1. Sympathetic neurotransmission and
noradrenaline content of the tail artery of Wistar rats treated for 7 days with the
adenosine antagonist, 1,3-dipropyl-8-sulphophenylxanthine (
DPSPX), were examined. 2. Systolic blood pressure of the
DPSPX-treated rats (164.0 +/- 2.9 mmHg; n = 6) was significantly greater than saline-treated controls (140.0 +/- 2.8 mmHg; n = 5) after 7 days treatment. 3. The pressor responses of the arterial rings to transmural nerve stimulation (65 V, 0.1 ms, 4-64 Hz, for 1 s) were markedly enhanced in the
DPSPX-treated compared with the saline-treated animals. Both noradrenergic and purinergic components of perivascular sympathetic neurotransmission were enhanced during
DPSPX-induced
hypertension. 4.
Vasoconstrictor responses to exogenous
noradrenaline (0.1-300 microM) and
adenosine 5'-triphosphate (0.01-3 mM) were unaffected after
DPSPX treatment, indicating prejunctional alteration of sympathetic cotransmission during
DPSPX-induced
hypertension. 5. Acute exposure to
DPSPX (10 microM) did not modify
vasoconstrictor responses to transmural nerve stimulation, thus supporting the claim that the enhancement of sympathetic neurotransmission only results from long-term
DPSPX treatment. 6. The
noradrenaline content of the tail arteries of
DPSPX-treated (4.498 +/- 0.26 ng cm-1; n = 4) was significantly greater than saline-treated (3.440 +/- 0.30 ng cm-1; n = 5) animals. 7. These findings show that chronic inhibition of the actions of endogenous
adenosine by
DPSPX results in an elevation of systolic blood pressure accompanied by enhanced sympathetic cotransmission and enhanced
noradrenaline content of the rat tail artery.