Tsukamoto K, Sved A F
Department of Behavioral Neuroscience, University of Pittsburgh, PA 15260.
Hypertension. 1993 Dec;22(6):819-25. doi: 10.1161/01.hyp.22.6.819.
Previous studies demonstrated that stimulation of type B gamma-aminobutyric acid (GABAB) receptors but not type A (GABAA) receptors in the nucleus tractus solitarius of spontaneously hypertensive rats elicited a larger increase in arterial pressure compared with control rats of the Wistar-Kyoto strain. The present studies extended that observation by examining the cardiovascular response to injection into the nucleus tractus solitarius of a selective GABAB receptor antagonist, CGP 35348, in these strains as well as examining the cardiovascular responses to stimulation or blockade of GABAB receptors in the nucleus tractus solitarius in another model of hypertension, the rat treated with deoxycorticosterone acetate and salt. In both groups of hypertensive rats the pressor response to injection into the nucleus tractus solitarius of the GABA uptake blocking drug nipecotic acid was significantly greater compared with control rats (P < .01 in each model). Similarly, in both models of hypertension, the depressor response elicited by blockade of GABAB receptors in the nucleus tractus solitarius by injection of CGP 35348 was approximately 75% greater compared with control rats (P < .05 in each model). These results suggest that alterations in GABAB-mediated neural transmission in the nucleus tractus solitarius may contribute to the elevated arterial pressure observed in these models of hypertension.
先前的研究表明，与Wistar-Kyoto品系的对照大鼠相比，刺激自发性高血压大鼠孤束核中的B型γ-氨基丁酸（GABAB）受体而非A型（GABAA）受体，会引起动脉压更大幅度的升高。本研究通过检测在这些品系中向孤束核注射选择性GABAB受体拮抗剂CGP 35348后的心血管反应，以及在另一种高血压模型（用醋酸脱氧皮质酮和盐处理的大鼠）中检测孤束核中GABAB受体刺激或阻断后的心血管反应，扩展了该观察结果。在两组高血压大鼠中，与对照大鼠相比，向孤束核注射GABA摄取阻断药物尼克酸后的升压反应均显著更大（在每个模型中P < 0.01）。同样，在两种高血压模型中，通过注射CGP 35348阻断孤束核中GABAB受体所引起的降压反应，与对照大鼠相比均大约大75%（在每个模型中P < 0.05）。这些结果表明，孤束核中GABAB介导的神经传递改变可能导致了在这些高血压模型中观察到的动脉压升高。
