Where is adrenergic receptors found

These are easier since there are only two types, muscarinic receptors and nicotinic receptors. And I will make it even easier by getting rid of the nicotinic receptors after I tell you they are involved in muscle contraction and are affected by substances such as curare used on those poison-tipped arrows that cause muscle paralysis by blocking these nicotinic receptors. Medications such as succinlycholine are available to block the nicotinic receptors and induce paralysis necessary for certain medical procedures.

We are left with the one parasympathetic receptor you must learn, the muscarinic receptor. When this receptor is stimulated, it causes a decrease in the heart rate, a decrease in heart contractility and a decrease in the size of the bronchioles. When we are at rest, we can slow down and conserve energy. The parasympathetic nervous system helps us do this.

What would happen if we block the muscarinic receptors? That would cause the heart rate and contractility to increase, dilation of the bronchioles and less production of secretions in the body.

This is the exact effect of atropine, a drug we use to counteract too much parasympathetic activity such as from over-stimulation of the vagus nerve or the effects of certain chemical warfare nerve agents and organophosphate poisoning. Atropine is a parasympatholytic, we can also call it a parasympathetic antagonist or parasympathetic blocker or an anticholinergic medication.

All these terms mean the same; it means they block the action of acetylcholine at the parasympathetic receptors. The effect of blocking any receptor causes the opposite effect we would expect from stimulating the receptor. Ipratroprium is another example of a parasympathetic blocker medication but this one is inhaled so most of the effect occurs in the lungs, and when we block parasympathetic receptors in the lungs we cause the bronchioles to dilate and decrease production of secretions like mucus.

That makes ipratroprium useful in the patient with COPD who produces excessive pulmonary mucous and in combination with albuterol for any wheezing patient. But remember that the primary rescue medication for bronchospasm is a beta 2 agoinist such as albuterol although ipratrorium is often added and is available as a combination inhaler with albuterol called Combivent. It is important to remember that it is the balance between the sympathetic and parasympathetic nervous system that keeps our automated body functions in balance and working properly.

Outside forces, including drugs, medications or poisons can change the functioning of the autonomic nervous system. Activation of adrenergic receptors in the heart will modify the cardiac action potentials of pacemaker cells and contractile myocytes to increase heart rate and cardiac contractility, which will improve cardiac output.

Activation of adrenergic receptors on the vasculature will lead to vasoconstriction and increased systemic vascular resistance. Vasoconstriction in addition to the increased cardiac output above will increase blood pressure to improve perfusion to vital organs. Activation of adrenergic receptors will also lead to bronchodilation to open the airways, mydriasis to optimize vision, and gluconeogenesis to increase glucose levels to meet the needs of increased metabolism during the fight or flight response.

Below is a reminder of the sympathetic events that occur leading up to adrenergic receptor activation discussed previously in the autonomic nervous system. This blog will now serve as a continuation and discuss the adrenergic receptors in more detail, their location, and the effects they produce.

Of note, there will be a future similar post discussing cholinergic receptors on the parasympathetic side. Postganglionic sympathetic neurons release norepinephrine onto adrenergic receptors of target organs to generate the sympathetic response.

Postganglionic parasympathetic neurons release acetylcholine onto muscarinic receptors of target organs to generate the parasympathetic response. Preganglionic neurons arise from the central nervous system at the thoracolumbar level. They release acetylcholine onto nicotinic cholinergic receptors on the cell bodies of the postganglionic neurons. Postganglionic neurons then release norepinephrine onto adrenergic receptors on the target organs. Preganglionic neurons also terminate on the adrenal medulla which causes secretion of epinephrine and norepinephrine into the bloodstream.

These circulating catecholamines will also bind to adrenergic receptors to produce a sympathetic response. As discussed above, the beta adrenergic receptors are involved in generating a sympathetic fight or flight response when catecholamines such as norepinephrine and epinephrine bind to them. While both norepinephrine and epinephrine can act on beta receptors, epinephrine has a higher affinity for beta receptors compared to norepinephrine, especially the beta2 receptors in which there is very little to no norepinephrine activity.

More on this later. This is in contrast to what we saw with alpha receptors in which norepinephrine has a higher affinity than epinephrine. This makes sense when thinking about norepinephrine and epinephrine as pressor medications used to treat various types of shock.

Epinephrine has quite a bit of beta effect and some alpha, while norepinephrine has quite a bit of alpha effect and some beta.

This is also why epinephrine is given during anaphylaxis as it has a much higher affinity for the beta2 receptors in the lungs which will lead to bronchodilation and improvement in respiratory distress. General Function on Smooth Muscle. Beta receptor activation leads to smooth muscle relaxation. For example, one of the main locations of beta receptors is in the lungs and activation will lead to bronchodilation via smooth muscle relaxation. This is in contrast to what we saw with alpha receptors in which activation led to smooth muscle contraction vasoconstriction, urethral sphincter constriction, pylorus constriction, prostate contraction, iris dilator muscle contraction, etc.

Below are some tricks to help remember receptor affinity and the effect each receptor has on smooth muscles. Epinephrine has a much higher affinity for beta receptors than norepinehrine. Alternatively, norepinephrine has a much higher affinity for alpha receptors than epinephrine.

Alpha receptors lead to smooth muscle contraction and beta receptors lead to smooth muscle relaxation. There are 3 main types of beta receptors: beta1, beta2, and beta3. All beta receptors are coupled with Gs proteins which increase levels of cAMP.

Beta1 receptors are fairly easy to remember as there are 2 main locations to know: the heart and kidneys. Beta1 receptors on the heart will increase heart rate and cardiac contractility when activated. Heart rate will be increased through beta1 activation of the SA node, AV node, and conduction system of the heart. This will increase the phase 4 action potential slope of pacemaker cells resulting in more frequent depolarization.

Beta1 activation will also increase cardiac contractility by influencing phase 2 of the action potential of cardiac myocytes, which will increase stroke volume. Remember that heart rate and stroke volume are the 2 variables for cardiac output. If they are both increased, then cardiac output will increase.

The increased cardiac output will subsequently augment blood pressure and perfusion. Any adrenergic effects on cells are generally mediated by G protein-coupled receptors. Other areas of smooth muscle contraction are: Ureter. Vas deferens. Hair arrector pili muscles.

Uterus when pregnant. Urethral sphincter. Blood vessels of ciliary body stimulation causes mydriasis. Induction of glucagon release from the pancreas. Contraction of sphincters of the gastrointestinal tract. Negative feedback in the neuronal synapses—presynaptic inhibition of noradrenalin release in CNS. Increases renin secretion from the juxtaglomerular cells of the kidney. Increases ghrelin secretion from the stomach. Beta-agonists bind to the beta receptors on various tissues throughout the body.

Beta-1 receptors are predominantly found in three locations: the heart, the kidney, and the fat cells. The beta-1 adrenergic receptor is a G-protein-coupled receptor communicating through the Gs alpha subunit. Targeted activation of the beta-1 receptor in the heart increases sinoatrial SA nodal, atrioventricular AV nodal, and ventricular muscular firing, thus increasing heart rate and contractility.