pharmacological treatment of hypertension

stages of contraction of cardiomyocytes

1 Na+ enters via slow Na+ channel in pacemaker cell causuing small depolarisation

2 Ca2+ enters cell via T-type voltage gated Ca2+ channel (further depolarisation)

3 Ca2+ enters via

L-TYPE

Voltage gated Ca2+ channel causing a large depolarisation

4 depolarisation spreads thru gap junctions to both pacemaker and contractile cells (contracticle cells contain L-type Ca2+ channels which causes further release of Ca2+ from SR via RyRs)

5 depolarisation occurs in neghbouring cells

6 this causes Contraction of cardiomyocyte

ARB vs ACE

They both cause a dec in overall BP

however ACE inhibitors come with an extra side effect causing patients to present with a constant dry-cough.

ACE inhibitors inhibit ACE which stops the conversion of angiotenisn I to angiotensin II and it also inc bradykinen production which causes vasodilation (this is also what causes the dry cough as it can cause slight bronchoconstriction)

ARBs cause inhibition of the AT1 receptor which Angiotensin II binds to in order to have any effect on the BP/vasculature tone

it does not have any effect with bradykinen and so causes no cough