Hydralazine or Dihydralazine is a directly acting arteriolar vasodilator with little action on venous capacitance vessels; reduces t.p.r. It causes greater reduction of diastolic than systolic BP. Reflex compensatory mechanisms are evoked which cause tachycardia, increase in c.o. and renin release — increased aldosterone — Na and water retention.
The disproportionate cardiac stimulation appears to involve direct augmentation of NA release and myocardial contractility as well. Thus, a hyperdynamic circulatory state is induced—angina may be precipitated due to increased cardiac work as well as steal phenomenon. There is no reduction in renal blood flow despite fall in BP. However, fluid retention and edema may occur by the above mechanism. Tolerance to the hypotensive action of Hydralazine develops unless diuretics or beta blockers or both are given together to block the compensatory mechanisms.
The mechanism of vascular smooth muscle relaxant action of hydralazine is not clearly known. It is partly endothelium dependent: may involve generation of NO (nitric oxide) and stimulation of cGMP. Direct effects on membrane potential and on Ca2 fluxes have also been proposed.
Hydralazine is used in moderate-to-severe hypertension not controlled by the first line drugs. Usually, low doses are added to the diuretic and beta blocker already being administered. Hydralazine is not used alone. Large doses are not recommended for long periods.