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Intestinal dopaminergic activity in obese and lean Zucker rats: response to high salt intake.

机译:肥胖和瘦的Zucker大鼠的肠道多巴胺能活动:对高盐摄入的反应。

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The present study examined intestinal dopaminergic activity and its response to high salt (HS, 1% NaCl over a period of 24 hours) intake in obese (OZR) and lean Zucker rats (LZR). The basal Na+,K+-ATPase activity (nmol Pi/mg protein/min) in the jejunum of OZR was higher than in LZR on normal salt (NS) (OZR-NS = 111.3 +/- 6.0 vs. LZR-NS = 88.0 +/- 8.3). With the increase in salt intake, the basal Na+,K+-ATPase activity significantly increased in both animals (OZR-HS = 145.9 +/- 11.8; LZR-HS = 108.8 +/- 6.7). SKF 38393 (10 nM), a specific D1-like dopamine receptor agonist, inhibited the jejunal Na+,K+-ATPase activity in OZR on HS intake, but failed to inhibit enzyme activity in OZR on NS intake and LZR on NS and HS intakes. The aromatic L-amino acid decarboxylase (AADC) activity in OZR was lower than in LZR on NS intake. The HS intake increased AADC activity in OZR, but not in LZR. During the NS intake the jejunal monoamine oxidase (MAO) activity in OZR was similar to that in LZR. The HS intake significantly decreased MAO activity in both OZR and LZR. The jejunal COMT activity in OZR was higher than in LZR on NS intake. The HS intake reduced COMT activity in OZR but not LZR. It is concluded that inhibition of jejunal Na+,K+-ATPase activity through D1 dopamine receptors is dependent on salt intake in OZR, whereas in LZR, the enzyme failed to respond to the activation of D1 dopamine receptors irrespective of their salt intake.
机译:本研究检查了肥胖(OZR)和瘦Zucker大鼠(LZR)的肠道多巴胺能活性及其对高盐(HS,1%NaCl在24小时内)摄入的反应。 OZR空肠中的基础Na +,K + -ATPase活性(nmol Pi / mg蛋白/分钟)高于生理盐(NS)的LZR(OZR-NS = 111.3 +/- 6.0 vs. LZR-NS = 88.0 +/- 8.3)。随着盐摄入量的增加,两只动物的基础Na +,K + -ATPase活性均显着增加(OZR-HS = 145.9 +/- 11.8; LZR-HS = 108.8 +/- 6.7)。 SKF 38393(10 nM)是一种特定的D1类多巴胺受体激动剂,在HS摄入量时可抑制OZR中的空肠Na +,K + -ATPase活性,但在NS摄入量中却不能抑制OZR中的空肠Na +,K + -ATPase酶活性,而在NS和HS摄入量中则不能抑制LZR中的空肠Na +,K + -ATPase活性。摄入NS后,OZR中的芳香族L-氨基酸脱羧酶(AADC)活性低于LZR。 HS摄入增加了OZR中的AADC活性,但不增加LZR中的AADC活性。在NS摄取期间,OZR中的空肠单胺氧化酶(MAO)活性与LZR中的相似。 HS摄入显着降低了OZR和LZR中的MAO活性。摄入NS后,OZR的空肠COMT活性高于LZR。 HS摄入降低了OZR的COMT活性,但没有降低LZR。结论是,通过D1多巴胺受体抑制空肠Na +,K + -ATPase活性取决于OZR中的盐摄入量,而在LZR中,无论其盐摄入量如何,该酶均无法响应D1多巴胺受体的激活。

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