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Purinergic receptors are a super-family of membrane receptors which facilitate cellular responses in reaction to the presence of extra-cellular purines. Naturally occuring ligands for purinergic receptors are largely derivatives of adenine (ATP, ADP, and adenosine), though derivatives of uracil are also endogenous ligands.

History
Purines were first proposed as extracellular signalling molecules in 1929 by Albert Szent-Györgyi who observed that when purified adenine compounds were injected, they produced a temporary reduction in heart rate. In 1959 Pamela Holton, working at St Mary's Hospital medical school showed that ATP was released from sensory neurons upon antidromic stimulation, the first evidence that ATP may act as a neurotransmitter.

In the 1960s, the classical view of autonomic smooth muscle control was that sympathetic neurons released noradrenaline, whilst the responses of antagonistic parasympathetic neurons were mediated by acetylcholine. However, in a number of systems responses could still be observed in the presence of cholinergic and adrenergic blockers. In 1972 Geoffrey Burnstock proposed that the non-adrenergic, non-cholinergic (NANC) neurotransmitter was ATP. This proposal was met with initial criticism, since ATP was known to be a critical ubiquitous [adenosine triphosphate#biosynthesis|intracellular molecular energy source]] so it seemed counter-intuitive that cells might also actively release this vital molecule as a neurotransmitter.

newly characterized plasma membrane molecules involved in several and as yet only partially known cellular functions such as vascular reactivity, apoptosis and cytokine secretion.

Little is known about the effect extracellular microenvironment has on their function.

Fibroblasts share several features with smooth muscle cells and are an important constituent of the atherosclerotic plaque.

This receptors have their effect of high glucose concentration on ATP-mediated responses in human fibroblasts.

The members of the family include the following: