Effect of nitric oxide and renal nerves on renomedullary haemodynamics in SHR and Wistar rats, studied with laser Doppler technique.

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-ω-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 (S i n = 8, S d n = 8) and in Wistar rats (W i n = 10, W d n = 10). An innervated non-treated Wistar group served as control (C i 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 S i group ; W i -19 ± 8 (P < 0.05), W d -17 ± 6 (P = 0.07), S i -50±9 (P < 0.01) and S d -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.