Pharmacology for Dentistry

Antihypertensive Agents 183

opathy, peripheral vascular disorders, con-
gestive heart failure, acute myocardial inf-
arction, myocardial preservation during
surgery, migraine, oesophageal spasm and
exercise induced bronchial asthma.

AMLODIPINE

Amlodipine is a long-acting calcium
channel blocker that inhibits the transmem-
brane influx of calcium ions into vascular
smooth muscle and cardiac muscle. By in-
hibiting calcium ion influx it directly dilates
vascular smooth muscle.

After oral administration of S-
amlodipine besylate, bioavailability is 65-
80%. Approximately 93% drug is bound to
plasma proteins. It is extensively converted
to inactive metabolites via hepatic
metabolism. It is excreted in urine as 10%
parent drug and 60% of the metabolites.

Amlodipine is generally well tolerated.
The most commonly observed side effects
are headache, edema, fatigue, flushing and
dizziness.

Other side effects include nausea,
abdominal pain, somnolence, palpitations,
muscle cramps, frequency of micturition or
nocturia, cough, breathlessness, epistaxis,
impotence, nervousness and conjunctivitis.

It is indicated in the treatment of
essential hypertension and angina pectoris.

DIRECT VASODILATORS

HYDRALAZINE

It acts directly on arteriolar smooth muscle
to cause relaxation. It decreases diastolic

pressure more than systolic blood pressure

by lowering peripheral vascular resistance.

Due to preferential arteriolar dilatation, pos-

tural hypotension is uncommon. It increases

heart rate and cardiac output.

After oral administration its absorption

is almost complete and rapid. It is subject to

significant first pass metabolism in liver.

Adverse effects include nausea, vomiting,

tachycardia, dizziness, fatigue, weakness, pal-

pitations, headache, paresthesia, tremor, con-

stipation, anxiety, nasal congestion, lupus like

syndrome and sleep disturbances.

It is indicated in hypertension (moderate

or severe) and hypertension with renal

involvement.

SODIUM NITROPRUSSIDE

It has a brief duration of action. It relaxes

directly arteriolar and venous smooth

muscle. It decreases both preload and

afterload thus both cardiac output and

peripheral resistance are reduced.

It is given parenterally and onset of ac-

tion occurs quickly (within 1 minute). On

stopping IV infusion, the effect dissipates

rapidly. It is converted to NO by endothe-

lial cells and RBCs which relaxes vascular

smooth muscle. It is converted to thiocyan-

ate in liver which is excreted slowly.

Adverse effects include nausea, vomiting,

nervousness, palpitation, sweating, headache,

disorientation, methaemoglobinaemia.

It is indicated in hypertensive crisis,

congestive heart failure and acute mitral

regurgitation.