Impaired Interaction Between Efferent and Afferent Renal Nerve Activity in SHR Involves Increased Activation of α2-Adrenoceptors
Impaired Interaction Between Efferent and Afferent Renal Nerve Activity in SHR Involves Increased Activation of α2-Adrenoceptors
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DOI：
10.1161/hypertensionaha.110.166595
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发表时间：
2011-03-01
期刊：
影响因子：
8.3
通讯作者：
Smith, Lori A.
中科院分区：
文献类型：
--
作者：
Kopp, Ulla C.;Cicha, Michael Z.;Smith, Lori A.
传出肾交感神经活动（ERSNA）的激活增加了传入肾神经活动（ARNA），导致在维持低ERSNA的总体目标中通过肾肾反射的激活降低ERSNA。自发性高血压大鼠（SHR）对各种刺激的肾-肾反射反应受损。由于SHR肾组织中α 2-肾上腺素能受体（AR）密度增加，我们检测了ERSNA诱导的AR NA增加是否在SHR中受损，如果是，则检测了α 2-AR的作用。对ERSNA增加的ARNA反应在SHR中受损，为2390 +/-460%.秒，而在Wistar-Kyoto大鼠中为6620 +/-1690%.秒。6250 pmol/L去甲肾上腺素（NE）不能改变SHR肾盂P物质的释放，但在Wistar-Kyoto大鼠中，250 pmol/L NE可增加肾盂P物质的释放，从5.7 ± 0.7 pg/min增加到12.5 ± 1.3 pg/min。肾盂给予α（2）-AR拮抗剂rauwolscine可增强ERSNA诱导的ARNA增加，4170 ± 900%.s，而在Wistar-Kyoto大鼠中没有。在萝芙木碱存在下，250 pmol/L NE增加SHR骨盆P物质释放，从5.2 ± 0.3 pg/min增加到11.2 ± 0.8 pg/min。由于血管紧张素II抑制SHR肾机械感觉神经的激活，我们研究了氯沙坦是否改善ERSNA诱导的ARNA反应。Losartan对SHR的ARNA反应或NE诱导的P物质增加无影响。然而，氯沙坦+萝芙木碱导致进一步增强的反应性的肾感觉神经增加ERSNA和NE在SHR，但不是在WKY。我们的结论是，肾脏α（2）-AR和血管紧张素II 1型受体的激活增加有助于在SHR ERSNA和ARNA之间的相互作用受损。（高血压。2011;57[第2部分]：640-647。
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 alpha(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 alpha(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 alpha(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 alpha(2)-ARs and angiotensin II type 1 receptors contributes to the impaired interaction between ERSNA and ARNA in SHR. (Hypertension. 2011;57[part 2]:640-647.)