Beta 1 Beta blockers A - Propranolol,
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1 Pharma Lecture 3 Beta blockers that we are most interested in are the ones that target Beta 1 receptors. Beta blockers A - Propranolol, it s a non-selective competitive antagonist of beta 1 and beta 2 receptors, it will bock the action of norepinephrine, it s used in many cardiac conditions. Effects: - A- Decrease Cardiac output B- Decreased Heart rate C- Decrease in contractile force D- Decrease in AV conduction E- Reduce sympathetic nervous system outflow F- Small vasoconstrictive effect (Increase in PVR) - Because these drugs work on beta adrenergic receptors on skeletal muscles that usually cause vasodilation when stimulated, but these drugs will inhibit them and vasoconstriction will therefore occur. G- Reduce renin release (Beta 1) - They are effective In patients with high renin activity, especially in younger patients who usually have hypertension due to high renin levels. H- Neutralize reflex tachycardia induced by Vasodilators- These group of drugs are beneficial as an adjuvant treatment for anti-hypertensive agents that cause tachycardia as their side effect. For example, some vasodilators cause reflex tachycardia and beta blockers such as propranolol are good drugs to neutralize this.
2 Side effects: - 1- Hypotension Generally all anti- hypertensive drugs cause hypotension 2- AV block, Bradycardia - They might predispose to arrythmias; therefore, we should be careful in giving these drugs to patients who have conduction problems or bradycardia. 3- Bronchial Constriction/spasm - They can act on smooth muscles of the bronchi and cause vasoconstriction; therefore, these drugs should be avoided in patients that suffer from Asthma. 4- Acute withdrawal syndrome (receptor super sensitivity) - For patients on beta blocker treatment for a long time we don t advise them to stop taking these drugs abruptly. This is because the body always tries to maintain homeostasis, so when you are constantly on beta blocker treatment, the body will be getting a lesser signal and will therefore upregulate the number of receptors or will increase their sensitivity. Now the patient will have the same amount of Norepinephrine as everyone else, but the number of receptors they may have will be greater than normal, all this norepinephrine will bind to these receptors and can predispose this patient to an ischemic attack. 5- Increase triglyceride levels and decrease HDL levels This will cause a problem in patients who have alterations in their lipid profiles. 6- Induce glucose intolerance We have to be careful in diabetic and obese patients. 7- May cause nightmares/depression They are lipid soluble and therefore can cross the blood brain barrier, the mechanism on how they may cause nightmares is unclear.
3 Contraindications:- 1- Bronchial Asthma Because they block Beta 2 receptors on skeletal muscles causing vasoconstriction 2- Peripheral vascular disease Because they cause an increase in PVR 3- Conduction problems/av block B- Atenolol It's a Beta 1 selective antagonist, less lipid soluble than other betaadrenergic antagonists, administered once daily. C- Metoprolol It's a Beta 1 selective antagonist, It s useful in Asthmatic patients. D- Nadolol It's Non-selective. Its advantage is that it is only administered once daily. Indications:- 1- Treatment of mild-moderate hypertension 2- Very useful for patients who are taking vasodilators, to prevent reflex tachycardia 3- Useful in controlling blood pressure in patients with underlying heart diseases.
4 ACE Inhibitors (Angiotensin converting enzyme inhibitors) These drugs work by acting on the Renal angiotensin system, mainly in the kidneys, and also in the blood vessels. *The doctor started talking about the history of these drugs, I didn t include it* Mechanism of Renin-angiotensin system: - Upon certain stimuli, such as low blood flow to the kidney, the kidney will start to secrete renin which will convert a peptide called angiotensinogen into angiotensin 1 and this will be worked upon by an enzyme called Angiotensin converting enzyme (ACE) in different parts of the body, to be converted into angiotensin 2. Angiotensin 2 has different functions in the body, one of the most important functions is that it regulates the blood pressure. Any decrease in blood pressure, will stimulate the renin release to produce angiotensin 2. Angiotensin 2 has two receptors, called AT1 & AT2. Now there will be changes when angiotensin binds to its receptors. 1- In the blood vessels we have AT1 receptors causing Vasoconstriction, cell growth & proliferation 2- In the kidneys we also have AT1 receptors causing aldosterone release, and when aldosterone is released it will cause sodium retention and will thus increase intravascular volume. 3- In the central nervous system it can cause central sympathetic activation. 4- AT2 receptor activation causes Vasodilation, restrains cell growth & proliferation, mediates Prostacyclin & NO release in the kidney, helps excrete sodium in the kidneys. In hypertension, we have elevated production of angiotensin 2. The effects of angiotensin 2 are seen more on AT1 receptors in this case.
