Frequency characteristics of blood pressure oscillations evoked by sympathetic transmitters, noradrenaline and adenosine triphosphate

Mean arterial pressure (MAP) was recorded beat-to-beat in chronically instrumented, conscious, unrestrained rats under control conditions and after pharmacological inhibition of vascular sympathetic influences by means of: (1) ganglion blockade with chlorisondamine; (2) α-adrenoceptor antagonist phentolamine; (3) P2 receptor blockade with pyridoxalphosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS). Angiotensin II was continuously infused to prevent drastic MAP decrease during chlorisondamine and phentolamine administration. Overall MAP variability increased after ganglion blockade and combined blockade of adreno- and purinoceptors. It increased also after inhibition of purinergic influences, but was not significantly changed after vascular adrenergic blockade. Spectral analysis of spontaneous MAP fluctuations in intact rats revealed a peak centered at 0.4–0.5 Hz. Ganglion blockade suppressed MAP fluctuations with frequencies from 0.1 to 0.8 Hz. After blockade of α-adrenoceptors, MAP spectral density was suppressed only within the 0.1–0.45-Hz band, but increased in the 0.45–0.8-Hz band. In the latter case, sympathetically-induced peak of MAP spectrum was centered on 0.6 Hz, being evoked, presumably, by adenosine triphosphate (ATP). Blockade of P2 receptors by PPADS enhanced MAP fluctuations in the 0.1–0.45-Hz frequency band, i.e. the noradrenaline-induced peak was centered on 0.2 Hz. No peaks were observed in the 0.1–0.8-Hz frequency band during combined blockade of adreno- and purinoceptors. The present study supports the concept that sympathetic purinergic co-transmission is essential for stabilization of MAP level. MAP fluctuations evoked by noradrenaline and ATP can be distinguished by their frequency characteristics.