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225 Cards in this Set
- Front
- Back
__________ __________ innervation of the striated m. of the esophagus and external anal sphincter.
|
Parasympathetic cholinergic
|
|
3 sympathetic prevertebral ganglia to the gut
|
celiac ganglion
inferior mesenteric ganglion superior mesenteric ganglion |
|
Is afferent signals carried within the ANS innervation of the gut?
|
For sure, in both PSNS and SNS
|
|
Distal rectum and anal canal receive sympathetic innervation from where?
|
hypogastric plexus
|
|
Parasympathetic is Stimulatory or Inhibitory within the gut?
|
stimulatory
|
|
Sympathetic is Stimulatory or Inhibitory within the gut?
|
Inhibitory
(decreases tone and motility, usually decreases secretion) [NE, α2,β2(epi)] |
|
What does parasympathetic stimulation do to sphincters?
|
relax the sphincter
[ACh, M receptor] |
|
What does sympathetic stimulation do to sphincters?
|
contract sphincter
[NE, α1 receptor] |
|
Layers of the duodenum (out to in)
|
serosa, muscularis externa, submucosa, mucosa
|
|
Location of Auerbach's plexus in the gut
|
between the outer longitudinal and inner circular layer of the muscularis externa
-primarily involved with motility |
|
Location of Meissner's plexus
|
submucosa
-primarily involves fluid secretion and absorption |
|
Sympathetic _____- ganglionic synapse primarily on _______ _____, and occasionally directly on target cells
|
POST (synapse in one of the prevertebral ganglion)
enteric nerves |
|
Parasympathetic ___- ganglionic synapse primarily onto enteric _____.
|
PRE
ganglia (from there innervate enteric nerves) |
|
CCK is a hormone or a NT
|
it is both
|
|
2 classic excitatory NT in the GI
|
ACh and Substance P
|
|
2 classic inhibitory NT in the GI
|
VIP and NO
|
|
Long reflex of the gut
|
afferent -> CNS, efferent -> gut
|
|
Short reflex of the gut
|
reflex takes place entirely within the gut wall
(local reflex, intramural reflex) |
|
What receptors does the vagovagal (long) reflex carry info from to the CNS?
|
chemo and mechanoreceptors
|
|
Autocrine cell signaling
|
hormone that acts on the surface receptor of the same cell
|
|
Paracrine cell signaling
|
hormone released to neighboring cell or tissue rather than into the bloodstream
|
|
Endocrine cell signaling
|
hormone released from endocrine cell into the bloodstream
|
|
Neuroendocrine cell signaling
|
hormone released from neuron into the bloodstream
|
|
5 major GI hormones
|
Gastrin, CCK, Secretin, GIP, Motilin
|
|
Which of the 5 major GI hormones is released in the Antrum (bottom 1/2 of stomach)?
|
Gastrin
|
|
Which 2 GI hormones is still present in the ileum
|
CCK and Secretin
|
|
What stimulates the release of Gastrin?
|
peptides, amino acids, distention, Vagal stimulation
|
|
What stimulates the release of CCK?
|
peptides, amino acids, fatty acids >8C
|
|
What stimulates the release of Secretin?
|
mostly acid and partially fat
|
|
What stimulates the release of GIP?
|
glucose, amino acids, fatty acids
|
|
What stimulates the release of Motilin?
|
Nerves and to a lesser extent fat and acids
|
|
Where is Gastrin released?
|
Antrum and the duodenum to a lesser extent
|
|
Where is CCK released?
|
Duodenum and Jejunum
|
|
Where is Secretion released?
|
Duodenum
|
|
Where is GIP released?
|
Duodenum and Jejunum
|
|
Where is Motilin released?
|
Duodenum and Jejunum
|
|
Action of Gastrin?
|
Stimulate:
-gastric acid secretion -growth of gastric oxynitic gland mucosa |
|
Action of CCK?
|
Stimulate:
-gallbladder contraction -pancreatic enzyme secretion -pancreatic bicarbonate secretion -growth of exocrine pancreas Inhibits: -gastric emptying |
|
Action of Secretin?
|
Stimulate:
-pancreatic bicarbonate secretion -bilary bicarbonate secretion -growth of exocrine pancreas -pepsin secretion Inhibit: -gastric acid secretion -trophic effect of gastrin |
|
Action of GIP?
|
Stimulate:
-Insulin release Inhibit: -gastric acid secretion |
|
Action of Motilin?
|
Stimulate:
-gastric motility -intestinal motility |
|
3 inputs to the parietal cell
|
1. PS synapse
2. histamine from ECL cell 3. gastrin |
|
What cell type produces gastrin?
|
G cell
|
|
What cell type produces IF and H+?
|
Parietal cell
|
|
What cell type produces pepsinogen?
|
Cheif cell
|
|
What 2 cell types does Secretin inhibit?
|
G cell and Parietal cell
|
|
What is the goal of Somatostatin?
|
wants to inhibit everything!
