Inhibits Gastric Secretions From Gastrin Cells Secondary

Sympathetic Stimuli: Decrease motor activity • Inhibits GI activity via direct effects on SM and inhibitory effects on neurons of ENS • T5-L2 Preganglionic Fibers ○ Pre-ganglionic fibers enter sympathetic chain to postganglionic neurons in the celiac, mesenteric ganglia ○ Mostly post-ganglionic to the gut Parasympathetic Activity: Increase Motor Activity • Preganglionic to the gut: • Cranial Divison: Vagus (Esophaguslarge intestine) • Sacral Division: Pelvic Nerves (sigmoidalanal regions) • Post-ganglionic neurons: • In myenteric and submucosal plexuses Enteric Nervous System: • Afferent sensory nerve fibers entirely within ENS: ○ Cell bodies in ENSaxons terminate in prevertebral sympathetic ganglia (celiac, mesenteric, hypogastric)gut ○ Cell bodies in dorsal root ganglia or cord or in CN gangliamedullaGI via vagus • Stimulated by: ○ 1)mucosal irritation ○ 2)gut distention ○ 3)Chemical presences • Submucoal Plexus (Meissner) ○ Secretion, absorption, contraction • Myenteric Plexus (Auerback’s) ○ Increases Tonic Contractions, rhythmic contractions, conduction velocity ○ VIP- inhibits sphincter tone (pyloric/ileocecal valve) Depolarization Stimuli: Stretch, Achetylcholine, PNS, gastrin, motilin Hyperpolarizing Stimuli: Norepinephrine, Epinephrine, SNS, Secretin, CCK Inhibitory Substances: VIP ↑cAMP, NO↑cGMP, Sympathetic Stimulation Reflexes within ENS: secretion, peristalsis, mixing, contractions, local inhibition Reflexes from gut Prevertebral sympathetic Ganglia GI 1) Gastrocolic Reflex (evacuation of Colon w/ stomach filling) 2) Enterogastric reflex (stomach motility/secretion inhibited w/ intestinal filling) 3) Colonoileal Reflex (inhibition of ileal motility w/ colon filling 4) Intestinointestinal- distention of one portion of the intestinedecreased contractions caudad of the bolus 5) Gastroileal- stomach activityileocecal relaxation- empty small intestine to process next meal Reflexes from gutSC/Brainstem GI tract

1) Stomach/duodenum to brain and back (Vagus)-control gastric motility/secretion 2) Pain reflexes (inhibition of GI motility) 3) Defactation reflexes afferent signals via SC (distention of colon, rectum causing reflex contractions of these organs and abdomen Vasovagal: vagal sensory nerves relay stretch information to brainstem releasing vagal efferents to cells (parietal/Gcells in stomach) • Example: eat fooddistends stomachbrainstemreduces in wall tone in stomach to keep pressure in stomach low Splanchnic Circulation: GI Blood Flow: Reticuloendothelialcells to clean blood of bacteria, Nonfat water soluble nutrients absorbed in gut Fat based nutrients absorbed into intestinal lymphatics and are taken to blood via thoracic duct, bypassing liver GUT, Spleen, Pancreas, LiverPortal VeinLiver SinusoidsHeptatic VeinVena Cava Vasoconstrictors: Ang II, Endothelin, NE (alpha2 agonists), PGF, Vasopressin Vasoodialators- Ach, Adenosine, Bradykinin, CGRP, histamine, NO, VIP, B2 Agonist, cck, vip, gastrin, secretin Postprandial Hyperemia- blood flow increases to response to a meal Dilators: CCK, VIP, gastrin, Secretin GI glands: kallidin, bradykinin Ingestion of Food: 1) Voluntary Phase- initiates swallowing 2) Pharyngeal Stage – involuntary passage of food thru pharynx Esophagus 3) Esophageal Peristalsis –involuntary phase transports food pharynxstomach a. Primary peristalsis- continuation of the wave from the pharynx b. Secondary peristalsis: If not completely emptied, stretch initiates secondary peristalsis Factors that increase intestinal motility: Gastrin, CCK, insulin, serotonin Factors that decrease gastric motility: secretin, CCK, glucagon, GIP, VIP Hormone Cholecystokini n

Stimulus for secretion Fats, FA, Monoglycerides , small peptides and Amino Acids

From

Action

ICells Duodenum/Jej un

↑Gallbladder contraction and relaxation of sphincter (oddi) tone ↑pancreatic enxyme and HCO3secretion (via + acinar cells) ↓Stomach

