 Dear students, in this topic we shall discuss the effects and mode of action of catecholamine hormones. The catecholamine hormones that is epinephrine and norepinephrine have numerous cardiovascular and metabolic effects. They also effect contraction of smooth muscles and induce vasoconstriction. They also stimulate glycolysis and lipolysis. They also stimulate sympathetic nervous system for fight or flight response. This fight and flight response is a very important response for survival, which is shown in any dangerous or stressful situation. In this response, different tissues are activated at a time and the body is prepared for an emergency response. Fight and flight mechanism or response is an important role in these requirements. These requirements include first, mobilization of energy resources of the body. Number two, increasing the heart rate. Number three, diverting blood flow to the skeletal muscles. And number four, dilating the pupil of the eye so that maximum light can enter the eye and increase vision. These hormones during their action bind to the receptors which are called adrenergic receptors or adenoreceptors. These receptors are G protein coupled receptors. There are two types of adenoreceptors, alpha, receptors and beta adenoreceptors. Alpha and beta are two types of adenoreceptors. These receptors are alpha-1, alpha-2 and beta-1 and beta-2. These types of adenoreceptors are found in different tissues. These types of adenoreceptors vary in the mode of action of catecholamine hormones. We will look at these four types of adenoreceptors in detail. First, we will study the mode of action of catecholamine by binding through alpha-1 adenoreceptors. These receptors are coupled to a G protein which is inhibitory in its actions. When we say that it is inhibitory in a hormonal pathway, it means that it decreases the concentration of cyclic AMP after its activation. These alpha-1 adenoreceptors mediate smooth muscle contraction in many tissues. After their stimulation, the concentration of cyclic AMP is reduced in the cell and also the inositol trisphosphate pathway is activated. Dear students, when the inositol trisphosphate pathway is activated, it leads to elevation of intracellular inositol trisphosphate. This increased inositol trisphosphate causes release of calcium ions from the stores within the cells. These stores are mitocondria and endoplasmic reticulums in which calcium ions are stored in the body. As a result, calcium ion concentration in cytosol is increased. Increased calcium ions cause contraction of muscles. Dear students, now we shall discuss the mechanism of action. of catecholamines by binding through alpha-2 adenoreceptors. These types of receptors are found in the pre-synaptic cells at norendenergic adenergic synapses. They are also located on some post-synaptic sites in liver, brain and smooth muscles. Stimulation causes an auto-inhibition of release of norepinephrine through a negative feedback. This action is mediated by an inhibitory effect of these receptors on an enzyme adenolate cyclase. Dear students, now we shall discuss the mode of action of catecholamines through beta-1 adenoreceptors. Beta-1 adenoreceptors' stimulation is due to the neuronal release of norepinephrine. All adenoreceptors are different types of stimulation. These receptors are also linked to a G-protein, but this G-protein is a stimulatory G-protein. Through these receptors, when catecholamine hormones act, they cause activation of adenolate cyclase enzyme, which results in increase in the concentration of cyclic AMP in the cell. Elevation of cyclic AMP in the cytosol causes increase in calcium conductance. As a result, calcium levels in the cell are raised. This results in increased contraction of cardiac muscles. It also results in the release of fatty acids from adipose tissue. Dear students, now we shall discuss the mechanism of action of catecholamines through beta-2 adenoreceptors. These receptors are stimulated due to higher levels of circulating catecholamines. These receptors are also a stimulatory G-protein coupled with which results in the increase of CAMP level in the cell. Here, when CAMP rises, it causes the activation of calcium pump. Rather than increasing the conductivity of calcium, it activates calcium pump. When calcium pump activates, the result is that calcium ions are sequestered into the mitochondria end endoplasmic category. This results in decrease in the concentration of calcium ions in the cell. When this calcium ion level decreases in the cell, it causes relaxation of smooth muscles. Relaxation of smooth muscles results in bronchodilation and vasodilation.