Bergström G, Rudenstam J, Taghipour K, Göthberg G, Karlström G
Department of Physiology, Göteborg University, Sweden.
Acta Physiol Scand. 1996 Jan;156(1):27-36. doi: 10.1046/j.1365-201X.1996.429150000.x.
The threshold for activation of the humoral renal antihypertensive system, presumably residing in the renomedullary interstitial cells (RIC), is substantially reset upwards in the spontaneously hypertensive rat (SHR). Depressor reactions, normally elicited by an increased renal perfusion pressure, can be inhibited either by high frequency renal nerve stimulation or blockade of nitric oxide synthesis, i.e. manoeuvres decreasing renal blood flow at this high perfusion pressure. The present study was designed to explore the effects on regional renal haemodynamics of blocking NO synthesis with N-omega-nitro-L-arginine (L-NNA) in chloralose anaesthetized SHR and Wistar rats. Mean arterial blood pressure (MAP), heart rate (HR), renal blood flow (RBF), cortical blood perfusion (CBP) and papillary blood perfusion (PBP) were measured in renally innervated and denervated SHR (Si n = 8, Sd n = 8) and in Wistar rats (Wi n = 10, Wd n = 10). An innervated non-treated Wistar group served as control (Ci n = 12). The laser Doppler technique was used to record CBP and PBP. MAP increased in all groups receiving L-NNA while HR, RBF and CBP simultaneously decreased. The relative decreases in RBF were more marked into the two SHR groups than in the corresponding Wistar groups. After L-NNA PBP also decreased in all four groups despite the increased MAP and more so in the Si group; Wi -19 +/- 8 (P < 0.05), Wd -17 +/- 6 (P = 0.07), Si -50 +/- 9 (P < 0.01) and Sd -25 +/- 9% (P < 0.05). We conclude that NO is important for maintaining PBP especially in SHR. The more marked decrease in PBP in the innervated SHR suggests a NO/renal nerve interaction in the control of renomedullary blood flow in SHR. This finding may be of importance for the regulation of the humoral renal depressor mechanism.
体液性肾降压系统的激活阈值，推测存在于肾髓质间质细胞（RIC）中，在自发性高血压大鼠（SHR）中显著上调。通常由肾灌注压升高引发的降压反应，可通过高频肾神经刺激或一氧化氮合成的阻断来抑制，即在这种高灌注压下减少肾血流量的操作。本研究旨在探讨在水合氯醛麻醉的SHR和Wistar大鼠中，用N-ω-硝基-L-精氨酸（L-NNA）阻断NO合成对局部肾血流动力学的影响。在有肾神经支配和去神经支配的SHR（Si n = 8，Sd n = 8）和Wistar大鼠（Wi n = 10，Wd n = 10）中测量平均动脉血压（MAP）、心率（HR）、肾血流量（RBF）、皮质血流灌注（CBP）和乳头血流灌注（PBP）。一个有神经支配的未处理Wistar组作为对照（Ci n = 12）。激光多普勒技术用于记录CBP和PBP。接受L-NNA的所有组中MAP升高，而HR、RBF和CBP同时降低。两个SHR组中RBF的相对降低比相应的Wistar组更明显。给予L-NNA后，尽管MAP升高，但所有四组中的PBP也降低，在Si组中更明显；Wi -19 +/- 8（P < 0.05），Wd -17 +/- 6（P = 0.07），Si -50 +/- 9（P < 0.01）和Sd -25 +/- 9%（P < 0.05）。我们得出结论，NO对维持PBP很重要，尤其是在SHR中。有神经支配的SHR中PBP的更明显降低表明在SHR肾髓质血流控制中存在NO/肾神经相互作用。这一发现可能对体液性肾降压机制的调节具有重要意义。