(acid and gastrin are the most potent triggers) |
|
What nerve releases Gastrin-releasing Peptide (GRP)?
|
Vagus
|
|
What is the action of GRP?
|
gastrin release from G cell
|
|
What does VIP stimulate?
|
pancreatic and intestinal secretion
|
|
Opiates _______ motility and _______ intestinal secretion.
|
decrease, decrease
|
|
4 neurocrines of the GI
|
1. VIP
2. GRP 3. Enkephalins, opiates 4. Neurotensin |
|
Action of Neurotensin?
|
increase blood glucose
(stimulate glycogenolysis and glucagon release and inhibit insulin release) |
|
2 paracrine hormones of the GI
|
Somatostatin
Histamine |
|
What causes the release of Pancreatic polypeptide?
|
protein, fat, glucose
|
|
What is the action of Pancreatic polypeptide?
|
decrease pancreatic bicarb and enzyme secretion
|
|
What causes the release of Peptide YY?
|
Fat
|
|
What is the action of Peptide YY?
|
decrease:
-gastric secretion -gastric emptying |
|
What causes the release of Enteroglucagon?
|
hexose and fat
|
|
What is the action of Enteroglucagon?
|
decrease:
-gastric secretion -gastric emptying Increase: -insulin release |
|
Location of striated muscle in the GI tract
|
pharynx, upper 1/2 of esophagus, and external anal sphincter
|
|
What 3 regions of the GI have phasic muscle contractions?
|
esophagus, antral stomach, small intestine
|
|
Regions of the GI that have tonic muscle contractions?
|
sphincters, orad stomach
|
|
What is the organization of the smooth muscle within the GI?
|
single- unit smooth muscle
(gap junctions - contract as one) |
|
Describe the propulsive segment of peristalsis.
|
relaxation of the longitudinal muscle and contraction of circular muscle
|
|
Describe the recieveing segment of peristalsis.
|
Contraction of the longitudinal muscle and inhibition of circular muscle.
|
|
What is the action and mechanism of segmentation within the GI?
|
action: mixing
mechanism: alternating propulsive and recieving segments |
|
Physiologic ileus within the GI.
|
absence of motility (normal)
|
|
Trituration
|
crushing and grinding of food in the stomach
|
|
When an inhibitory motor neuron is ACTIVE what is the state of contraction of the smooth muscle?
|
lack of contraction
|
|
Inhibitory motor neurons to the lower esophageal sphincter are normally _____ and must be turned ____ for the sphincter to relax.
|
off, on
|
|
Describe the pressure difference within the esophagus.
|
UES: + pressure
esophagus to diaphragm: - pressure due to thoracic pressure esophagus below the diaphragm: + pressure |
|
What is the innervation of the upper esophageal sphincter?
|
excitatory somatic nerves (travel through the vagus)
|
|
Innervation of the lower esophageal sphincter
|
excitatory: ACh and substance P
inhibitory: VIP and NO |
|
What is the difference between primary and secondary peristalsis?
|
primary: follow the pharyngeal wave, able to complete the active movement
secondary: occurs if food does not make it the entire way down |
|
Where does the afferent signal from the pharynx go to?
|
swallowing center located in the medulla
|
|
What does the nucleus ambiguus within the swallowing center control?
|
skeletal muscle
|
|
What does the dorsal motor nucleus within the swallowing center control?
|
smooth muscle
|
|
What 2 things are able to activate the enteric inhibitory nerves -> opening the LES
|
distention and vagus
|
|
Does CCK have any control over the LES?
|
yes, able to relax the sphincter
|
|
Achalasia
|
defective enteric inhibitory nerve -> sphincter will not open
|
|
Basic innervation of the stomach.
