Central administration of kisspeptin-10 inhibits water and sodium excretion of anesthetized male rats and the involvement of arginine vasopressin.
Ten. Shi-Chao SC; Gu. Shou-Yong SY; Niu. Yun-Fei YF; An. Xiao-Fei XF; Yan. Ming M; He. Ming M
Key Findings
- Central (icv) kisspeptin-10 reduced urine flow and sodium excretion in anesthetized male rats
- Plasma AVP levels rose after kisspeptin-10 injection, while ANP levels stayed the same
- The reduction in urine and sodium persisted even after renal sympathetic nerves were cut, indicating a nerve‑independent mechanism
Practical Outcomes
- For biohackers, the study shows kisspeptin can influence fluid balance via vasopressin, but it requires direct brain delivery, which isn’t feasible outside a lab. Oral or peripheral kisspeptin supplements are unlikely to replicate these effects, so the finding is more of scientific interest than a usable protocol for improving hydration or electrolyte management.
Summary
In rats, giving kisspeptin-10 directly into the brain lowered how much urine they made and how much sodium they excreted, mainly because it raised the hormone vasopressin (AVP) in the blood. This effect didn’t depend on the kidney’s sympathetic nerves or on another hormone called ANP, and it didn’t change blood pressure, heart rate, or potassium loss.
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.
Study Information
pubmed
2010
2010-08-01T00:00:00.000Z
10.3109/07435801003769995
19
19