Differences in purinoceptor modulation of norepinephrine release between caudal arteries of normotensive and hypertensive rats.

The effects of 2-chloroadenosine, a purinoceptor agonist, on the overflow of endogenous norepinephrine (NE) was examined in the electrically field-stimulated (EFS) caudal artery obtained from Wistar-Kyoto (WKY) rats and age-matched spontaneously hypertensive rats (SHRs). 2-Chloroadenosine at 10(-6) and 10(-5) M reduced the EFS-evoked release of NE from arteries of WKY rats but was without effect on the release of NE from arteries of SHRs. Methoxamine (10(-5) M), an alpha adrenoceptor agonist, caused the release of ATP, ADP, AMP and adenosine from caudal arteries of Wistar rats, WKY rats and SHRs, and decreased the release of EFS-evoked release of endogenous NE in arteries from normotensive rats, but not from arteries of SHRs. Thus, both exogenously applied and endogenously released purines are ineffective in reducing the evoked release of NE in this model of hypertension. The enhanced release of NE from sympathetic nerves of SHRs may be due in part to the loss of prejunctional modulation by purines.