A Type of Drug-Food Interaction 5
October 5th 2009 06:53
Patient was given Phentolamine. How does it act? Why was it useful in this case? Phentolamine is a non-selective alpha-adrenoceptor antagonist. It inhibits alpha 1 receptors usually found in the smooth muscles of blood vessels, allowing the walls to relax and the lumen to dilate. This will decrease vascular resistance and blood pressure. However it inhibits presynaptic alpha 2 receptors as well. Alpha 2 modulates release of catecholamines in the presynaptic terminals. Phentolamine, therefore, will inhibit such modulation. Its potential effect is usually seen in the heart as tachycardia.
The use of phentolamine for hypertensive emergencies is justified with the rationale that we would want to counteract overexpression of sympathomimetic effect, as occurring with the presence of tyramine. According to Hoffman (2007) phentolamine and other alpha blockers theoretically bring about such effect.
In the management of emergency hypertension, we would not want to abruptly decrease the pressure for this may cause hypoperfusion. A 25% initial decrease in blood pressure is ideal. Phentolamine being a non-selective drug should help in acquiring this effect. Because of phentolamine, peripheral resistance decreases (alpha 1 antagonism), but cardiac output potentially increases (alpha 2 antagonism). The decrease of pressure is due to decreased vascular resistance. But such decrease is only gradual for blood flow and cardiac output will increase.
Why didn’t the physician use a Beta-adrenoceptor antagonist to treat the condition? Beta blockers were not used because such application may cause unopposed alpha-adrenergic action to the blood vessels, further constricting the blood vessels, elevating blood pressure, and mostly affecting the coronary arteries. This will bring about cardiac ischemia. As we all know Beta 1 receptors usually are situated in the heart. If we give drugs to block Beta 1, then the effect would only manifest as decreased cardiac rate and strength of contraction, but the overemphasized alpha adrenergic effect will continue to manifest as vasoconstriction. Beta 2 on the other hand is usually found in the smooth muscles of the blood vessels. But the receptors are dominated by the alpha receptors. Giving a drug to counteract beta 2 might not be potent enough to counteract alpha-adrenergic action (vasoconstriction) in the blood vessels.
In the management of emergency hypertension, we would not want to abruptly decrease the pressure for this may cause hypoperfusion. A 25% initial decrease in blood pressure is ideal. Phentolamine being a non-selective drug should help in acquiring this effect. Because of phentolamine, peripheral resistance decreases (alpha 1 antagonism), but cardiac output potentially increases (alpha 2 antagonism). The decrease of pressure is due to decreased vascular resistance. But such decrease is only gradual for blood flow and cardiac output will increase.
Why didn’t the physician use a Beta-adrenoceptor antagonist to treat the condition? Beta blockers were not used because such application may cause unopposed alpha-adrenergic action to the blood vessels, further constricting the blood vessels, elevating blood pressure, and mostly affecting the coronary arteries. This will bring about cardiac ischemia. As we all know Beta 1 receptors usually are situated in the heart. If we give drugs to block Beta 1, then the effect would only manifest as decreased cardiac rate and strength of contraction, but the overemphasized alpha adrenergic effect will continue to manifest as vasoconstriction. Beta 2 on the other hand is usually found in the smooth muscles of the blood vessels. But the receptors are dominated by the alpha receptors. Giving a drug to counteract beta 2 might not be potent enough to counteract alpha-adrenergic action (vasoconstriction) in the blood vessels.
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