What Are Beta Receptors?

Beta receptor is an adrenal receptor. Adrenergic receptors are divided into two categories: those that combine with corresponding transmitters to cause vasoconstriction and dilated pupils are called alpha adrenaline receptors, referred to as alpha receptors; those that combine with corresponding transmitters cause cardiac excitement, blood vessels, and bronchi Those with dilation and metabolic changes (glycolysis and lipolysis) are called beta adrenergic receptors, or beta receptors for short.

The concept of adrenaline receptors can be traced back to 1905. Langley studied the mechanism of action of nicotine and arrow poison on muscles and proposed that the drug only acts on certain parts of muscle cells or nerve endings, which is called the receptor site. There are two types of receptor substances, excitatory and inhibitory. Dale (1906) found that the excitatory effect of adrenaline can be blocked by ergotamine, while the inhibitory effect is not blocked, providing an example of the concept of two receptors.

In 1948, Ahlquist studied 6 similar epinephrine drugs with similar structures and compared the strength of the effects of these drugs on whole animals and isolated organs. There are two different organ effects: a effect: mainly includes the contraction of peripheral blood vessels. Epinephrine has the strongest effect, followed by norepinephrine, and isoproterenol is the weakest. effect: mainly includes the excitability of the heart and the expansion of peripheral blood vessels. The effect of isoproterenol is the strongest, and adrenaline is the second. Norepinephrine is the weakest. Based on the significant differences in the effects of these drugs, two hypotheses of adrenaline receptors were proposed, and the former was named a receptor and the latter was named B receptor, which provided a theoretical basis for the classification of adrenaline receptors. ^[1]

Adrenergic receptors fall into two categories: alpha receptors that bind to the corresponding transmitters to cause vasoconstriction and dilated pupils, and beta receptors that bind to the corresponding transmitters to cause cardiac excitement, blood vessel and bronchiectasis, and metabolic changes. According to their different responses to agonists or blockers, alpha receptors can be divided into two subtypes: those that can be stimulated by phenylephrine and methoxamine and are called alpha receptors blocked by prazosin Is the alpha ₁ receptor. This receptor is located on the cell membrane (postsynaptic membrane) of a noradrenergic innervating effector. Any alpha receptor that can be excited by clonidine and blocked by yohimbine is called alpha ₂ receptor. It is located on the presynaptic membrane, adipocytes, and some visceral and vascular smooth muscle cell membranes. receptors are traditionally divided into two subtypes: the receptors of the myocardium are mainly ₁ types, and ₂ receptors also exist, and the ratio of the two is about 80:20. Studies have suggested that alpha receptors also exist on the myocardium; beta ₂ receptors are predominant on bronchial and vascular smooth muscle. Studies have shown that ₃ receptors are predominant in brown adipose tissue. ^[1]

When the beta receptor binds to the GS protein, it activates

Beta receptor blockers can selectively bind to beta receptors and competitively block the binding of noradrenergic neurotransmitters or epinephrine drugs to B receptors, thereby antagonizing their -type epinephrine effects , So it is also called -type anti-adrenalin drugs. Experiments in the right atrium of isolated guinea pigs have demonstrated that beta-blockers can shift the concentration-response curve of the agonist isoproterenol to accelerate heart rate in parallel to the right. Under the action of different concentrations of blocking drugs, although the effects of agonists are antagonized, increasing the concentration of agonists can still achieve the maximum effect, which is a typical competitive antagonism.

In whole animals, -blockers are similar to -blockers, and their anti--adrenergic effect depends on the ratio of local agonist and blocker concentrations in the tissue and the sympathetic tone of the body. For example, it has a weaker effect on the heart at rest, but when the sympathetic tone of the heart increases (pathological conditions such as exercise or heart failure), it has a significant inhibitory effect on the heart. An important feature of -blockers is that they have a high degree of specificity. Although they can block the effects of adrenergic nerve stimulation on enhancing myocardial contraction and heart rate, they cannot block calcium, digitalis and ammonia. The excitatory effect of theophylline or glucagon on the heart can not counteract the vasodilating effect of acetylcholine.

The chemical structure of beta-blockers is similar to that of beta-agonist isoprenaline. They all have the following basic structure: a secondary amine with an isopropyl group at one end and an aromatic ring at the other end, which can be one or two benzene rings, or a heterocyclic ring. The former seems to be related to the affinity of the beta receptor; the latter may determine that it exerts an agonistic or antagonistic effect after binding to the beta receptor. ^[1]