Maintenance of internal chemical environment of the body to a constant is called homeostasis. Hormones play a major role in maintaining homeostasis by their intergrated action and feed back controls.

Feedback control is mostlly negative, rarely positive. In a negative feedback control, synthesis of a hormone slows or halts when its level in the blood rises above normal. Some of examples of feedback control is given below.
Rise of testosterone level in the blood above normal inhibits ICSH secretion by the anterior pituitary lobe. This negative feedback checks oversecretion of testosterone

Hypothalamus in response to some external stimulus, produces a thyrotrophin-releasing hormone for the secretion of thyrotrophic hormone. The thyrotrophin-releasing hormone (TRH) stimulates the anterior pituitary lobe to secrete thyrotrophic hormone. The latter in turn stimulates the thyroid gland to produce thyroxine. If thyroxine is in excess, it exerts an influence on the hypothalamus and anterior pituitary lobe, which then secrete less releasing hormone and thyroid-stimulating hormone (TSH) respectively. A rise in the TSH level in the blood may also exert negative feed back effect on the hypothalmus and retard the secretion of TRH. This restores the normal blood-thyroxine level.
Sometimes, accumulation of a biochemical increases its own production. For example uterine contraction at the onset of labour stimulates the release of the hormone oxytocin, which intensifies uterine contractions. The contractions futher stimulate the production of oxytocin. The cycle of increase stops suddenly after the birth of the baby. This is a positive feedback control

How does the neuroendocrine control work? The hormones are released in very small quantities, yet they can cause widespread dresponses in cells or tissues all over the body. These responses in cells or tissues all over the body. These responses can be quite specific and selective in different cells. All vertebrate hormones belong to one of four chemical groups. Some hormones, such hormone, such as adrenaline and thyroid hormone, are small molecules derived from the amino acid tyrosine, others such as vasopressin and oxytocin, are short peptides, still other hormones, like insulin and glucagons, are longer polypeptide chains. Testosterone and estrogen are steroid hormones. Catecholamines, peptide and protein hormones are not lipid-soluble, and so, cannot enter their target cells through the bilipid layer of plasma membrane. Instead, these water-soluble hormones interact with a surface receptor, usually a glycoprotein, and thus, initiate a chain of events within it. The hormone insulin provides a well-studied example of how this happens.

- The membrane bound receptors of insulin is a heterotetrameric protein consisting of four subunits, two -subunits protrude out from surface of the ell and bind insulin, and two -subunits that span the membrane and protrude into the cytoplasm.

- Such receptors range from fewer than 100 in most cells in our body to more than 1,00,000 in some liver cells. Let us now consider the mechanisms whereby hormones induce their actions at the cellular and molecular levels.

Binding of insulin to the outer subunits of the receptor causes a conformational change in the membrane spanning -subunits, which is also an enzyme, a tyrosine kinase. The activated -subunits add phosphate groups of specific tyrosine residues located in cytoplasmic domain of the receptor, as well as a variety of insulin receptor substrates.

As a result of -subunit activity, a transducer G protein activates enzyme phosphodiesterase. This enzyme makes phosphatidylinositol 4,5-biphosphate (PIP2) into a pair of mediators inositoltriphosphate (IP3) and diacylglycerol (DG). In turn, IP3, which is water-soluble, and so diffuses into cytoplasm triggers the release of another messenger Ca2+ ions from intracellular endoplasmic reticulum activating many calcium-mediated processes. While DG remains in the membrane where it activates an enzyme called protein kinase C, which in turn, activates many other enzymes, such as pyruvate dehydrogenase, and so brings about the physiological effects.

Mediators amplify the signal in an expanding cascade of response. A single -subunit of insulin receptor, for example, activates many molecules of DG, and each protein kinase C molecule activated by DG will, in turn, activate many other enzyme molecules. DG and IP3 are examples of second messengers, intermediary compounds that amplify a hormonal signal and so set into action a variety of events within the affected cell. A variety of events within the affected cell. A variety of hormones use another second messenger, the cyclic form of adenosine monophosphate, (cAMP). The enzyme adenylate cyclase converts adenosine triphosphate (ATP) into cAMP. Because an enzyme can be used over and over again, a single molecule of active adenylate cyclase can catalyse production of about 100 molecules of cAMP. In muscle or liver cells, when hormones, such as, adrenaline bind receptors, the receptors change shape and bind to G protein, causing it, in turn, to bind the nucleotide guanosine triphosphate (GTP) and activate another protein adenylate cyclase. The result of this complex cascade of interactions is the production of large amounts of cAMP.

cAMP activates the enzyme protein kinase A, which, in turn, activates the enzyme phosphorylate kinase. Each molecule of protein kinase A activates roughly 100 molecules of enzyme, phosphorylate kinase and so on. The net result is that a single molecule of adrenaline may lead to release of as many as 100 million molecules of glucose within only 1 or 2 minutes. No wonder only very small quantities of hormone are needed.

Many cells use more than one second messenger. In heart cells, cAMP serves as a second messenger, speeding up muscle cell contraction in response to adrenaline, while cyclic guanosine monophosphate (cGMP) serves as another second messenger, slowing muscle contraction in response to acetylcholone. It is in this way that the sympathetic and parasympathetic nervous systems achieve antagonistic effect on heartbeat. Another example of antagonistic effect is insulin, which lowers blood sugar level, and glucagons, which raises it.

Another type of hormonal interaction is known as synergistic effect. Here, two or more hormones complement each others actions and both are needed for full expression of the hormone effects. For example, the production, secretion and ejection of milk by mammary glands require the synergistic effects of estrogens, progesterone, prolactin and oxytocin.

We have discussed many dramatic effects of hormone, for instance, testosterone. Yet, its concentration in the plasma of adult human male is only 30 to 100 ng per ml. How can hormones in such tiny quantities have such widespread and selective actions? Unlike catecholamine and peptide hormones, steroid and thyroid hormones are lipid-soluble hormones and readily pass through the plasma membrane of a target cell into the cytoplasm. There they bind to specific intracellular receptor proteins, forming a complex that enters the nucleus and bind to specific regulatory sites on chromosomes. The binding alters the pattern of gene expression, initiating the transcription of some genes (DNA), while repressing the transcription of others. This results in the production of specific mRNA translation products, proteins and usually enzymes. The actions of lipid-soluble hormones are slower and last longer than the actions of water-soluble hormones. These cause physiological responses that are characteristic of the steroid hormones.