|
parasympathetic and sympathetic innervation. myenteric NS is prominent, but submucossal plexus is present
|
|
Receptive relaxation
|
relaxation of the orad portion of the stomach to accommodate food from the esophagus
(vagovagal reflex) |
|
Adaptive relaxation
|
distention in the stomach (stretch receptors) triggers vago-vagal reflex (efferents go to inhibitory ENS neurons)
|
|
Feedback relaxation
|
receptors in the small intestine, involves both hormones as well as local reflex
|
|
Propulsion
|
bolus is pushed toward the closed pylorus
|
|
Retropulsion
|
bolus is pushed back into the proximal stomach
|
|
What are Migrating Motor complex (MMC) and when do they occur?
|
MMC are periodic bursts of high-amplitude contractions that sweep the stomach clean. Occur during fasted or interdigestive state
|
|
What are interstitial cells of Cajal
|
maintain a basic electrical rythm, specialized smooth m. cells
|
|
What is the pacemaker current that facilitates slow waves?
|
opening of voltage gated Ca2+ channels -> depolarizing influx of Ca2+ activation of Ca-activated K+ currents
|
|
What is able to affect the frequency of slow waves?
|
temperature and metabolic activity
|
|
Vagal stimulation to the stomach Increases or Decreases contractions.
|
Increases
|
|
3 hormones that increase contractions of the stomach
|
ACh, gastrin, and CCK
|
|
Spike potentials
|
action potential that is able to initiate a contraction with a slow wave.
|
|
What 2 motility patterns are occuring during small intestine fed (digestive) state?
|
mixing (segmentation) and propulsion
|
|
What is occuring in the small intestine 2-3 hours after a meal?
|
few or no contractions but migrating motor complex (MMC) are occuring
|
|
Where does the MMC start and end?
|
start in the stomach and end in the terminal ileum
|
|
How often does a MMC cycle and why?
|
90 minutes (only occur during fasting) because that is how long it take it to travel.
|
|
What is thought to initiate MMC?
|
motilin
|
|
Peristalic Reflex
|
'law of the intestines'
-move the entire length of the small intestine and depends on the enteric NS -not important in healthy individuals |
|
Intestino-intestinal reflex
|
if area of small intestine is grossly distended the rest of the bowl is inhibited
(depends on extrinsic innervation) |
|
Power propulsion
|
long, large contractions in response to noxious stimuli
[vomiting - retrograde direction diarrhea - orthograde direction] |
|
Gastro-ileal reflex
|
relaxation of the ileal-cecal sphincter and contraction of the ileum upon eating or shortly there afterwards
|
|
Potential mediators of the gastro-ileal reflex
|
CCK, gastrin, extrinsic
|
|
Ileal break
|
inhibition of gastric and pancreatic secretions and motility due to lipids and/or carbs infusied in the ileumin amount suffidient to cause malabsorption
|
|
What occurs to haustrations in the colon during a mass movement?
|
they disapear while the colon sweaps it's contencts in the aboral direction
|
|
Gastrocholic reflex
|
food in the stomach -> stretch -> increased motility and mass movement in the LI
(efferent: CCK, gastrin, PNS) |
|
Which 2 GI hormones is still present in the ileum
|
CCK and Secretin
|
|
What stimulates the release of Gastrin?
|
peptides, amino acids, distention, Vagal stimulation
|
|
What stimulates the release of CCK?
|
peptides, amino acids, fatty acids >8C
|
|
What stimulates the release of Secretin?
|
mostly acid and partially fat
|
|
What stimulates the release of GIP?
|
glucose, amino acids, fatty acids
|
|
Where is the salivary nucleus?
|
medulla
|
|
What parasympathetic cranial nerves are involed with salvation?
|
CN VII and IX
|
|
What is the mode of action of parasympathetic stimulation to the saliavary glands?
|
ACH acts on M3 receptors with cause in increase in Ca2+
|
|
Describe sympathetic stimulation to the salivary gland.
|
T1-T3 -> superior cervical ganglion -> NE acts on β receptor and via cAMP second messanger cause in increase in Ca2+
|
|
Both _______ and _______ NT can stimulate exocytosis by salivary acinar cells
|
chalinergic and adrenergic
|
|
The osmolality of saliva is significantly _______ than that of plasma
|
lower
|
|
Is the potassium concentration in saliva greater or less than that of plasma?
|
greater
|
|
What happens to Na+ and Cl- as saliva passes through the duct?
|
they are reabsorbed
|
|
Is saliva Hpotonic or Hypertonic compared to plasma?
