Chapter 5: Thirst, Hunger, Elimination Flashcards
Extracellular Thirst
Accounts for 1/3 of total water in body
Water outside cells (in blood, CSF, body cavities)
Induced by perspiration, blood loss, diarrhea, heavy menstrual bleeding
Blood volume and blood pressure decrease
Requires replacement of electrolytes and water
Extracellular Thirst Mechanisms
Drop in blood pressure lead to…
Leads to activation of baroreceptors (blood pressure receptors) in kidneys
Activation of baroreceptors triggers release of renin from kidneys
Renin is an enzyme that produces angiotensin in blood
Angiotensin causes vasoconstriction
Angiotensin causes hypothalamus and pituitary to increase production of vasopressin (anti-diuretic hormone –prevents urination)
Angiotensin causes adrenal gland to release aldosterone from adrenal cortex
Aldosterone causes kidneys to increase sodium reabsorption
Vasopressin causes kidneys to increase water reabsorption
How does angiotensin stimulate production of vasopressin
Subfornical Organ
• Located outside BBB
• Contains osmoreceptors and also responds to angiotensin
• Neurons in subfornical organ project to hypothalamus
Cellular Thirst
Accounts for 2/3 of total water in body
Water inside cells
Induced by excess salt consumption or severe thirst (dehydration)
Excess salt consumption or severe thirst leads to increased extracellular sodium
Osmotic force draws water out of cells (cell shrinks)
Extracellular thirst will occur before cellular
Concentrated saline (salt) applied around third ventricle …
induces drinking
Distilled water applied around third ventricle …
causes drinking cessation
Feeding (Absorptive) Phase
Insulin release from pancreas
Glucose from blood moves into cells, glucose–>glycogen
Energy stored
Parasympathetic
Fasting (Utilization) Phase
Glucagon release from pancreas
Glycogen stores from cells metabolized to glucose and released into blood
Liberates stored energy
Sympathetic
Ghrelin
- Secreted by epithelial cells lining empty stomach, as well as intestines and pancreas
- Ghrelin levels in blood rise during fasting
- Signals hunger & stimulates feeding
- Inhibits vagus nerve (signals parasympathetic system)
- Crosses BBB via transport system (get into hypothalamus)
Cholecystokinin (CCK)
- Released when food reaches the intestines (duodenum)
- Stimulates digestion of fat and protein
- Injecting CCK reduces feeding and food seeking behaviour
- Receptors in many areas, influence on hypothalamus directly and through vagus nerve
- Receptors in many areas of brain stimulate vagus nerve
Orexin
- Produced in the Lateral Hypothalamus
- Causes craving of food
- Increases meal size by suppressing inhibitory feedback
Neuropeptide Y (NPY)
- NPY neurons found in arcuate nucleus of hypothalamus
- NPY active during hunger
- NPY less active in well-fed state
- Stimulates hunger
- Injecting NPY into hypothalamus of rats leads to ravenous and frantic eating behaviours
- Obesity can be associated with excessive NPY
- Chronic stress and a high fat, high sugar diet are associated with excess NPY in studies of mice and monkeys
Leptin
- Secreted by adipose tissue
- Decreases food intake
- Increases metabolism
- Involved in long-term regulation of body weight and fat stores
- Does not necessarily have immediate effects on hunger and satiety
Lesion the ventromedial hypothalamus (VMH)
Hyperphagia (overeating)
Therefore, Natural role of VMH is to inhibit/reduce feeding
Lesion the lateral hypothalamus (LH)
Aphagia (failure to eat/drink)
Therefore, Natural role of LH is to stimulate/promote eating behaviour