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Central administration of kisspeptin-10 inhibits water and sodium excretion of anesthetized male rats and the involvement of arginine vasopressin

Study · animal · Endocrine research · 2010 · DOI 10.3109/07435801003769995 · PMID 20712435

Plain-language summary

Paraphrased from the published abstract below — not a verdict on whether anything works.

This rat study examined effects of central (intracerebroventricular) administration of kisspeptin-10 on water and sodium excretion in anesthetized male rats, including the possible role of arginine vasopressin (AVP) and renal sympathetic nerves. Intracerebroventricular injection of 5 nmol kisspeptin-10 significantly decreased urine flow, sodium excretion, and free water clearance from 30 to 60 min post-injection (p < 0.05), and significantly increased plasma AVP at 30 min (p < 0.05), while plasma ANP, blood pressure, heart rate, and potassium excretion did not significantly change. The effect on urine flow and sodium excretion persisted after bilateral renal sympathetic denervation. The authors concluded central kisspeptin-10 inhibits sodium excretion and urine flow, likely mediated by increased plasma AVP and independent of plasma ANP or renal sympathetic nerve activity.

Abstract

To investigate the effect of hypothalamus kisspeptin on water and sodium excretion and the possible mechanism. The intracerebroventricular (icv) administration and radioimmunoassay were used to observe the effect of kisspeptin-10 on urine flow, sodium and potassium excretion, plasma arginine vasopressin (AVP), and atrial natriuretic peptide (ANP) concentrations in anesthetized male rats. The mediation of renal sympathetic nerve was also investigated by studies conducted on rats with bilateral renal sympathetic denervation. The urine flow, sodium excretion, and free water clearance decreased significantly by icv injection of 5 nmol kisspeptin-10 (p < 0.05) from 30 to 60 min post-injection. Meanwhile, plasma AVP concentrations increased significantly 30 min after the icv injection of 5 nmol kisspeptin-10 (p < 0.05), whereas the equal dose of kisspeptin-10 did not significantly change plasma ANP concentrations. The mean arterial blood pressure, heart rate, and potassium excretion did not significantly change during the experiment. Furthermore, pretreatment with 5 nmol kisspeptin-10 could still significantly decrease urine flow and sodium excretion in renal sympathetic denervated rats. Central administration of kisspeptin-10 could inhibit sodium excretion and urine flow in anesthetized male rats, which is probably mediated by increasing the plasma AVP concentration and is independent of plasma ANP concentration and renal sympathetic nerve activity.

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