Naked Science Forum
Life Sciences => Physiology & Medicine => Topic started by: Jennajenna on 20/02/2016 19:33:56
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Hi guys
I just donot fully understand why non selective β blocker can contribute hypertenstion.
for β-1 receptor part, non selective blocker can decrease HR, contractility, CO and decrease renin release to decrease BP.
how about fro β-2 receptor part? β-2 receptor blocker can vasoconstrict to increase BP? how this part can contribute the hypertension??
thanks!
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You are right that beta-2 receptors provoke vasodilatation, and blocking those would, logically, have a hypertensive effect, but because the beta-1 mediated effects on cardiac output are the dominant determinant of the mean arterial pressure, using non-specific blockers, like propranolol, produces a net antihypertensive outcome.
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THANKS FOR YOUR REPLY
why do not we use only β-1 selective blockers instead of non selective beta blockers? what is the benefit to use non-selective blockers?
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Beta-1 blockers are cardioselective, whereas first generation blockers non-selectively antagonize both beta-1 and beta-2 adrenoceptors - thus affecting not only the heart, but the kidneys, liver, lungs, GI tract, liver, vascular smooth muscle, skeletal muscle ect. This can ultimately lead to reduced cardiac and/or renal output ect.
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why do not we use only β-1 selective blockers
Jenna, we do use beta-1 selective blockers, which include drugs like atenolol or metoprolol, because they tend to be more cardio-selective than propranolol and therefore have a better side effect profile and are safer in people at risk from asthma (asthmatics should avoid beta blockers full stop, but sometimes they are used - judiciously and cautiously - in people with stable and mild asthma where it is judged that the cardiovascular benefits outstrip any respiratory risk).
But propranolol is a very safe drug with a long track record of use; we know it is well tolerated and likely to suit most people.