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REVIEW: hypovolemia

REVIEW: hypovolemia. A Decrease in Blood Pressure:. Heart baroreceptors cause posterior pituitary to secrete VP VP increases vasoconstriction VP increases water pores in the collecting duct, increasing water absorbtion from filtrate Cells in glomerulus secrete renin  angiotensin II

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REVIEW: hypovolemia

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  1. REVIEW: hypovolemia A Decrease in Blood Pressure: • Heart baroreceptors cause posterior pituitary to secrete VP • VP increases vasoconstriction • VP increases water pores in the collecting duct, increasing water absorbtion from filtrate • Cells in glomerulus secrete renin •  angiotensin II • Increases aldosterone • Increases vasoconstriction • Increases VP • Stimulates drinking •  aldosterone • Increase sodium retention

  2. What about an increase in blood pressure? • Baroreceptors in heart stop sending releasing signals to SON and PVN • Glomerulosa cells produce less renin • Under conditions of excessively high blood pressure: • The atria of the heart secrete Atrial Natriuretic Peptide (ANP) • ANP: • Shuts down secretion of VP, renin, and ALDO • Increases sodium excretion in the urine • Increases diuresis (water loss in urine)

  3. Osmotic Imbalance Review High blood osmolality causes: • Osmoreceptors in the brain to signal SON and PVN nuclei to increase VP secretion • VP increases water retention in the kidney • Glomerular cells decrease secretion of Renin • Decrease Aldosterone secretion • Decrease Angiotensin II levels

  4. INSULIN • Regulation of Secretion • Hyperglycemia stimulates release • Glucose sensors in  cells • Gastric Inhibitory Peptide • Released from cells of the small intestine • Potent stimulator of insulin secretion • Somatostatin: inhibits insulin release (paracrine) • Autonomic nervous system • Parasympathetic activation increases insulin release • Sympathetic activation blocks insulin release • Epinephrine (from adrenal) blocks insulin release

  5. INSULIN • Action at Target Tissues • Activation of insulin receptor: • Increases transport of glucose, amino acids, and fatty acids into cells Glucose transporter:

  6. Type 1 DiabetesInsulin Dependent: IDDM • Possibly results from autoimmune reaction • The body’s immune system attacks the  cells • Pancreatic  markedly reduced • Symptoms only appear after ~80% loss of cells • No insulin……physiological repercussions? • Treatment • Insulin injections • Recent methods

  7. Type 2 Diabetes:Non-Insulin Dependent: NIDDM • Accounts for 90-95% of all Diabetes cases • Usually occurs in overweight individuals over 40 years of age • But ages are getting younger and younger • Associated with abdominal fat in women • Target cells become resistant to insulin • insulin receptor • Fewer receptors • Receptors have lower affinity • Receptor blocked (possibly by antibody) • Post-receptor mechanisms

  8. Diabetes Prevelence in US % Incidence of diagnosed diabetes 1980 1990 2000 2007

  9. 2004 % of adults >20 2007

  10. Type 2 Risks 2006 • 7th leading cause of death • With Type 2 diabetes • 2 to 4-fold increase in heart disease related death • 2-fold risk of death • Type 2 associated complications • 2-4 fold risk of stroke • 75% of adults with Type 2 have high blood pressure • leading cause of blindness in adults aged 20-74 • Leading cause of kidney failure

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