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Bartter’s syndrome (antenatal Bartter syndrome, hyperprostaglandin E syndrome) is an autosomal-recessive electrolyte disorder, producing hypokalemia, metabolic alkalosis, hyper-reninism, and hyperaldosteronisms.

• It has now been recognized to be caused by mutations in at least three transport proteins responsible for NaCl absorption in the loop of Henle. Besides mutations in the Na+/K+/2Cl-cotransporter, Bartter’s syndrome can also be caused by mutations in the K+ channel that is present in the apical membrane of the ascending limb (ROMK or KIR1.1).
• This K channel is a K-recycling pathway and its operation is a prerequisite for NaCl absorption through NKCC2.
• Clinically, Bartter syndromes types I and II are indistinguishable. In contrast, a milder form of Bartter’s syndrome is caused by mutations in the basolateral chloride channel (ClC-Kb), an exit pathway for cellular Cl.

A receptor on nerve endings within a synapse that responds to the released neurotransmitter from that neuron. This then feeds back to the same neuron and negatively regulates the synthesis and release of that neurotransmitter.

Autophagy derived from latin words “self eating” is a normal regulated cell process where cytoplasmic materials are degraded through the lysosomal machinery and the contents reused by the cell.

During this process, organelles like mitochondria together with long-lived proteins are sequestred in a double-membrane vesicle delivered and degrade in lysosomes inside the cell.

Autophagy is activated in case of nutrient deprivation and plays a crucial role in the destruction of bacteria, viruses, and unnecessary proteins aggregates in cell.

Autacoids are literally ‘self-medicating agents’ that are liberated from or produced by cells in response to a stimulus. They differ from hormones in that they usually act locally after release, rather than reaching their target organ via the bloodstream.

Arrestins act as adaptor proteins that bind to phosphorylated G protein-coupled receptors (GPCR) and link the receptors to clathrin-coated pits. β-Arrestins are essential in the internalization of many GPCRs.

alpha-2  antiplasmin, a naturally occurring inhibitor of fibrinolysis, is a single chain glycoprotein that forms a stable, inactive complex within plasmin and thereby prevents plasmin’s activity.

Annexins form an evolutionary conserved family of Ca2+ and phospholipid binding proteins implicated in membrane trafficking and the regulation of Ca2+ currents across membranes.

An allergen is usually an inert substance (e.g. pollen, house dust mite faeces) that in some individuals can trigger the generation of an (inappropriate) antigenic response. Mediated by TH2 lymphocytes, it causes B-Lymphocytes to produce lgE.

Subsequent exposure of a sensitized individual to the allergen is therefore able to cross-link IgE antibodies on the surface of mast cells and trigger an immune response and histamine release.

The sensation of pain, following injury or disease, in response to a previously non-noxious stimulus is termed ‘allodynia’.

Tactile allodynia is caused by recruitment of low-threshold (non-nociceptive) sensory fibres (Aβ) in nociceptive pathways.