Block gastrin, increase motility

Motility (↑p. Sphincter tone) Relaxes orad part of stomach so it can receive food ↑Intestinal motility Hyperpolarizin g stimuli + bile release from gallbladder Gastrin

Stretch/Meat Vagus (via GRP) Inhibited by H+ in stomach (via stimulation of somatostatin release) (not fats)

Stomach G cells Pyloric Glands

Gastric Inhibitory Peptide

FA, AA, CHO, oral glucose

Mucosa In duodenum and jejunum

Enterogastron e

Hypertonicity/li pids

Duodenum

Inceases Acid Secretion (parietal cells), enhance stomach motility, enhances pyloric pump ↑Intestinal morility Depolarizing stimulus ↑ LES tone, ↓Pyloric tone Slow emptying to small intestine (stomach inhibition) (↑Sphincter tone) Inhibit intestinal motility ↑insulin secretion ↓gastric H+ secretion Inhibit Stomach Emptying into

Similar to CCK

Secretin

Acid FA in duodenum

SCells Duodenal Mucosa

duodenum (↑Sphincter tone) Inhibits GI motility (↑Sphincter tone) Inhibit intestinal motility Increase pancreatic ductal HCO3 secretion Increase biliary HCO3 secretion + bile secretion Hyperpolarizin g stimuli ↑Intestinal motility Inhibit intestinal motility

Insulin VIP

Motilin

Serotonin

Empty stomach/ 90min

Duodenum

Absence of VIP causes achalasia and megaesophag us

Inhibit stomach motility Inhibits hastric H+ and stimulates HCO3secretion Relaxation of smooth muscle Analogous to secretin Waves of Prevent activity bacteria through the overgrowth stomach 90min Depolarizing stimuli ↑Intestinal

Glucagon Pepsin

Acid, or gastric ACH

Intrinsic Factor

Acid

Somatostatin

Secreted by cells throughout GI tract

Histamine

Enterochromaff in cells

Stomach Mucous neck cells and peptic/chief cells Parietal Cells High H+ in lumen Its secretions are inhibited by vagal simulations

Ach

Gland Type Mucus Glands Crypts of Lieberkuh n Oxyntic Glands

motility ↑ H+ production Inhibit intestinal motility Breaks down protein/ Collagen B12 absorption

Prevents percicious anemia

Inhibits release of all GI hormones Inhibits H+ secretions Activate gastric secretion of H+ (patietal cells) + gastric secretion of H+, pepsinogen, and mucus (all 3 stomach cell types) Stimulates pancreatic acini, (not ducts) to produce enzymes + bile release

Cells

Responds To

Sucretes

Location

Goblet Cells

Mechanical Stimuli

Mucus

All over

Mucous Neck: mucous + pepsinogen

Proxmal 80% of stomach

Mucous Neck, Peptic (chief) cells, Parietal

(oxyntic) cells

Pyloric Gland Tubular Glands

Mucus cells Few peptic Few parietal 1)Oxytinic/Pari etal Cells

Oxyntic Glands Complex Gland

2)Peptic/Chief Cells Saliva

1)Simple Mucous glands 2)Compou nd mucus glands Surface Mucus Glands

Goblet Cells

Goblet?

Mechanical stimuli Ach/ Protiens Gastrin Enterochomaffin Histamineparietal HCL 1) taste and tactile 2) CNS- smells 3) Reflex from stomach/duodenum

Chief: Pepsinogen Parietal: hcl and IF Pepsinogen, lots of mucus, and gastrin 1)Acid HCL Intrinsic Factor 2)Pepsinogen Mucus Gastrin Primary(Acini) : NaCl, Ptyalin (alpha amylase), Mucus, ECF Secondary(Du cts): ↑K+ HCO3-

lining

Distal 20% of stomach lining Stomach/up per dudenum

Outside of GI tract (Salivary, Pancreatic, Hepatic)

Esophageal Secretion

Stretch/Ach

Viscous, Very alkaline Mucus

Stomach

Regulation of Gastric Sucretions: Ach, Gastrin, Histamine Feedback of Gastric Sucretion: -Low ph, inhibits gastric secretions from gastrin cells secondary to release of somatostatin from Dcells -Inhibitory nervous reflexes inhibit gastric secretion through inhibition of GRP release