regulating BP lect1

• • CO = HR x SV
  • BP = CO x TPR
  • Total peripheral resistance = resistance blood encounters as it passes through the circulation
  • when you think TPR:
  • think arterioles
  • think change in arteriole calibre - vasoconstriction or vasodilation
• Arterioles

  • aka resistance vessels
  • smooth muscle walls capable of vasoconstriction or vasodilation
  • innervated by sympathetic nervous system
  • also responsive to hormones and chemical factors
  • response 1 = vasoconstriction -> increase TPR -> increase resistance to flow
  • e.g. excitation of SNS, catecholamines (NE), angiotensin II
  • response 2 = vasodilation -> decrease TPR -> decrease resistance to flow
  • e.g. o2 lack, increase hydrogen ions, increase co2 (exercise), atrial naturetic factor, nitric oxide, inhibition of SNS etc
• Vasomotor Centre (VMC):

  • VMC is a collection of neurones in medulla, governing degree of contraction/relaxation of smooth muscle of primarily veins and arterioles
  • it also communicates with the cardioinhibitory and cardioexcitatory centres, which also sit in the medulla
  • only has one type of output - this is a sympathetic output to arterioles

  
• • normally arterioles are held in a mild degree of vasoconstriction (called vasomotor tone) by a low frequency of action potentials coming from the vasomotor centre via the sympathetic nervous system
  • altering frequency of action potentials, baseline vasomotor tone can either by increased (causing vasoconstriction) or decreased (causing vasodilation)
  • this will then increase/decrease resistance to blood flow -> increase/decrease TPR -> increase/decrease BP

  
• • veins have nothing to do with TPR
  • veins play a role in BP, as venoconstriction/venodilation of veins affect venous return, therefore pre-load, therefore SV, therefore determine CO - and BP = CO x TPR
• VMC & veins (capacitance vessels):

  • VMC controls sympathetic input to veins
  • increase VMC activity/action potentials
  • causes venoconstriction
  • increase venous return
  • increase SV -> increase CO
  • decrease VMC activity/action potentials
  • causes venodilation
  • decrease venous return
  • decrease SV -> decrease CO