Receptors That Are Stimulated By Noradrenalin Or Adrenaline Biology Essay

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Adrenaline is a non-selective adrenergic agonist which acts directly on receptors and activates them to produce similar effects to those that occur after the release of the hormone epinephrine from the adrenal medulla or stimulation of sympathetic nerves. It mimics the actions of the sympathetic nervous system except the actions on the arteries of the face and sweat glands; thus is it called sympathomimetic.

Pharmacologically several classes of adrenoceptors can be distinguished in the sympathetic nervous system. Based on the different responses that the receptors show to the adrenergic agonists epinephrine, norepinephrine and isoproteremol two receptor families and were distinguished.

The order of potency is epinephrine ≥ norepinephrine >> isoproterenol for -adrenoceptors. Based on the different affinities adrenoceptors show for -agonist and blocking drugs they are subdivided into two subgroups, 1 and 2 adrenoceptors.

1 receptors mediate many of the classic effects involving constriction of smooth muscle and they are located on the post synaptic membrane of the effector organs. Inositol-phospholipid signaling pathway is activated when adrenaline binds to 1 receptors on the liver cells that signal and activate phosphorylation of glycogen synthase and inactivate phosphorylase kinase which results in activateion of glycogenphosphorylase which leads to the release of glucose into bloodstream.

2 receptors are present on cells of pancreas and in certain vascular smooth muscle cells where they control insulin output. They are also present primarily on presynaptic nerve endings where they control adrenergic neuromediator. Upon stimulation of sympathetic adrenergic nerve norepinephrine is released and travels across the synaptic cleft to interact with 1 receptors. On the neuronal membrane a portion of norepinephrine circulates back to interact with 2 receptors and stimulate them. This causes the inhibition of further norepinephrine production and release from the stimulated adrenergic neuron which in turn leads to a decrease in the adrenergic neuron output. Norepinephrine acts as a local modulating mechanism for sympathetic neuromediator output reduction when sympathetic activity is high; here receptors are acting as inhibitory autoreceptors. When norepinephrine is released from a presynaptic sympathetic neuron and diffuses to presynaptic parasympathetic neurons where 2 receptors are also found and it interacts with them causing the inhibition of acetylcholine release; these receptors are then thought to be acting as inhibitory heteroceptors. The effects of 2 receptors are mediated by adenylyl cyclase inhibition and the decrease in intracellular cAMP levels in contrast to 1 receptors.

Adrenaline increases heartbeat which causes an increase in glucose and oxygen to the muscles. It also increases the respiratory rate which results increasing the rate of CO2 removal and increases the oxygen level in the blood. It also increases arteriolar constriction which causes the blood to divert from the digestive system and skin to the muscles.

Tissue such as vasculature to skeletal muscles have both 1 and 2 receptors

The responses of the recptors are different from those of receptors. The order of potency is isoproterenol > epinephrine > norepinephrine for -adrenoceptors. Based on the different affenities for adrenergic agonist and antagonist that -adrenoceptors show, these receptors can be subdivided into 1, 2 and 3 subgroups. 1 receptors have similar affinities for adrenaline and noradrenalin, while 2 receptors have greater affinity for adrenaline than for noradrenalin. Thus, tissues such as vasculature of skeletal muscles which have 2 receptors as the dominant receptors are particularly responsive to the effects of adrenaline that is releases from adrenal medulla. Activation of adenylyl cyclase occurs upon binding of a neurotransmitter at any of the three receptors leading to an increase in intracellular cAMP.

In general we can say that at high doses of adrenaline effects on the vascular system are strongest causing (vasoconstriction), whereas at low doses effects predominate causing (vasodilatation).

Adrenaline has major actions on the cardiovascular system. It has (positive inotropic: 1 action) where it strengthens the contractility of the myocardium and has (positive chronotropic: 1 action) where it increases the rate of contraction; therefore it increases the cardiac output.

Adrenaline is a type of catecholamines which are sympathomimetic amines that contain, 3,4-dihydroxybenzene group and the following characteristics:

High potency: Drugs that have the highest potency in directly activating or are catechol derivatives (with OH groups in the 3 and 4 position on the benzene ring).

Poor penetration into the CNS: Catecholamines do not readily penetrate into the CNS due to their polar nature; however most of these drugs have effects that are related to action on the CNS such as (anxiety, headache and tremor).

Rapid inactivation: Catecholamines are metabolised by two enzymatic pathways MAO intraneuronally and by COMT postsynaptically. They are also ineffective when given orally and have a short period of action when given parentally due to inactivation by COMT in the gut wall and MAO in the liver and gut wall. Metanephrine and vanillylmandelic acid are the final metabolites that are found in urine.

