Receptor sensitivity in noradreanline is α1=α2, β1>>β2
Thus its actions are somewhat different from that of adrenaline.
Both systolic and diastolic blood pressures are increased due to:
- Increased force of contraction
- Beta 1 effect
- Beta 2 effect is absent, thus vessels are vasoconstricted increasing total peripheral resistance.
Reflex bradycardia occurs. This is because as blood pressure is increased, through baroreceptors an increase in vagal discharge slows down the heart. It is forceful but slow.
Cardiac output may not change much because of slowing down of the heart.
Vasoconstriction is generally seen, apart from coronary vessels because of local factors which may increase blood flow. Cerebral blood flow may also increase as systolic pressure is increased.
If atropine is given, it blocks the muscarinic receptors and as acetyl choline slows down the heart rate by virtue of M2 receptors, therefore, if atropine is given before noradrenaline, heart rate is not slowed down.
Baroreceptor reflex is seen.
There has been a tremendous decrease in therapeutic uses of noradrenaline over the years. In hypotension noradrenaline may be used to prevent shock.
Side effects are same as that of adrenaline, apart from tachycardia. There is also a perception of forceful and slow heart beat.