|
Hypotonic
|
|
Describe the direct and indirect methods of vasodilation and increased blood flow to salivary glands.
|
direct: PS nerve releases VIP on the vasculature
indirect: cascade that originates from enzyme released secretatory cell |
|
How does the sympathetic NS increase blood flow to the salivary gland?
|
Biphasic: SNS act on α1 to vasoconstrict -> increased vascular-dilator metabolites and increased cellular metabolites cause vasodilation
|
|
2 divisions of the gastric mucosa
|
oxyntic gland area and pyloric gland area
|
|
4 cell types of the oxyntic gland area
|
Parietal, Peptic (Chief), ECL cells, mucous
|
|
Secretion of the Peptic (Chief) cell
|
pepsinogen, gastric lipase
|
|
Secretion of Oxyntic (parietal) cell
|
HCl, IF
|
|
3 cell types of the pyloric gland area
|
G cells, D cells, Mucous
|
|
Secretion of D cells
|
somatostatin
|
|
Alkaline Tide
|
Upon eating the action of the parietal cells is increased causing an increase of bicarb entering the blood -> the blood leaving the gut is more alkaline compared to its arrival
|
|
Where is the H/K pump located within the parietal cell?
|
on the apical membrane (facing the lumen)
|
|
Where is the Cl/HCO3 exchanger in the parietal cell?
|
on the basolateral membrane (toward the interstitial space)
|
|
What is meant by potentiation within the GI?
|
whole is > sum of parts
|
|
3 mechanisms to reduce acid secretion within the stomach
|
1. vagotomy
2. H2 histamine blockers (Zantac, Tagamet) 3. PPI's: proton pump inhibitors |
|
4 main physiological events of the Cephalic phase
|
1. Vagus (ACh) stimulates parietal cell
2. Vagus (ACh) stimulates ECL cell (histamine from ECL cell stimulated parietal cell) 3. Vagus (GRP) stimulates G cell (gastrin goes to ECL cell and parietal cell) 4. Vagus (ACh) inhibits D cells -> somatostain inhibited |
|
Somatostatin like to inhibit both __ ______ and ______ ______.
|
G cells and parietal cells
|
|
What stimulates and inhibits D cell secretion of somatostatin?
|
Lumen H+ will stimulate
vagal input will inhibit |
|
What input from the luminal side will stimulate gastrin secretion?
|
protein products
|
|
_______ and _____ stimulate the release of somatostatin
|
Gastrin and acid
|
|
What is the effect of acid in the duodenum?
|
stimulates secretin, which in turn inhibits both parietal and G cells and stimulates somatostatin release
|
|
What stimulates enterogasterone and what does it do?
|
acid, fat, and hyperosmolar solutions
it inhibits the parietal cell |
|
What do Fatty acids in the duodenum and jejunum cause?
|
stimulate GIP, which inhibits both the G cell and the parietal cell
|
|
2 functions of the mucous layer
|
1. diffusion barrier to H+ and pepsin
2. traps bicarb for future use |
|
2 stimuli for the release of mucous by mucous cells
|
vagal stimulation and chemical stimulation
|
|
Describe the action of H. Pylori
|
gram negative bacteria that lives in the antral mucosa that has urease to use urea to make the environment livable
*inhibits somatostatin secreting D cells |
|
What does H. pylori do to gastrin levels?
|
increase levels
|
|
Where are the receptors for cobalamin-IF complex
|
ileum
|
|
Pernicius anemia
|
destruction of parietal cells that result in B12 deficiency
|
|
What do acinar cells secret?
|
digestive enzyme
|
|
What do ductal and centroacinar cells secret?
|
watery juice that contain Na+ and HCO3-
|
|
acid tide caused by the pancreatic ductal cell
|
an increase in H+ within the blood
|
|
Where is 90% of HCO3- in pancreatic juice derived from?
|
plasma
|
|
What does the rate of HCO3- secretion depend on the availability of ______
|
luminal Cl-
|
|
How does secretin increase the release of bicarb?
