Cellular mechanisms underlying the excitatory actions of ATP in vascular smooth muscle

✍ Scribed by Charles Kennedy

• Publisher: John Wiley and Sons
• Year: 1993
• Tongue: English
• Weight: 434 KB
• Volume: 28
• Category: Article
• ISSN: 0272-4391
• DOI: 10.1002/ddr.430280343

✦ Synopsis

It i s now clear that noradrenaline (NA) is not the sole excitatory cotransmitter in perivascular sympathetic nerves, as both adenosine 5'-triphosphate (ATP) and neuropeptide Y (NPY) are co-stored with NA in synaptic vesicles and co-released during nerve stimulation. The relative contribution of these compounds to neurogenic contractions i s dependent upon the species, vessel and parameters of stimulation studied. Stimulation of the perivascular nerves evokes excitatory junction potentials (ejps) which, in most vessels are resistant to a-adrenoceptor antagonists. The ejps are mediated by ATP, as they are selectively abolished by desensitisation of the P,,-purinoceptor by (.r,P-MeATP or by the selective P,-antagonist, suramin. in many vessels a component of the neurogenic contraction also shows resistance to a-adrenoceptor blockade but can be inhibited by a,P-MeATP or suramin. In the limited number of vessels studied t o date, ATP has been found to act via several ionic mechanisms, including an increase in a non-specific, cationic current and an increase in a chloride current. These currents appear to have a variable distribution and are not all present in all vessels. This may allow vessels a differential response to ATP depending on their function. However, the distribution, role and relative importance of these effects i s not yet known. As well as its direct contractile effects, ATP also interacts in a synergistic manner with NA and NPY. The mechanisms which underlie these effects are unclear but may involve an increase in the current through L-type calcium channels. Clearly, vascular neurotransmission is not the simple process previously envisaged.