Amino acids are well known to be an important class of compounds for the maintenance of body homeostasis and their deficit, even for the polar neuroactive aminoacids, can be controlled by supplementation. However, for the amino acid taurine (2-aminoethanesulfonic acid) this is not true. Due its special physicochemical properties, taurine is unable to cross the blood-brain barrier. In addition of injured taurine transport systems under pathological conditions, CNS supplementation of taurine is almost null. Taurine is a potent antioxidant and anti-inflammatory semi-essential amino acid extensively involved in neurological activities, acting as neurotrophic factor, binding to GABA A/glycine receptors and blocking the excitotoxicity glutamate-induced pathway leading to be a neuroprotective effect and neuromodulation. Taurine deficits have been implicated in several CNS diseases, such as Alzheimer’s, Parkinson’s, epilepsy and in the damage of retinal neurons. This review describes the CNS physiological functions of taurine and the development of new derivatives based on its structure useful in CNS disease treatment.

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It has been proposed that the acetylcholine (ACh)-induced relaxation of the rat aorta is entirely mediated by endothelium derived-nitric oxide (NO). However, some authors have reported that indomethacin pretreatment attenuates ACh-induced relaxation of rat aortic ring preparations. Moreover, it has also been suggested that cAMP accumulation may regulate either nitric oxide synthase (NOS) or cyclooxygenase (COX) expression in different tissues. Thus, in this in vitro study we have investigated the endothelial mechanisms involved in the ACh-induced relaxation of ring preparations of the rat thoracic aorta, as well as the influence chronic treatment with the selective β2-agonist salbutamol had upon such mechanisms. Results of functional experiments show that N Gmonomethyl-L-arginine (L-NMMA, 3 × 10 -4 M) considerably inhibited the ACh-induced relaxation of rat aortic ring preparations. However, indomethacin (10 -5 M) was also found to partially attenuate this ACh response, suggesting that although NO is the most important mediator of the ACh-induced relaxation of the rat aortic ring preparations, vasorelaxation may also involve prostanoids. Moreover, the results suggest that treatment with salbutamol failed to produce any change in the ACh-induced relaxation of rat aortic ring preparations.