AIM: To investigate the possible role of hypothalamic kisspeptin in the regulation of body fluid metabolism and maintenance of internal homeostasis. METHODS: Natriuresis and diuresis were induced by blood volume expansion (VE) in anesthetized male rats and kisspeptin-10 was intracerebroventricularly (icv) administered. Radioimmunoassay (RIA) was used to measure the plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations during the VE. The mediation of the renal sympathetic nerve was also investigated in rats with bilateral renal sympathetic denervation. RESULTS: The increased urine flow and sodium excretion induced by VE were significantly inhibited by icv injection of 5 nmol kisspeptin-10 (P<0.05), which peaked 20 min after the decrease in VE. The mean arterial blood pressure and heart rate did not change during the experiment. Plasma AVP concentrations were significantly increased 20 min after icv injection of 5 nmol kisspeptin-10 during VE (P<0.05), while pretreatment with 5 nmol kisspeptin-10 did not significantly change plasma ANP concentrations. Furthermore, pretreatment with 5 nmol kisspeptin-10 could significantly inhibit VE-induced natriuresis and diuresis in renal sympathetic denervated rats (P<0.05). CONCLUSION: Central administration of kisspeptin-10 inhibited VE-induced natriuresis and diuresis. This effect was likely mediated by increasing AVP release independent of plasma ANP concentration and renal sympathetic nerve activity.
AIM: To investigate the possible role of hypothalamic kisspeptin in the regulation of body fluid metabolism and maintenance of internal homeostasis. METHODS: Natriuresis and diuresis were induced by blood volume expansion (VE) in anesthetized male rats and kisspeptin-10 was intracerebroventricularly (icv) administered. Radioimmunoassay (RIA) was used to measure the plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations during the VE. The mediation of the renal sympathetic nerve was also investigated in rats with bilateral renal sympathetic denervation. RESULTS: The increased urine flow and sodium excretion induced by VE were significantly inhibited by icv injection of 5 nmol kisspeptin-10 (P<0.05), which peaked 20 min after the decrease in VE. The mean arterial blood pressure and heart rate did not change during the experiment. Plasma AVP concentrations were significantly increased 20 min after icv injection of 5 nmol kisspeptin-10 during VE (P<0.05), while pretreatment with 5 nmol kisspeptin-10 did not significantly change plasma ANP concentrations. Furthermore, pretreatment with 5 nmol kisspeptin-10 could significantly inhibit VE-induced natriuresis and diuresis in renal sympathetic denervated rats (P<0.05). CONCLUSION: Central administration of kisspeptin-10 inhibited VE-induced natriuresis and diuresis. This effect was likely mediated by increasing AVP release independent of plasma ANP concentration and renal sympathetic nerve activity.
Authors: Sophie Messager; Emmanouella E Chatzidaki; Dan Ma; Alan G Hendrick; Dirk Zahn; John Dixon; Rosemary R Thresher; Isabelle Malinge; Didier Lomet; Mark B L Carlton; William H Colledge; Alain Caraty; Samuel A J R Aparicio Journal: Proc Natl Acad Sci U S A Date: 2005-01-21 Impact factor: 11.205
Authors: José Antunes-Rodrigues; Margaret de Castro; Lucila L K Elias; Marcelo M Valença; Samuel M McCann Journal: Physiol Rev Date: 2004-01 Impact factor: 37.312
Authors: Alexander J Seymour; Victoria Scott; Rachael A Augustine; Gregory T Bouwer; Rebecca E Campbell; Colin H Brown Journal: J Physiol Date: 2016-10-02 Impact factor: 5.182