Pharmacology of HTN 2

• Where are B1 receptors?

  Heart (increases rate & force of contraction)

  Juxtaglomerular apparatus of kidney (renin secretion)
• What activates B1 receptors?

  Noradrenaline
• Where are B2 receptors?

  Lungs (bronchodilation)

  Smooth muscle (vasodilation)
• What binds to B2 receptors?

  Adrenaline
• Where are B3 receptors?

  Adipocytes (lipolysis)
• Beta receptor blocking depends on adrenaline & noradrenaline.
• What are the physiological hypotheses for beta blockers in HTN?

  Decreases CO

  Decreases peripheral vascular resistance

  Change in baroreceptor sensitivity

  Decrease renin secretion

  Decrease sympathetic outflow to CNS

  -> Response to beta blockers is likely to be multifactorial
• Why should beta blockers be avoided in cocaine-induced HTN?

  Cocaine -> increase release of adrenaline -> increase action on alpha (vasoconstriction), b1 (increase HR) and b2 (vasodilation)

  If you then give a beta blocker, you will leave the action of alpha receptors 'unopposed', which means it removes the effects of the b2 receptors (vasodilation) -> worsens HTN
• What is the effect of adrenaline on BP?

  Increase (increases HR & decrease TPR)
• What is the effect of noradrenaline on BP?

  Increase (by vasoconstriction, with reflex bradycardia)
• What is the effect on isoprenaline on BP?

  Decrease (vasodilator)