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) alpha-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 alpha-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.
Golubinskaya
V O
VO
Department of Human and Animal Physiology, Faculty of Biology, M.V. Lomonosov Moscow State University, Russian Federation.
Tarasova
O S
OS
Borovik
A S
AS
Rodionov
I M
IM
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002714:Chlorisondamine / Q000494:pharmacology; D003243:Consciousness; D005583:Fourier Analysis; D005730:Ganglionic Blockers / Q000494:pharmacology; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D010507:Periodicity; D010646:Phentolamine / Q000494:pharmacology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D011983:Receptors, Purinergic / Q000502:physiology; D013564:Sympathetic Nervous System / Q000737:chemistry / Q000187:drug effects / Q000502:physiology; D013565:Sympatholytics / Q000494:pharmacology; D013566:Sympathomimetics / Q000494:pharmacology*
D005730:Ganglionic Blockers; D010975:Platelet Aggregation Inhibitors; D011983:Receptors, Purinergic; D013565:Sympatholytics; D013566:Sympathomimetics; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; D011732:Pyridoxal Phosphate; D000255:Adenosine Triphosphate; D002714:Chlorisondamine; D009638:Norepinephrine; D010646:Phentolamine