10. Hypertension

• primary hypertension has no identifiable cause while secondary hypertension is associated with a specific disease like renal disease
• primary hypertension may be due to sodium retention leading to increase in blood pressure

  • increases cardiac output
• primary hypertension associated with vasoconstriction and increased wall thickness

  • increases total peripheral resistance
• ace inhibitors treat hypertension by blocking angiotensin II production, leading to vasodilation, decreased aldosterone (less water retention) and increased bradykinin
• calcium channel blockers:

  • dihydropyridines (DHPs) bind to L type calcium channels when inactivated, while non DHPs bind when open
  • means DHPs are more selective to vascular smooth muscle as this has increased inactivated channels at rest
  • leads to decreased calcium influx, decreasing resistance and arterial blood pressure
• calcium channel blockers side effects = headache, flushing and ankle oedema
• thiazide diuretics are used to treat hypertension

  • side effects = hypokalaemia, diabetes, gout
• beta blockers block NAd binding and decrease cardiac output and blood pressure

  • decrease contractility, heart rate, renin release (therefore decreases angiotensin and aldosterone)

  side effects = cold hands, fatigure
• alpha blockers:

  • mostly found on vascular smooth muscle cells
  • cause arterial and venous dilation
  • modulate noradrenaline release

  side effects = lethargy, headache and dizziness
• clonidine acts as an a2 receptor agonist, decreasing sympathetic activity, decreases resistance and blood pressure
• methyldopa acts as a false neurotransmitter and a a2 receptor agonist
• hydralazine and nitrovasodilators lead to NO in blood stream, causing dilation