Impaired interaction between efferent and afferent renal nerve activity in SHR involves increased activation of alpha2-adrenoceptors.

Activation of efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), leading to decreases in ERSNA by activation of the renorenal reflexes in the overall goal of maintaining low ERSNA. The renorenal reflex responses to various stimuli are impaired in spontaneously hypertensive rats (SHR). Because renal tissue density of α(2)-adrenoceptors (ARs) is increased in SHR, we examined whether the ERSNA-induced increases in ARNA are impaired in SHR and, if so, the role of α(2)-ARs. The ARNA responses to increases in ERSNA were impaired in SHR, 2390 ± 460%·seconds, versus in Wistar-Kyoto rats, 6620 ± 1690%·seconds. Renal pelvic release of substance P was not altered by 6250 pmol/L norepinephrine (NE) in SHR but was increased by 250 pmol/L NE in Wistar-Kyoto rats, from 5.7 ± 0.7 to 12.5±1.3 pg/min. Renal pelvic administration of the α(2)-AR antagonist rauwolscine enhanced the ERSNA-induced increases in ARNA, 4170 ± 900%·seconds, in SHR but not in Wistar-Kyoto rats. In the presence of rauwolscine, 250 pmol/L NE increased substance P release, from 5.2 ± 0.3 to 11.2 ± 0.8 pg/min, in pelvises from SHR. Because angiotensin II suppresses the activation of renal mechanosensory nerves in SHR, we examined whether losartan improved the ERSNA-induced ARNA responses. Losartan had no effect on the ARNA responses or the NE-induced increases in substance P in SHR. However, losartan+rauwolscine resulted in further enhancement of the responsiveness of the renal sensory nerves to increases in ERSNA and NE in SHR but not in WKY. We conclude that increased activation of renal α(2)-ARs and angiotensin II type 1 receptors contributes to the impaired interaction between ERSNA and ARNA in SHR.