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首页> 外文期刊>Journal of Functional Foods >In vivo antihypertensive mechanism of lactoferrin-derived peptides: Reversion of angiotensin I-and angiotensin II-induced hypertension in Wistar rats
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In vivo antihypertensive mechanism of lactoferrin-derived peptides: Reversion of angiotensin I-and angiotensin II-induced hypertension in Wistar rats

机译:乳铁蛋白衍生肽的体内降压机制:Wistar大鼠中血管紧张素I和血管紧张素II诱导的高血压的逆转

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Novel peptides with antihypertensive effects in SHR rats have previously been identified in lactoferrin (LP) hydrolysates. To investigate their in vivo antihypertensive mechanism, we have assessed the blood pressure lowering effects of two of these LF-derived peptides (RPYL and DPYKLRP) in Wistar rats subjected to either angiotensin I- or angiotensin II-induced hypertension. Blood pressure was measured by the tail-cuff method, hypertension was induced by subcutaneous infusion of angiotensins, and then captopril, valsartan or LF-derived peptides orally administered. Angiotensin I- and angiotensin II-induced hypertension were reversed by captopril and valsartan, respectively. RPYL and DPYKLRP reversed angiotensin I-induced hypertension, while DPYKLRP but not RPYL produced a modest reversion of angiotensin II-elicited hypertension. Neither RPYL nor DPYKLRP modified normotension. Thus, in vivo ACE inhibition is involved in the antihypertensive effects of LF-derived peptides like RPYL and DPYKLRP, while inhibition of AT(1) receptor-mediated vasoconstriction plays a less relevant role. (C) 2015 Elsevier Ltd. All rights reserved.
机译:先前已在乳铁蛋白(LP)水解物中鉴定出了在SHR大鼠中具有降压作用的新型肽。为了研究它们的体内降压机制,我们评估了这两种LF衍生肽(RPYL和DPYKLRP)在接受血管紧张素I或血管紧张素II诱导的高血压的Wistar大鼠中的降血压作用。通过尾套法测量血压,皮下注射血管紧张素诱导高血压,然后口服卡托普利,缬沙坦或LF衍生肽。卡托普利和缬沙坦分别逆转了血管紧张素I和血管紧张素II引起的高血压。 RPYL和DPYKLRP逆转了血管紧张素I引起的高血压,而DPYKLRP却未逆转RPYL产生了适度的血管紧张素II引起的高血压逆转。 RPYL和DPYKLRP均未改变血压。因此,体内ACE抑制与LF衍生肽(如RPYL和DPYKLRP)的抗高血压作用有关,而对AT(1)受体介导的血管收缩的抑制作用则不那么重要。 (C)2015 Elsevier Ltd.保留所有权利。

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