Activation of A2a adenosine receptors in the nucleus tractus solitarius inhibits renal but not lumbar sympathetic nerve activity.
The activation of adenosine A2a receptors in the nucleus tractus solitarius (NTS) via microinjection of the selective agonist CGS 21680 elicits long-lasting, dose-dependent decreases in mean arterial pressure (MAP) and heart rate (HR) and preferential dilation of the iliac vascular bed in comparison to the renal and mesenteric vascular beds. We investigated whether differential changes in regional sympathetic output occur with A2a receptor activation. In 24 chloralose/urethane anesthetized male Sprague-Dawley rats MAP, HR, renal (RSNA) and lumbar sympathetic nerve activity (LSNA) were recorded simultaneously. Data were analyzed as both the maximum decrease and the integral of the decrease over the duration of the depressor response. Microinjection of CGS 21680 (2 and 20 pmol in 50 nl volume) into the subpostremal NTS caused significant and dose-dependent decreases in MAP, HR and RSNA, however, did not significantly decrease LSNA in comparison to the effect of vehicle. Maximum responses of RSNA vs. LSNA in delta% of control values were: -32 +/- 4 vs. -9 +/- 2, and -59 +/- 4 vs. -19 +/- 5 for low (n = 9) and high (n = 8) doses of CGS 21680 respectively; integral responses of RSNA vs. LSNA in delta% x min were: -487 +/- 112 vs. -19 +/- 35 and -1258 +/- 164 vs. -175 +/- 126 for low and high doses of CGS 21680 respectively. Microinjections of vehicle (n = 7) did not alter integral hemodynamic or neural parameters. We conclude that activation of A2a adenosine receptors in the NTS evokes differential changes in visceral vs. somatic sympathetic nerve activity which cannot explain differential vascular responses in terms of simple sympathetic withdrawal. Lack of significant inhibition of LSNA combined with preferential vasodilation in hindquarter vascular bed suggests that active vasodilation may be triggered by activation of A2a adenosine receptors in the subpostremal NTS.
Scislo
T J
TJ
Department of Physiology, Wayne State University, School of Medicine, Detroit, MI 48201, USA.
O'Leary
D S
DS
D000241:Adenosine / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D007668:Kidney / Q000294:innervation*; D008161:Lumbosacral Region; D008297:Male; D009433:Neural Inhibition / Q000502:physiology; D010627:Phenethylamines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018047:Receptors, Purinergic P1 / Q000187:drug effects / Q000502:physiology*; D017552:Solitary Nucleus / Q000502:physiology*; D013116:Spinal Cord / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*
D010627:Phenethylamines; D018047:Receptors, Purinergic P1; C061282:2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine; D000241:Adenosine