Internal Regulation

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homeostasis

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process that maintains various physiological states within a fixed range

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set point

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a specific value of an internal state that the body defends

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set point can be compared to a

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thermostat setting

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flow of set point

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air temp-->temp. sensor-->compare with thermostat setting -->heat a/c

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body water content

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between 45%-70% of the body is water (varies across individuals) individuals with more fat have less water

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distribution of body water

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1/3 extracellular; 2/3 intracellular

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in osmosis water moves

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across cell membrane from an area of low solute concentration to an area of high solute concentration

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osmosis

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occurs until the concentration of dissolved particles in the intracellular and extracellular fluid are equal

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the intracellular and extracellular particles are referred to as

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osmolarity

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what is the normal concentration of dissolved particles in the intracellular and extracellular fluids

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~300 mM

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isotonic

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300 mM, normal concentration of solute in extracellular and intracellular fluid

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hypotonic

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<300 mM, less than normal concentration of solute in extracellular and intracellular fluid

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hypertonic

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>300 mM, greater than normal concentration of solute in extracellular and intracellular fluid

Front 14

ingestion of water: ECF volume and ICF volume?

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ECF increase ICF increase

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Hypertonic NaCl: ECF volume and ICF volume?

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ECF increase ICF decrease

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hemorrhage ECF volume and ICF volume?

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ECF decrease ICF no change

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IV isotonic NaCl ECF volume and ICF volume?

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ECF increase ICF no change

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water deprivation ECF volume and ICF volume?

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ECF decrease ICF decrease

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two mechanisms for thirst

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osmotic thirst, hypovolemic thirst

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osmotic thirst is caused

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when solute concentration in ECF increases

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when ECF increases (causing osmotic thirst)

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the ICF volume decreases causing cells to shrink

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during osmotic thirst, osmoreceptor neurons

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especially in the organum vaculosum of the laminae terminalis (OVLT), respond

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osmoreceptors in the OVLT stimulate neurons in the

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paraventricular nucleus (PVN) and the supraoptic nucleus (SON) to release vasopressin (also known as antidiuretic hormone (ADH)) in the circulation of the posterior pituitary

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in osmotic thirst, circuits controlling drinking behavior are

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stimulated and ADH causes kidneys to reabsorb water

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Hypovolemic thirst is caused by

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loss of both solutes and water from ECF

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hypovolemic thirst causes

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blood pressure to drop

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blood pressure change is sensed by

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baroreceptors in several parts of the body; kidney, aorta, heart

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change in [Na+] is sensed in

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the kidney

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baroreceptors in the heart and aorta

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send input to the brain through glossopharyngeal and vagus nerves

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hypovolemic thirst flow chart

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memorize

Front 31

stimulus for osmotic thirst

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high solute concentration outside cells causes loss of water from cells

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osmotic thirst is best relieved by

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drinking water

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receptor location for osmotic thirst

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OVLT, a brain area adjoining the third ventricle

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hormone influence for osmotic thirst

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accompanied by vasopressin secretion to conserve water

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stimulus for hypovolemic thirst

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low blood volume

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hypovolemic thirst is best relieved by

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water containing solutes

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receptor location for hypovolemic thirst

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1. receptors measuring blood pressure in the veins 2. subfornical organ, a brain area adjoining the third ventricle

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hormone influences of hypovolemic thirst

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increased by angiontensin II

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most mammals eat in discrete bouts called

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meals

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oral factors

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the taste, smell, texture, and temp of the food can promote or discourage feeding

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oral factors include

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sham feeding and sensory specific satiety

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sham feeding

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the food, after being eaten, does not enter the stomach, but issues from a gastric fistula, the chewing and swallowing of food causes an abundant secretion of gastric juices

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the stomach; excitatory

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grehlin is an orexigenic hormone that is released by a subset of cells lining the stomach. Its circulating blood levels increase with fasting and decrease after a meal

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the stomach; inhibitory

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gastric filling stretched the stomach and activates sensory receptors in the stomach wall and these signals are transmitted to the brain through two routes: vagus nerve and splanphic nerves (spinal)

Front 45

what are intestinal factors?

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the intestines appear to be sensitive to stretch and has chemoreceptors as well. it transmits these signals through the vagus and splanchnic nerves; cck

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cholecystokinin (CCK) is a

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hormone released by duodenal cells that close the pyloric sphincter between the stomach and the intestines and stimulates receptors on the vagus nerve

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CCK does not

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cross blood-brain barrier, but some brain neurons responsive to neural signals from the intestines release CCK. Thus, brain CCK seems to be involved in the regulation of food intake just like intestinal CCK is.

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Postabsorbtive factors are

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fast and complex carbs are broken down into fatty acids and simple monosaccharides in the gut and then are absorbed through the wall of the intestines into the circulation where they can contact a variety of tissues and endocrine glands

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examples of postabsorptive factors

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liver (glycogenolysis, glycogenesis), pancreas (glucagon, insulin), adipocytes (leptin)

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what is leptin

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an anorexigenic hormone released by adipose tissue in proportion to fat mass.

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insulin flowchart

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memorize

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glucagon flowchart

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memorize

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central feeding circuits are based on

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lesion data (early views)

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central feeding circuits include

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ventromedial hypothalamus (VMH)="satiety center"
lateral hypothalamus (LH)="hunger center"

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central feeding circuits flowchart

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memorize

Front 56

lateral hypothalamus lesions cause

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sensory-motor neglect and some of the feeding and drinking deficits might be secondary

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damage to the dopaminergic systems systems

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sending fiber tracts that course through the LH can cause similar effects (however, fiber-sparing lesions of cells bodies are also effective)

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LH lesions cause a decrease in

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insulin. thus, some of the weight loss may be secondary to this hormonal effect.

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Ventromedial hypothalmic lesions cause

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metabolic disturbances including increases in circulating insulin. in fact, VMHX rats will still gain weight even if their food intake is restricted.

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damage to VMH must be large

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usually including areas surrounding the VMH, to produce consist effects

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damage to fiber tracts passing through the area,

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such as the ventral noradrenergic bundle, can also lead to the effects on feeding and weight gain

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rats with VMH lesions will not

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overeat all food. They eat less of unpalatable foods than control animals do. Thus, it is not as thought VMHX rats are "so they will eat anything"

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how is the preoptic area of the hypothalamus effected by lesions

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deficit in physiological mechanisms of temperature regulation

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how is the lateral preoptic area of the hypothalamus effected by lesions

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deficit in osmotic thirst due partly to damage to cells and partly to interruption of passing axons

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how is the lateral hypothalamus area of the hypothalamus effected by lesions

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undereating, weight loss, low insulin level (bc of damage to cell bodies); underarousal, underresponsiveness (because of damage to passing axons)

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how is the ventromedial hypothalamus area of the hypothalamus effected by lesions

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increased meal frequency, weight gain, high insulin level

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how is the paraventricular nucleus area of the hypothalamus effected by lesions

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increased meal size, especially increased carb intake during the first meal of the active period of the day

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hypothalmic involvement in feeding: despite the caeats associated with the early oversimplified views of the LH and VMH, it is clear that these and other areas of the hypothalamus (PVN, arcuate nucleus) play a

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significant role in feeding and energy regulation

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there are a variety of neuropeptides and neuropeptide receptors found in

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neurons of the hypothalamus that are known to be involved in increasing or decreasing feeding

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HORMONAL/NEUROPEPTIDE
INFLUENCES ON CELLS IN THE ARCUATE
NUCLEUS AND PARAVENTRICULAR

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memorize chart