Na or Ca=channels open=depolerization
-K and Cl bind=hyperpolerization
i.e. nicotinic AcH=excititory
GABA-A=inhibitory

Front 6

G proteins

Back 6

-do most hor binding
-stimulate 2nd messengers
-integral proteins
-7 transmemb glycoprotein family
-have 3 subunits:
alpha-binds GTP & GDP
beta
gamma-stays bound to beta

Front 7

cAMP

Back 7

-2nd messenger
-Gi receptor
- hormone binds to alpha s.u. activates adenylate cyclase=cAMP from ATP

Front 8

Function of cAMP

Back 8

prokaryotes-lac operon regulator of transcription
eukaryotes-cAMP binds to regulatory proteins=frees protein kinase A =phosphorylates proteins or goes into nucleus to
activate KREB proteins
-is degraded by phosphodiesterases (caffeine)=turn cAMP into AMP

Front 9

Adenylate cyclase is stimulated by

Back 9

-glucagon
-epinepherine(beta receptors=Gs)
-dopamine
-PTH
-ACTH
-MSH
-vasopressin
-LH,FSH,TSH

Front 10

Adenylate cyclase is inhibited by

Back 10

-epinepherine (alpha receptor=Gi)
-dopamine
-somatostatin

Front 11

Clinical conditions invloving cAMP

Back 11

Pseudohypothyroidism:
abn Gs
PTH can't activate adenylate cyclase=
-hypocalcemia
-mental/neuro probs
-PTH levels are norm or inc
-toxic nodule
Cholera:
toxin activates Gs GTP can't be hydrolyzed to turn off cAMP=
-inc cAMP prod.
-inc H2O/electrolytes
-diarrhea
Whooping cough:
pertusis inactivates Gi=
overproduction of cAMP

Front 12

FUnction of phospholipase C

Back 12

-Gq
-Phos C cleaves lipids=PIP formed=IP3= binds to Ca ch. & causes release of stored
Ca in ER =Ca then binds to:trop C,calmodulin,PKC=exocyt of prods in sec vesicles,muscle cont.
-PLC=PIP=IP3=DAG=activtes PKC that in presence of Ca phosphorylates protein side chains

Front 13

Overall effect if cAMP is decreased

Back 13

dec in PKA=dec in:
- HR
-symp outflow
-insulin release

Front 14

Overall effect if IP3 is made

Back 14

Ca levels inc:inc in
-vasc sm. musc. cont
-exo gland secretion
-nasal/bronchial mucus prod,cont of bronchioles
-pain

Front 15

Overall effect if cAMP is made

Back 15

PKA is made=inc in:
-HR,contractility
-vasodilation,bronchdil
-H2O permeability in kidney
-gastric acid secretion
-relaxation of renal sm. musc.

Front 16

How Cyclic GMP is made

Back 16

-ANF receptors on cell surface made of guanylate cyclase
-ANF binds=conf change that activates intracellular guan cycl.=changes GTP->cGMP

Front 17

Function of cGMP in retinal rods

Back 17

retinal rods:cGMP bound to Na ch.& keeps open till lite present
-lite dec cGMP levels =transducin (Gi) activates phosphodiesterase that cleaves cGMP
-ch. close

Front 18

NO & effect on cGMP

Back 18

NO activates cytoplasmic guanylate cyclase:
-inc levels of cGMP
-PKG is acted on =vasc.sm. musc. relaxation

Front 19

Desensitation and Regulation of Hormone Receptors

Back 19

-cAMP ativates PKA=phosphorylation of HR's=they can't bind to Gs=downregulation of receptors

Front 20

Downregulation of receptors

Back 20

-ligands go to cell
-are endocytosed
-vesicles take them up w/ lysosome
-ligand is degraded
-some go back to cell surface
degredation=cause for type II diabetes:
-overeating=overexposure of insulin receps to insulin