 Pyrite cells are in either resting state or in a stimulated state, but when and how the cells are stimulated. Pyrite cells have receptors for acetylcholine known as muscarinic receptors which are of M3 type. Then there are receptors for gastrin that is released from G cells from pylori glands. Also there are receptors for histamine which are of H2 type. So all these three acetylcholine, gastrin, histamine can stimulate parietal cell and can cause increase in HCl secretion. But not only that, they also affect release of each other. We can actually simplify it as levels of control of HCl secretion. These levels can be arranged as neural, hormonal and parafine manner. So vegas is the one which releases acetylcholine acts in a neural manner, gastrin is released in blood and acts in hormonal manner. HCl cells release histamine and which acts on parietal cells in pyrocrine manner. The machinery appears little complex but if you think in terms of levels of control you will get a sense of it. At the top is wegel control which stimulates acid secretion by directly stimulating parietal cells as we saw that there are acetylcholine receptors, M3 receptors. Then it also causes release of gastrin from G cells. Not only that it also stimulates these enterochromophen like cells which release histamine. Now D cells release somatostatin which have an inhibitory effect on these. So since the effect of vegas is to stimulate HCl secretion, vegas actually inhibits these D cells. Gastrin forms a second level and when gastrin is released it stimulates again the lower levels that is the ECL and also the parietal cells. But again it will have an inhibitory effect on D cells. Then ECL cells which release histamine acting in a pyrocrine manner that also stimulates parietal cells and inhibits D cells releasing somatostatin which is having negative effect. So if you see in terms of level the top post level is stimulating all three lower levels. Second level is gastrin is stimulating the lower two levels and the lowest level histamine is stimulating parietal cells with all inhibiting the D cells. But these are all stimulatory effects for release of HCl. So there should be a negative control also on the secretion. The secreted acid itself that is the H plus ions have a negative influence of parietal cells since they stimulate D cells causing release of somatostatin. This somatostatin inhibits parietal cells ECL cells and G cells and decreases their secretion thus decreasing H plus ions. So here is a negative feedback going on to control the level of hydrogen ions. So this is how machinery is arranged but when are these stimulants activated? Now neural stimulation via vagus occurs when you see smell or think of food. This is known as cephalic phase of HCl secretion. So the thought process itself will stimulate HCl secretion. When food enters into stomach, local distention of the stomach and peptides in its food stimulate these G cells causing release of gastrin. So this is a local effect. This is known as gastric phase. Now distention of the stomach also activates local reflexes causing stimulation of the vagus again. But what happens when partially digested food of stomach that is chyne enters the diodenum. Now depending on the contents of the chyne there are secretions in diodenum which also have effect on HCl secretion. The fat content in chyne causes release of CCK, polycystokynein. Acidic content causes release of another hormone secretin both of which have inhibitory effect on release of gastrin. So this effect of intestine on the release of HCl secretion is known as intestinal phase. Now this phase is also very important because it ensures proper pH in diodenum and that it does not become too acidic since enzymes are acting alkylene environment only. So if it becomes too acidic there is a signal back to the stomach to decrease the HCl secretion. So there are different phases of acid secretion which act via different mechanism. There is a phallic phase which acts on thought smell of food. There is a gastric phase which occurs when food enters into the stomach and when food enters into the diodenum there is intestinal phase.