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How Do Antihistamines Bind At The H1 Receptor Sites?

Antihistamines prevent escalation of allergic reactions. They work by blocking the H1 histamine G-protein receptor. G-protein receptors are cell-surface proteins that act like cellular switches that start a cascade of complex chemical reactions inside the cell. By outcompeting histamine at the H1 binding site, antihistamines stop allergic reactions before they start, or can stop a severe allergy attack within seconds of application. This is the most important action in reversing acute allergic reactions.

In order to fully understand how antihistamines can block histamine from these receptors, one should think of the H1 G-protein receptor as a lock that has two keys that fit. Antihistamines and histamines are keys that both fit that lock. There are only so many keyholes. Therefore, if there are many more keys than locks, then there are likely to be keys without locks. Histamine release is part of the nonspecific immune response. Typically, the body releases histamine whenever a cellular injury or infection occurs. However, the immune system can be easily fooled into mistaking benign particles as harmful disease causing agents. These benign particles are often protein residues that rub off when touching certain plants or insects, but sometimes certain proteins characteristic to specific foods can trigger the reaction internally.

About Histamine Chemicals

Histamine is a versatile chemical that plays many different important roles inside the human body. Importantly, antihistamines medication only disrupts the allergy causing pathways initiated by histamine binding. When an antihistamines dose is far larger than the body's release of histamine, harmful side effects are likely to occur. In short, antihistamines only have to mimic the binding site where histamine-H1 interactions occur and be present in concentrations high enough to block nearly all available binding sites.

How Histamines Cause Allergic Reactions

When histamine is released from mast cells, it will bind to an H1 G-protein receptor. This ignites a cascade of biochemical reactions inside the individual cell that eventually result in vasodilation (expanding of blood vessels) and increased vascular permeability. Increased vascular permeability allows fluid to release into tissues causing characteristic swelling, runny nose and watery eyes. The more histamine that is released in the immune system's response to the foreign particle, the stronger the symptoms of an allergic reaction will be. Antihistamines binding at the H1 site prevent these cascades from even starting.

Antihistamines Prevent H1 Receptor Binding

Antihistamines prevent histamine binding to H1 receptors through brute force. When a person takes antihistamines, either orally, nasally, topically or as a suppository, they flood the bloodstream. Since most H1 receptors are in the blood vessels, most allergy causing histamine-H1 interactions are combated by getting antihistamines quickly into the bloodstream. Antihistamines work quicker when applied closest to the source of the outbreak (think applying topical antihistamines on a poison ivy infection). When antihistamines are present at the site of an allergic reaction in great numbers, they simply outnumber the histamines present and occupy all the H1 binding sites preventing the histamine-H1 interaction that starts the chemical pathways associated with allergic reactions. Antihistamines stop histamine-H1 interactions by occupying all the H1 binding sites.

 

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