Vasodilators

Front 1

How vascualr smooth muscle is controlled

Back 1

Controlled by vasodilators and vasoconstricters that alter the sensativity of the contratile machinery:
1) entry and exist of calicum so via Na/Ca exchange, second messenger systems causing ion channels to open, vasoconstrictors angiotensin and endothelin

2)sequestration of ca within the cell : IP3 activation via phopholiapse c increasing SR storages.

3) Linking of ca2+ with contraction via activation of myosin light chain kinase

Ca2+ sensatisaition: increase in MLCK activity and desensatiation is a decrease in MLCK activity

Front 2

Vasodilator AIM

Back 2

Aims to decrease intracellular calcium levels thus inhbiits calcium channels activates atp dependant calcium pump and Na/Ca atpase that regualte clcoum from out of the cell Opens k+ channels so cause hyperpolarisation
2) increase in cAMP or cGMP to cause increase in myosin phosphatase

Front 3

ACE inhibitors:
captopril and enalapril

Back 3

inhibit the conversion of angiotensin 1 into angiotensin 11:
preventing: a) aldosterone realese b)vasopressin realse b) inhibiton of bradykinin breakdown leading to increased vasodilation c)increase in blood pressure by keepin symph. tone up
d)prolonging the life of NA

side effets: hypokalaemia and dry cough -- due to bradykinin accumlation

Front 4

Angiotensin 11 receptor antag:

Losartan and valsartan

Back 4

Alternative to ace causes less side effects no dry cough.. prevents the effect of increasing glomerolous filtration rate and thus pressure at the efferent arteriole. Blocks the effects of angiotensin 11 thus all the above it does with less side effect. Side effect include hypotension

Front 5

Calcium channel anta:
Dihyrdopyridines e.g. amlodipine and nifedipine

Verapamil and diltiazem

Back 5

Block calcium voltage sensative channels resulting in relaxtion and dilation of resistance and capacitance vessesls. could cause tachycardia. Verapamil used on the heart muscle, to cause a reduction in AV and SA node conduction, remember these are used if you dont respond to b-blockers and dont have left ventricular dysfunction. causes heart block thus arrthymias

Front 6

K+ activators such as pinacidal and minoxidal

Back 6

Hyperpolarizes the membrane due to increased influx of potassium switching of ca voltage gated channels, the potassium conductance is sensitve to ATP. Meaning that ATP in normal conditions supresses potassium function allowing depolarisation to occur, but k+ channel activators antagonise ATP thus hyperpolarisation takes place thus causing relaxation .

Front 7

Other vasoconstricters

Back 7

Also nitrates, Adenosine, ANP (aterial narteric peptide)-- increases cGMP thus casuing affect on calcium direct , prostacylcin