Leenen F H, Klement G, Yuan B
Hypertension Unit, University of Ottawa Heart Institute, Canada.
J Hypertens. 1992 Sep;10(9):929-37.
To determine in vivo whether in young spontaneously hypertensive rats (SHR) dietary sodium restriction decreases adrenergic transmitter release from the sympathetic nerve terminal.
Dietary sodium restriction was initiated in young and mature SHR and Wistar-Kyoto (WKY) rats, and subsequently changes in pressor responsiveness to norepinephrine and to the indirectly acting sympathomimetic tyramine were determined in relation to their effects upon plasma catecholamines.
In young SHR sodium restriction for 3-6 weeks prevented the development of hypertension, whereas in mature SHR sodium restriction did not affect blood pressure. Sodium restriction caused modest decreases in pressor responsiveness to the exogenous alpha-agonist, not different in young and mature SHR compared with WKY rats. In contrast, sodium restriction markedly inhibited pressor-responses to tyramine in young SHR and WKY rats, but not at all in mature rats. Tyramine increased plasma norepinephrine 5-10-fold. However, sodium restriction did not affect this response. The pressor response to tyramine was related to increases in total peripheral resistance, with minimal changes in cardiac output, and could be blocked by alpha 1-receptor blockade in rats on either control or low-sodium diets.
These results show that sodium restriction causes only a small decrease in the pressor response to norepinephrine, but a more marked inhibition of the pressor response to tyramine in young SHR and WKY rats without affecting the plasma norepinephrine response to tyramine. These results suggest that dietary sodium can indeed affect presynaptic functions in vivo, but that plasma norepinephrine responses to tyramine may not reflect changes in arterial norepinephrine release, or that sodium restriction affects a co-transmitter rather than norepinephrine release per se.
确定在年轻的自发性高血压大鼠(SHR)体内,饮食中限制钠的摄入是否会减少交感神经末梢肾上腺素能递质的释放。
对年轻和成熟的SHR以及Wistar-Kyoto(WKY)大鼠开始进行饮食中钠的限制,随后根据其对血浆儿茶酚胺的影响,确定对去甲肾上腺素和间接作用的拟交感神经药酪胺的升压反应性变化。
在年轻的SHR中,限制钠摄入3 - 6周可预防高血压的发展,而在成熟的SHR中,限制钠摄入对血压无影响。限制钠摄入使对外源性α - 激动剂的升压反应性适度降低,与WKY大鼠相比,年轻和成熟的SHR中此反应无差异。相反,限制钠摄入显著抑制了年轻SHR和WKY大鼠对酪胺的升压反应,但在成熟大鼠中完全没有抑制作用。酪胺使血浆去甲肾上腺素增加5 - 10倍。然而,限制钠摄入并未影响此反应。对酪胺的升压反应与总外周阻力增加有关,心输出量变化最小,并且在对照饮食或低钠饮食的大鼠中,α1受体阻断可阻断此反应。
这些结果表明,限制钠摄入仅使对去甲肾上腺素的升压反应略有降低,但在年轻的SHR和WKY大鼠中更显著地抑制了对酪胺的升压反应,而不影响血浆去甲肾上腺素对酪胺的反应。这些结果表明,饮食中的钠确实可以在体内影响突触前功能,但血浆去甲肾上腺素对酪胺的反应可能不反映动脉去甲肾上腺素的释放变化,或者限制钠摄入影响的是一种共递质而非去甲肾上腺素本身的释放。