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首页> 外文期刊>Metabolism: Clinical and Experimental >Role of gamma melanocyte-stimulating hormone-renal melanocortin 3 receptor system in blood pressure regulation in salt-resistant and salt-sensitive rats.
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Role of gamma melanocyte-stimulating hormone-renal melanocortin 3 receptor system in blood pressure regulation in salt-resistant and salt-sensitive rats.

机译：γ刺激黑素细胞的激素-肾黑素皮质素3受体系统在耐盐和盐敏感性大鼠的血压调节中的作用。

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摘要

Melanocortin 3 receptor (MC3-R) has high affinity and specificity to gamma melanocyte-stimulating hormone (gammaMSH), a natriuretic peptide involved in regulation of blood pressure (BP) and sodium excretion. Recent studies showing increased MC3-R expression and elevated plasma gammaMSH in normal rats fed a high-salt diet support the role of this system in sodium homeostasis. We hypothesized that dysregulation of MC3-R response to dietary salt may contribute to salt retention and BP elevation in salt-sensitive hypertension. We examined renal MC3-R expression, plasma gammaMSH concentration, and response to MC3-R agonist and antagonist in Dahl salt-sensitive (DSS) and Dahl salt-resistant (DSR) rats fed high-salt (8%) or low-salt (0.07%) diets for 3 weeks. Consumption of high-salt diet significantly increased BP in the DSS but not the DSR group. High-salt diet led to a 5-fold increase in plasma gammaMSH and a 2-fold increase in renal MC3-R in DSR rats. Plasma gammaMSH and renal MC3-R abundance in DSS rats were maximally elevated on low-salt diet and remained unchanged on high-salt diet. Administration of MC3-R agonist melanotan II significantly lowered BP and raised fractional Na excretion in the DSR but not the DSS rats consuming high-salt diet. In contrast, MC3-R antagonist SHU9119 significantly raised BP and lowered fractional Na excretion in both groups. Thus, the data suggest that gammaMSH-renal MC3-R pathway is activated and appears to be biologically functional in the DSS rats.
机译：黑皮质素3受体（MC3-R）对伽马黑素细胞刺激激素（gammaMSH）具有高亲和力和特异性，伽马黑素刺激激素是一种参与调节血压（BP）和钠排泄的利钠肽。最近的研究表明，高盐饮食的正常大鼠中MC3-R表达增加，血浆gammaMSH升高，支持了该系统在钠稳态中的作用。我们假设在盐敏感性高血压中，MC3-R对膳食盐反应的失调可能有助于盐分滞留和血压升高。我们检查了高盐（8％）或低盐的Dahl盐敏感性（DSS）和Dahl盐抗性（DSR）大鼠的肾脏MC3-R表达，血浆gammaMSH浓度以及对MC3-R激动剂和拮抗剂的反应（0.07％）节食3周。摄入高盐饮食会显着增加DSS而不是DSR组的BP。高盐饮食导致DSR大鼠血浆gammaMSH增加5倍，肾脏MC3-R增加2倍。在低盐饮食中，DSS大鼠的血浆γMSH和肾MC3-R丰度最高，而在高盐饮食中则保持不变。施用MC3-R激动剂melanotan II可以显着降低DSR的BP并增加Na分数的排泄，但DSS大鼠不食用高盐饮食。相反，两组中的MC3-R拮抗剂SHU9119均可显着提高BP并降低部分Na排泄。因此，数据表明，γ-MSH-肾MC3-R途径被激活并且在DSS大鼠中似乎具有生物学功能。

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