5 ACE inhibitors block conversion of Angiotensin 1 to angiotensin 2. It also prevents the degradation of bradykinin to its inactive peptide. Bradykinin causes vasodilation which helps in the treatment of hypertension. These drugs are very useful in Diabetic patients because they slow the progression of renal disease in diabetes. Most ACE inhibitors end with the suffix Pril such as Enalapril, Ramipril, Lisinopril, Captopril. 1- Captopril One of the oldest ones, it s associated with multiple side effects because it contains a sulfhydryl moiety, and this causes allergic reactions. It also causes alteration in taste sensation. 2- Enalapril- Secreted mainly in kidney, so we should be careful in patients with renal insufficiency. 3- Ramipril works really fast, so peak concentration will be reached quickly. 4- Lisinopril Slowly absorbed, administered less frequently. Side effects: - 1- Hypotension in hypovolemic patients 2- Hyperkalemia as we said, when we block the action of aldosterone, more sodium will be excreted, and more potassium will be retained. 3- Angioedema- rapid swelling of throat, nose, mouth larynx or tongue. However, this is very rare 4- Cough- This is the most common side effect of ACE inhibitors, because bradykinin causes constriction in the bronchi and edema. 5- Skin rash 6- Taste alterations
6 These side effects are higher in African Americans. Many studies have shown that ACE inhibitors don t work very well in African Americans and Chinese people. Contraindications: - 1 Avoid use with Potassium sparring diuretics as they already cause hyperkalemia. So, use with Thiazides & Loop diuretics is fine. 2- Pregnancy They are contraindicated, because they will affect proliferation and cell growth, so if this is inhibited, it will affect the growth of the fetus. Angiotensin Receptor Blockers (ARB s) These drugs are Competitive antagonists of the AT1 receptor. They prevent binding of Angiotensin 2. Some people prefer these drugs over the ACE inhibitors because they have less side effects and the function of AT2 receptors, which is protective for the CVS, is preserved. However, in relation to lowering of blood pressure, there was no great difference between ACE inhibitors and ARB s. 1- Losartan They work mainly on Blood vessels and prevent binding of angiotensin 2 on the AT1 receptor and thus there will be more Vasodilation, and a decrease in TPR. They also will intervene with angiotensin ability to release aldosterone, so we will have more sodium excretion.
7 Side Effects: - 1- Angioedema This is not related to bradykinin, it is related to the vasodilatory effect of the blood vessels 2- Contraindicated in pregnancy - for the same reason as ACE inhibitors. 3- Dizziness ACEI or ARB? We can use both ACEI and ARB s in hypertensive patients with heart failure, renal disease, and diabetes. We use ACEI as the first choice unless the patient cannot handle the angioedema or cough, then we resort to using ARB s. Peripheral Alpha 1 adrenergic receptor blockers Prazosin is one of these drugs, it is a competitive inhibitor of the alpha 1 adrenergic receptors. Norepinephrine usually binds to the Alpha 1 receptor and causes Constriction of the vessels. So, Prazosin prevents the binding of norepinephrine and there will be less constriction and there will be dilation. They decrease PVR & BP. These drugs aren t used a lot as anti-hypertensives because they have side effects, and other drugs have shown better efficacy. Side effects: - 1- Postural dizziness 2- Headaches 3- Drowsiness
8 4- First dose phenomenon - when we give the patient this drug, he usually experiences a syncopal reaction orthostatic hypotension (upon standing). So, we advise the patient to take the drug at bed time so that he will not experience this side effect, the patient then develops tolerance to this reaction after the first dose. Other drugs from this family include Doxazosin, Terazosin. They have different pharmacokinetics. Doxazosin and Terazosin have a Longer half-life than Prazosin. And these two drugs are mainly used to treat benign prostate hypertrophy. People with this condition have a problem in emptying their bladders as a result of the hypertrophy of the prostate. So alpha 1 adrenergic receptors are on the neck of the bladder and their function is constriction, when they are inhibited, the patient can empty their bladder with much more ease. Recent recommendations on Alpha 1 Blockers Alpha 1 blockers are less effective than diuretics in preventing cardiovascular events, mainly heart failure. The National Institiute of health recommends not to use Alpha 1 blockers as the first drug of choice in hypertension (not effective in preventing heart failure) We usually give it as an additional drug with other drugs if we do not see an improvement in reduction of blood pressure. Adrenergic Neuron blocking agents/sympatholytics As we know, Sympathetic activation is involved in elevation of Blood pressure either by increasing the Cardiac output or increasing the Total peripheral resistance. These drugs work by decreasing the production/secretion of norepinephrine, we will have less of the effect of NE and therefore will have less of the sympathetic stimulation.
9 However, NE is necessary for many functions in the body. We will therefore have a lot of side effects, this is why they aren t used as a first line of treatment. 1- Guanethidine; it is a false Neurotransmitter. It will use the uptake mechanism of NE, it can take the place of NE and enter into the vesicle, and instead of NE being secreted from the vesicle, Guanethidine will be released, and it will have no effect on NE receptors. This drug is effective Orally. It does not cross the Blood brain barrier. Important: - We only use it in cases of Moderate-Severe cases of hypertension. We save this drug for cases of refractory hypertension, in which hypertension is not being resolved by any other drugs. 2- Reserpine; Prevents the uptake of Dopamine inside the vesicle, dopamine is a precursor of NE, so less uptake of dopamine means less production of NE, the NE stores will be depleted. It can also affect the uptake of Serotonin, however this is related to some side effects, such as depression. Sympathetic tone will be decreased, so we will have decreased TPR & CO. Side effects: - 1- Orthostatic hypotension 2- Depression 3- Nasal congestion 4- Bradycardia 5- Incompetence (guanethidine) 6- Diarrhea (guanethidine) 7- Salt and water retention
10 Drug interactions: - Amine pump is involved in the uptake of dopamine. There are drugs that can block this pump such as; Tricyclic antidepressants, monoamine oxidase inhibitors, ephedrine, amphetamines, phenothiazines. After chronic use of guanethidine, the above agents could cause hypertension due to development of receptor super sensitivity. It is RARELY INDICATED because of its adverse effects. It is often only used as a last resort in refractory hypertension.
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