Physio L37- Cardiovascular Regulation- Hypertension

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Physio L37- Cardiovascular Regulation- Hypertension
2013-11-25 22:35:52
MSU Physio
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  1. Local Control
    • non-neural factors
    • Decrease P-> decrease flow-> homeostatic tissue response- increased flow
    • Autoregulation- each organ controls local blood flow
  2. Metabolic Vasodilators
    • Active tissues produce vasodilators
    • ATP use-> increases adenosine production
    • Adenosine is a strong vasodilator- active hyperemia
  3. Endothelial Factors
    • Pancreas
    • Released from endothelium, affect VSM (vascular smooth muscle)
    • Two examples: Nitric oxide and enothelin
  4. Nitric Oxide
    • Peptide- constricts VSM
    • Decreased flow-> increased BP
    • Stimulates of E increase gene activity that makes E (energy)
    • (released slow: goes through protein synthesis I)
  5. Endothelin
    • Hormones/ neural activation
    • Increased NO-> releases VSM-> increased blood flow
    • Manufactured all the time (released fast)
  6. Basoreceptors
    • Stretch receptors in carotid sinus and aortic arch
    • Changes in BP alter baroreceptor activity
    • Monitor your person BP (normal 120/80)
  7. Input to Medulla
    Baroreceptors send neurons in brainstem
  8. Control of Vasoconstriction/ Dilation
    • Cardiovascular control center (CCC) is in medulla
    • CCC controls symp and parasymp output
    • Homeostatic, short term control of blood pressure
    • symp: decrease in blood pressure- decreases baroreceptor input-> increases symp output-> increases BP (heart + VSM)
    • para: increase BP- increase baroreceptor input-> parasymp output-> decrease in BP (lower HR)
  9. Resetting
    • Body adjusts to own "normal" BP
    • Adaptation to prolonged BP change occurs over days
  10. Hypertension
    • Chronic elevated BP
    • Multiple causes- several small changes cause large increase in BP
  11. Cardiac Effects
    • Hypertrophy against increased load (diastolic pressure)
    • Increased oxygen use- heart attack when coronaries constrict
    • With age, increase systolic pressure, increase in stroke risk
  12. Essential Hypertension (90%)
    • Cause unknown, treat symptoms
    • Effective- reduces pathology
  13. Renal Hypertension (10%)
    • Also called secondary hypertension
    • Decreases blood flow to kidneys cause increase in kidney renin release
    • Renin converts angiotensinogen to angiotensin I (Ag-I)
    • Angiotensin converting enzyme (ACE) in lung capillaries converts A-I to A-II
    • A-II increases BP; is a strong vasoconstrictor and causes aldosterone release from adrenal cortex
    • Aldosterone increases Na+ reabsorption and H2O reabsorption by kidneys, more volume
  14. In Pregnancy
    • Placental factor causes vasoconstriction
    • Pre-eclampsia in hypertension during pregnancy
    • Magnesium sulfate treatment lowers BP (and decreases premature contractions...Brackston Hicks)
  15. Drug Treatments
    • Often used in combination
    • Varying side effects
  16. Diuretics
    • Increases Na+ excretion, lowers blood volume, decreases BP
    • (work in kidney tubules)
    • (ex: coffee)
  17. 1. ACE Inhibitors
    Block conversion of A-I to A-II (protease on kidneys)
  18. 3. Alpha-Adrenergic Receptor Blockers
    • Stops symp constriction of VSM, blocks NE effects
    • Fewer Ca+2 channels open, less Ca+2 entry, less force
  19. 2. Beta- Adrenergic Receptor Blockers
    • Blocks NE/ EPI effects on heart- less Ca+2 (to be enhanced effect- negative ->->prevent heart by pumping faster, ex: excessive exercise, hunt prey) entry
    • Decreases forces of cardiac contractions
  20. 4. Calcium Channel Blockers
    Decreases VSM contraction, blocks tone (more significant high BP)
  21. Shock
    • Very low blood pressure- loss of blood, toxic vasodilation
    • Reversible shock- can reverse from
    • Epi increases BP- side effects significant
    • Irreversible shock- multiple organ failure due to low BP...Death results