Sympathetic-mimetic drugs

The effects of sympathetic stimulation are mediated by the release of the neurotransmitters norepinephrine and adrenaline from the post-ganglionic nerve endings; these effects have a broad spectrum of action and are mimicked by particular drugs, which take the name of sympathomimetics. The primary role of these drugs is to enhance the signal of the orthosympathetic system. their mechanism of action and the type of receptors they activate. They are distinguished:

sympathomimetics direct action: they interact directly with the adrenergic receptor and activate it;
sympathomimetics indirect action: indirectly increase the bioavailability of catecholamines at the synaptic level, between the post-ganglionic fiber and the effector organ, inducing their release by the transport vesicles (depletion of the vesicles) and inhibiting their reuptake;
cute camouflage mixed action: they are drugs with a flexible chemical structure, able to interact directly with the adrenergic receptors and to stimulate the depletion of the transport vesicles.

Adrenergic neurotransmitters also act centrally; in particular we find the cell bodies of noradrenergic neurons in an area of the frontal cortex called the locus ceruleus; noradrenaline plays an important role in the control of mood and emotionality, for this reason sympathomimetics are commonly used as antidepressants; at the level of the limbic system it determines the emotional state with hyperexcitability, while at the central level there is also a control of the vascular, bladder and heart tone.

The adrenergic receptors of the ortho-sympathetic system are divided into two categories, alpha and beta, in turn characterized by their respective subgroups. Examining them individually, we identify:

Α1 receptors: they are metabotropic type receptors, mainly located at lpost-synaptic level, responsible for the activation of the effector enzyme phospholipase C, with consequent formation of IP3 and DAG; in summary it can be said that they are responsible for an excitatory response. These receptors are found at the vascular level and their stimulation causes the vessels themselves to contract, with a consequent increase in peripheral resistance and ultimately in blood pressure; they are also responsible for mydriasis at the ocular level and contraction of the bladder sphincter with subsequent water retention.
Α2 receptors: they are also metabotropic receptors, this time located on the noradrenergic termination at pre-synaptic level. These receptors have the task of controlling the release of noradrenaline: when this is in sufficient concentrations, its release is inhibited (“negative feedback” control) through the inhibition of the effector enzyme adenylate cyclase, with consequent reduction of AMPc. The α2 receptors are also located on the GABA-ergic terminations, where they perform the same inhibitory function. We can also find them in the pancreas, in particular in the β cells of the islets of Langerhans, where they inhibit the release of insulin, which results in the deposition of glucose in the form of glycogen.
Β1 receptors: they are metabotropic type receptors, which activate effector enzymes (adenylate cyclase or phospholipase C). These are mainly located at the cardiac level, where the rate and strength of cardiac contraction increase; in other words, after being stimulated, they generate tachycardia. In adipocytes they are responsible for the breakdown of triglycerides into fatty acids and glycerol, or for lipolysis. At the kidney level, they cause an increase in the hormone renin, which in turn generates the release of angiotensin: one of the most powerful vasoconstricting agents in our body.
Β2 receptors: metabotropic receptors located in the vessels of the musculature; specifically, at the level of the skeletal muscles they cause vasodilation with a consequent decrease in pressure resistance at the peripheral level; at the level of the smooth muscles they cause relaxation, in particular the relaxation of the uterine muscles, while at the bronchial level we will have bronchodilation (action widely exploited in the pharmaceutical field for the "antiasthmatic effect). This receptors are also responsible for the lysis of glycogen in the muscle and liver. This function once again supports the old name of the orthosympathetic system, also known as the ergotropic system.

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