|
activating CFTR channel
|
|
What is the electrical gradient of Na+ concerning pancreatic ductal cells
|
Na+ moves from plasma to lumen and water follows
|
|
How does the osmolality of pancreatic secretion compare to plasma
|
it is like it
(it rich in bicarbonate) |
|
3 primary controllers of pancreatic secretions
|
-vagovagal reflex
-secretin -CCK |
|
Pancreatic secretion during Cephalic Phase
|
VAGUS
-stimulate both ductule and acinar cells to secrete |
|
Pancreatic secretion during Gastric Phase
|
distention triggers vagovagal reflex
|
|
Methods for turning off pancreatic secretions
|
-once maximally stimulated, will decrease after a few hours
-peptide YY (PYY) -> stimulated by fat is the distal small intestine -somatostatin -glucagon -pancreatic polypeptide |
|
Components of Bile
|
-bile acids
-cholesterol -phospholipids -HCO3- and H2O -inorganic ions -bile pigments (bilirubin) |
|
Entrohepatic Circulation
|
release of bile acids into the duodenum -> absorption in the jejunum and ileum -> portal blood to the liver -> taken up by hapatocytes and resecreted
|
|
Primary bile acids are dehydroxylated in the intestine to form ______ _____ _____
|
secondary bile acids
|
|
Formation of bile salts
|
conjugation of either primary or seconday bile acids with taurine or glycine
(bile salts are ionized and H2O soluble) |
|
What is the major pathway for elimination of cholesterol from the body?
|
synthesis of bile acids
|
|
Function of micelle
|
-tuck lipid digestion into their interior
-deliver to unstirred water layer at the epithelial cell -enable product absorption |
|
________ and _________ bile acids can be absorbed passively all along intestine
|
deconjugation and dehydroxylation
|
|
_____ ______ bile acids (mostly conjugated) are absorbed by active transport at the terminal ileum
|
more hydrophilic
|
|
Rate of SYNTHESIS of new bile acids is _________ related to the return of bile acids by the portal circulation.
|
inversely
|
|
Rate of SECRETION is _______ related to the return of bile acids by the portal circulation
|
directly
|
|
Which electrolytes are secreted in the duct from the liver to the GB?
|
HCO3-, Na+, Cl-, H2O
(last 3 able to be secreted or absorbed) |
|
Stimulatory hormones for the secretion of electrolytes in the duct between the liver and gallbladder
|
Secretion (major), VIP, glucagons
|
|
2 stimuli for the opeing of sphincter of Oddi and GB contraction
|
PNS and CCK
|
|
3 levels of amplification at the small intestine
|
1. folds of Kerkring
2. microscopic villi and cryps of Lieberkuhn 3. submicroscopic microvilli |
|
What are carbohydrates broken down into?
|
monosaccharides
|
|
What are fats broken down into?
|
free fatty acids and 2-monoglyceride
|
|
What are proteins broken down into?
|
small peptides and amino acids
|
|
3 locations for digestion
|
1. lumen or cavity digestion
2. membrane digestion 3. intracellular digestion |
|
Products of amylase digestion
|
Maltose, Maltotriose, alpha-limit dextrans
|
|
Monosaccharide products that are finally absorbed
|
glucose, galactose, fructose
|
|
What carrier is responsible for glucose and galactose uptake into enterocyte?
|
SGLT1
(secondary active transport process) |
|
What is the carrier responsible for fructose uptake into the enterocyte?
|
GLUT 5
(facilitated diffusion) |
|
What transporter is located on the basilar membrane of the enterocyte?
|
GLUT 2
(all 3 monosaccharides compete for transporter) (facilitated diffusion) |
|
What enzymes are needed for protein digestion in the lumen and what does digestion yeild?
|
enzyme: gastric and pancreatic proteases
yeild: amino acids and oligopeptides |
|
Where does protein digestion begin?
|
Stomach with pepsin
|
|
5 processes in lipid assimilation
|
1. secretion of bile and various lipases
2. emulsification 3. enzymatic hydrolysis of ester linkages 4. solubilization of lipolytic products with bile salt micelles 5. transportation into and out of the enterocyte |
|
4 lipases of the digestive tract
|
1. food-bearing lipase
2. lingual lipase 3. gastric lipase 4. pancreatic lipase |
|
What hormone is released in response to fat and what does this hormone do to the sphincter of Oddi?
|
CCK
-opens the sphincter of Oddi |
|
What hormone is released in response to acid and how does this hormone affect ductal cells?
|
Secretin
-causes secretion of bicarb and fluid from ductal cells |
|
What do the pancreatic acinar cells release and what stimulates them?
|
release: enzymes
stimulation: ACh, CCK |
|
What do pancreatic centroacinar and ductal cells release and what are they stimulated by?
