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

@entity3160 @entity8 @entity101 @entity1808 @entity9886 @entity35 @entity1063
Activation of efferent renal sympathetic nerve activity (ERSNA) increases afferent @entity8 (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 @entity101 @entity35 (SHR). Because renal tissue density of a(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 a(2)-ARs. The ARNA responses to increases in ERSNA were impaired in SHR, 2390    460%  seconds, versus in @entity35 -Kyoto @entity35 , 6620    1690%  seconds. Renal pelvic release of substance P was not altered by 6250 pmol/L @entity1063 (NE) in SHR but was increased by 250 pmol/L NE in @entity35 -Kyoto @entity35 , from 5.7    0.7 to 12.5  1.3 pg/min. Renal pelvic administration of the a(2)-AR antagonist @entity3160 enhanced the ERSNA-induced increases in ARNA, 4170    900%  seconds, in SHR but not in @entity35 -Kyoto @entity35 . In the presence of @entity3160 , 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 @entity1808 suppresses the activation of renal mechanosensory nerves in SHR, we examined whether @entity9886 improved the ERSNA-induced ARNA responses. @entity9886 had no effect on the ARNA responses or the NE-induced increases in substance P in SHR. However, @entity9886 + @entity3160 resulted in further enhancement of the @entity8 to increases in ERSNA and NE in SHR but not in WKY. We conclude that increased activation of renal a(2)-ARs and @entity1808 type 1 receptors contributes to the impaired interaction between ERSNA and ARNA in SHR.
