Mechanism of action
·
Hydralazine apparently lowers blood pressure
by exerting a peripheral vasodilating effect through a direct relaxation of
vascular smooth muscle. It has also been suggested that cyclic 3',5'-adenosine
monophosphate (cyclic AMP) mediates, at least partly, the relaxation of
arterial smooth muscle by altering cellular calcium metabolism, which
interferes with the calcium movements within the vascular smooth muscle that
are responsible for initiating or maintaining the contractile state.
·
In hypertensive, the
hydralazine-induced decrease in blood pressure is accompanied by increased
heart rate, cardiac output, and stroke volume, probably because of a reflex
response to decreased peripheral resistance. The drug has no direct effect on
the heart.
·
Hydralazine may
increase pulmonary arterial pressure, as well as coronary, splanchnic,
cerebral, and renal blood flow. The preferential dilatation of arterioles, as
compared to veins, minimizes postural hypotension and promotes the increase in
cardiac output.
·
Hydralazine usually
increases renin activity in plasma, presumably as a result of increased secretion
of renin by the renal juxtaglomerular cells in response to reflex sympathetic
discharge. This increase in renin activity leads to the production of
angiotensin II, which then causes stimulation of aldosterone and consequent
sodium reabsorption. Tolerance to the antihypertensive effect of the drug
develops during prolonged therapy, especially if a diuretic is not administered
concurrently.
·
In CHF, hydralazine
decreases systemic vascular resistance and increases cardiac output.
Reference: Tripathi
K.D., "Essentials of medical pharmacology", Jaypee brothers medical
publishers, Seventh edition, New Delhi, page no. 520,522.
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