|
release: bicarb
stimulation: secretin (potentiated by: CCK and ACh) |
|
Zollinger-Ellison Syndrome
|
-gastric acid hypersecretion
-pH of duodenal contents is lowered (more acidic) -> lipase can not function or will be denatured |
|
Whipple's Disease
|
associated with malabsorption of fat concerning lymphatic transport
|
|
__-__ L water enter the small intestine
____ ml enter the colon ____ ml excreted |
7 to 10 L
600 100 |
|
In the intestines there is a net absorption of ___, ___, and ____ and a net secretion of ___ and _____
|
absorption: Na+, Cl- and water
secretion: K+ and bicarb |
|
What are the 2 major mechanisms of Na+ reabsorption
|
1. countertransport with H+
2. co-transport with solutes (sugars and AA) |
|
Which 2 GI hormones is still present in the ileum
|
CCK and Secretin
|
|
What stimulates the release of Gastrin?
|
peptides, amino acids, distention, Vagal stimulation
|
|
What stimulates the release of CCK?
|
peptides, amino acids, fatty acids >8C
|
|
What stimulates the release of Secretin?
|
mostly acid and partially fat
|
|
What stimulates the release of GIP?
|
glucose, amino acids, fatty acids
|
|
Where does the Na/H, Cl/HCO3 counter transporter appear?
|
in the ileum with increasing numbers in the distal ileum and into the colon
|
|
In the small intestine, there is a net ________ of K+; in the colon there is a net _______ of K+
|
absorption
secretion |
|
Major function of the colon?
|
absorption of Na+ Cl-
(some absorption/secretion of KCl) |
|
What do mineralocorticoids (aldosterone) control in the colon?
|
Na+ absorption; K+ secretion
|
|
Where is the intestines is the basolateral membrane permeable to K
|
only in the colon
|
|
Increased flow rate (as in diarrhea) increases K+ _______ into the colon
|
secretion
-K+ has a flow rate dependence |
|
How does VIP, cholera toxin, and serotonin affect secretion of K+?
|
increase secretion
-VIP and cholera toxin -> inc. cAMP -serotonon -> inc. Ca2+ |
|
What causes the high HCO3- and alkaline pH of stool water?
|
Cl-/HCO3- exchanger
(chloride in, bicarb out of cell and into lumen) |
|
What causes hypokalemic metabolic acidosis
|
prolonged diarrhea
(secretion of K+ and exchange of Cl-/HCO3- in the colon) |
|
Describe the mechanism of action of the oral rehydration therapy
|
-utilized the co-transport of Na+ with solutes (sugar and AA)
-increase concentration of glucose or AA in the intestinal lumen -> enhance absorption of water |
|
What form must iron be in to be absorbed?
|
ferrous state (Fe2+)
-use DMT-1 as transporter |
|
Hormones derived from Amino acids
|
thyroid hormone, peptide hormones, protein hormones
|
|
Hormones derived from fatty acids
|
prostaglandins, thromboxanes, leukotrienes
|
|
Hormones derived from cholesterol
|
steroids, vitamin D
|
|
Hormones that activate intracellular (nuclear) receptors?
|
steroid, thyroid hormones, vitamin D
|
|
Hormones that activate plasma membrane receptors
|
amino acid derived, fatty acid derived, steroid
|
|
Mechanisms of hormone secretion
|
-feedback loops (+/-)
-metabolic, osmotic, mechanical factors |
|
List the classic endocrine organs
|
hypothalamus, pituitary gland, pineal gland, parathyroid gland, thyroid gland, adrenal, pancreas, placenta
|
|
Solinocrine
|
hormonal communication
-messenger molecule secreted into lumen of ductal system |
|
Juxtacrine
|
hormonal communication
-messenger molecule remain associated with cell membrane of signaling cell and interacts with receptor on adjacent cell |
|
Hormones from amino acid derivatives
|
-dopamine, epinephrine, serotonin, thyroxin (T4), triodothyronin (T3)
|
|
Hormone of peptide/polypeptide derivative
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ACTH, atrial nariuretic peptide (ANP), vasopressin, calcitonin, CCK, growth hormone, inhibin, insulin, parathyroid hormone, somatostatin, THS, VIP
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Hormones of steroid derivative
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cortisol, aldosterone, esterdiol, progesterone, testerone
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Hormones of fatty acid derivatives
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prostoglandins, thromboxanes
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