Article ID Journal Published Year Pages File Type
2743797 Anaesthesia & Intensive Care Medicine 2006 5 Pages PDF
Abstract

In the pharmacological control of hypertension, drugs from several different mechanistic classes may be used alone or in combination. Thiazide diuretics transiently evoke hypovolaemia but their sustained hypotensive effect relies on arteriolar dilatation. The mechanism by which antagonists at β-adrenoceptors lower blood pressure is unclear, but may involve a reduction in cardiac output, inhibition of renin release, increased baroreceptor sensitivity or an effect on the central mechanisms of blood pressure control. Inhibitors of Ca2+ influx lower blood pressure principally by causing arteriolar dilatation. Inhibitors of angiotensin-converting enzyme lower blood pressure by preventing angiotensin-induced vasospasm (an action shared by antagonists at angiotensin AT1 receptors) and by promoting bradykinin-induced vasodilatation. Antagonists at α1-adrenoceptors lower blood pressure by preventing the vasoconstrictor action of noradrenaline on arteriolar smooth muscle. Methyldopa and clonidine are centrally-acting antihypertensive drugs that activate presynaptic α2-adrenoceptors, thereby inhibiting noradrenaline release. Hydralazine is a vasodilator that may interfere with IP3-induced Ca2+ release within the vascular smooth muscle cell. Sodium nitroprusside relaxes vascular smooth muscle by a process involving the production of nitric oxide. Of drugs used to control pulmonary hypertension, bosentan is an endothelin antagonist while iloprost is a prostacyclin analogue with vasodilator properties.

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