The role of H2 receptor blockers in acid reflux relief

Reflux of stomach contents into the esophagus is known to produce inflammatory changes in the esophageal lining. There are two components in that content responsible for such a damage. These are the hydrochloric acid and a biologically active substance called pepsin, an enzyme which digests protein. Both of acid and pepsin contribute to esophagitis. Inside the stomach acid is mainly produced to activate pepsin from a precursor known as pepsinogen. That reveals the dual effect of the stomach acid in relation to esophageal damage. The first effect being direct and the second indirect through the activation of pepsin which in turn irritates the esophagus.
It is well evident from the previous facts that reduction of acid production prevents damage of the esophageal lining. Acid is produced by cells lining the stomach known as parietal cells. These cells have chemical pumps called proton pumps which moves hydrogen ion from the inside of the parietal cell into the stomach lumen against a concentration gradient. Before this pumping activity the cell responds to signals initiating the process. These signals are: 1- Acetylcholine, a chemical substance released at the nerve endings supplying stomach glands, 2- Gastrin: a local hormone released from capillaries adjacent to stomach glands, and 3- Histamine: a biologically active chemical produced by specialized local cells in the stomach wall. These signals act upon specific sites in the membrane enclosing each parietal cell called receptors and each receptor is named after the name of stimulus which acts upon. Accordingly there are Aceylcholine, Gastrin and histamine receptors.
Acetylcholine is released through the various neurological mechanisms which follow food intake and its digestion. Gastrin is a local hormone produced by G cells located in the wall of the distal part of the stomach called the antrum in response to the chemical effect of digested proteins. Histamine is released mechanically by distention of the stomach and chemically by products of protein breakdown.
Theoretically speaking, we can block acid production by preventing the stimulatory effect of Acetylcholine, Gastrin and Histamine upon the parietal cells. Acetylcholine has well known antagonists but they have generalized effects as Acetylcholine is a universal neuro-transmitter. So far no Gastrin blocker is yet available. In 1964 the role of histamine as a parietal cell stimulant was discovered, however the use of traditional antihhistamine did not reduce acid secretion. That led scientists to postulate the existence of two histamine receptors, the one acted upon by traditional antihistamines (H1) and the other residing in parietal cell wall (H2).

H2-receptor antagonists have some similarity in structure to histamine, consequently they compete with its molecules and combine with receptors instead, of course they don't have the functional activity of histamine. Fortunately, this binding effect is simultaneously accompanied by a reduced stimulating effect of both Acetylcholine and Gastrin upon the parietal cell.
Examples of H2 receptor blockers include: Cimitedine (Tagamet),Ranitidine (Zantac), Nizatidine (Axid) and Famotidine (Pepcid).
They are equally effective, and the standard dose for mild to moderate acid reflux is: 400mg, 150mg, 150mg and 20mg respectively. This dosage is given twice daily for 6-12 weeks. Approximately 50% of patients with esophagitis heal on this regimen. However a high relapse rate of 50% has been reported within two months. Maintenance treatment is indicated in severe esophagitis associated with complications and if symptoms are relapsing immediately after treatment stops. The dosage may be given three times daily in some cases for proper relief of symptoms and healing of complications.
Generally speaking they are more effective than antacids but less effective than proton pump inhibitors.
Together with other measures for acid reflux relieve such as dietary control and lifestyle modifications, they have proven efficacy in mild to moderate symptoms. They are available as over the counter and prescription forms and have relatively lower cost.

Related Posts:
The role of Proton Pump Inhibitors in acid reflux relief
The role of Antacids in acid reflux relief

Rule out heart disease even if acid reflux is diagnosed

There are two types of pain related to acid reflux:
1- The classical heartburn characteristic of acid reflux resulting from irritation of the esophageal surface lining.
2- The chest pain which is similar to that associated with coronary artery disease (coronary arteries are blood vessels supplying the heart with its essential requirements of oxygen and nutrients). This pain is due to spasm of the esophageal wall muscles.
It is evident that acid as a pain stimulus acts on surface receptors in case of heartburn. On the other hand it stimulates deeper receptors when causing chest pain and that suggests the pre-existence of breaks in the esophageal surface lining in the form of erosions or ulcers or an increase in the distance of spaces between cells lining the esophageal surface. Both of these mechanisms favor further acid diffusion deeper into the wall of the esophagus.
At times differentiation between esophageal and cardiac causes is very difficult.
In this situation the priority is for considering causes related to the heart first, simply because heart disease is serious and the chest pain may be a symptom of myocardial infarction which is an emergency condition following obstruction of coronary blood supply to the heart and resulting in impending death of a localized area of the musculture of the heart. That is why exclusion of heart disease is important to save life.
Needless to say that this rule applies especially to older patients with hypertension or diabetes or known heart disease.
Actually, both acid reflux and ischemic heart disease may co-exist as they are common health problems and that complicates the decision making process.
Out of all cases, having chest pain similar to typical heart attack, though their coronary arteries are normal, acid reflux contributes to 40-60% of the causes. This finding is documented by ambulatory esophageal acid monitoring.
To recall chest pain associated with heart disease (called angina) is a sense of fullness or tightness, dull aching or crushing in nature, in the middle of the chest. That pain may spread into the neck, shoulder or arm and is associated with difficulty in breathing and a cold sweat. On the other hand, chest pain of esophageal origin spreads more frequently to the back, is initiated by the same factors that trigger heartburn like fatty foods, lying down immediately after meals and is lasting for minutes or hours. Esophageal pain may also be associated with other symptoms of acid reflux such as heartburn, regurgitation and difficult swallowing. It is characteristically relieved with antacids. Diagnosis is confirmed with esophageal manometry which detects abnormalities in esophageal motility.
Chest pain of cardiac origin usually follows exertion and is relieved by rest. Nitrates and calcium channel blockers which are known to alleviate angina, aggravates pain of esophageal origin at the same time as they relaxes the lower esophageal sphincter.