Enhanced sympathetic neurotransmission in the tail artery of 1,3‐dipropyl‐8‐sulphophenylxanthine (DPSPX)‐treated rats

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 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 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 Vasoconstrictor responses to exogenous noradrenaline (0.1–300 μ m ) and adenosine 5′‐triphosphate (0.01–3 mM) were unaffected after DPSPX treatment, indicating prejunctional alteration of sympathetic cotransmission during DPSPX‐induced hypertension Acute exposure to DPSPX (10 μ m ) 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 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 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.