Therapeutic indications:

Glaucoma: to reduce intraocular pressure in open-angle glaucoma a 2% epinephrine solution may be used topically which causes vasoconstriction of the ciliary body blood vessels and therefore decreases the production of aqueous humour.

Cardiac arrest: regardless of the cause; epinephrine can be used in patients with cardiac arrest to restore cardiac rythm. It acts on 1 adrenoceptors and cause vasoconstriction that leads to increased peripheral resistance so that the blood travels to the heart. It also it acts on 1 adrenoceptors which cause an increase in cardiac output and heart rate, which may sometimes lead to cardiac irritability. Other medications and treatments include vasopressin which doesn't lead to mayocardial irritability but effectively increase peripheral vascular resistance.

Bronchospasm: adrenaline is used essentially in emergency treatment of anaphylactic shock and acute asthma or in any condition that results in bronchoconstriction where it greatly improves respiratory exchange within only a few minutes after subcutaneous administration. However because it has a short duration of action; in the prolonged treatment of asthma albuterol and other drugs which are selective (2 agonists) are favoured since they have minimal cardiac stimulatory effects and a longer duration of action.

Anaesthetics: adrenaline increases the duration of local anaesthesia by causing vasoconstriction at the site of injection which in turn causes the local anaesthesia to persist at that site before it is absorbed into the circulation and metabolised; thus local anaesthetics usually contain 1:100000 parts epinephrine.

Anaphylactic shock: for the treatment of Type I hypersensitivity reactions in response to allergens due to its vasoconstriction effects.


Adrenaline has a short duration of action (due to rapid degradation) but a rapid onset. For the most rapid onset in emergencies it is given intravenously. It may also be given by inhalation, by endotracheal tube, topically to the eye or subcutaneously. Adrenaline is inactivated by the intestinal enzymes and only its metabolites are excreted in urine; thus it is ineffective when give orally.

Intracellular concentration of calcium plays a major role in maintaining smooth muscle tone in myocardium contraction. The contractile process of cardiac smooth muscle depends on the movement of extracellular calcium ions into smooth muscle cells and increasing the concentration of intracellular calcium. Agents can increase intracellular calcium by two main mechanisms:

The resting membrane potential of the smooth muscle cell is (Em= -60 mV). When excitatory neurotransmitters act on their receptors on smooth muscle depolarization of the membrane potential to (about -45 mV) this causes the special voltage dependent calcium channels to open which in turn results in calcium ions entering the muscle cells down an electrochemical gradient and increasing intracellular calcium

When calcium enters smooth muscle cells through voltage dependent channels the release of calcium from the mitochondria and sarcoplasmic reticulum occurs which leads to an increase in the cytosolic level of calcium.

The underlying cause of hypertension is an increased peripheral vascular resistance which is caused by an increase in active tension in the vascular smooth muscle; which in turn results in an increase in cytosolic free calcium

Calcium channel blockers:

When the preferred first-line agents are contraindicated or ineffective then calcium channel blockers are recommended and are effective in patients with angina or diabetes. Due to excessive vasodilatation and marked reflex cardiac stimulation the risk of myocardial infarction is increased; thus high doses of short-acting calcium channel blockers should be avoided.

Nefidipine is a calcium channel antagonist which selectively inhibits the calcium ions from entering the cardiac muscle and vascular smooth muscle without altering the concentration of serum calcium. It is a peripheral arterial vasodilator and it acts directly on vascular smooth muscle by binding to L-type calcium channels in the heart and in smooth muscle of the peripheral and coronary vasculature and blocks the inward movement of calcium through these channels. Due to the limited intracellular calcium stores in vascular smooth muscle; contraction is dependent upon the influx of extracellular calcium. Therefore intracellular calcium concentration decreases causing arterial vasodilation and decreased peripheral vascular resistance which leads to the reduction of arterial blood pressure.

Therapeutic uses: calcium channel blockers do not usually need the addition of a diuretic since they have an intrinsic natriuretic effect; they are useful in treating hypertension in patients with diabetes, asthma, angina or peripheral vascular disease.


To maintain good control of hypertension treatment needs to be given three times daily. Nifedipine has a short half life (3-8 hours). For less frequent doses sustained release preparations are available and may be used.

In conclusion:

Both adrenaline and nifedipine have major effects on vascular smooth muscle tone and are used therapeutically to treat cardiac conditions and hypertension respectively.