Central administration of kisspeptin-10 inhibits natriuresis and diuresis induced by blood volume expansion in anesthetized male rats

Abstract

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.

Development of an excitatory kisspeptin projection to the oxytocin system in late pregnancy

“…kisspeptin has been shown to increase plasma vasopressin concentrations in male rats (Han et al . ; Ten et al . ), and to increase mEPSC frequency in vasopressin neurones in brain slices from male rats (Yokoyama et al .…”

“…I.C.V. kisspeptin has been shown to increase plasma vasopressin concentrations in male rats (Han et al 2010;Ten et al 2010), and to increase mEPSC frequency in vasopressin neurones in brain slices from male rats (Yokoyama et al 2014). While this might represent a sex difference in the regulation of vasopressin neurones by kisspeptin, it is possible that paraventricular nucleus vasopressin neurones respond differently than supraoptic nucleus oxytocin neurones to I.C.V.…”

The Role of Neurotransmitters in Protection against Amyloid-β Toxicity by KiSS-1 Overexpression in SH-SY5Y Neurons

“…The actions of KP peptides are thought to be mediated via activation of either GPR-54 or NPFF receptors. However, in vivo actions on the opioid system [ 12 , 13 ], oxytocin/vasopressin systems [ 4 , 14 , 15 ], neurotransmitter systems [ 16 , 17 ], activation of endogenous antioxidants [ 18 ], activation of nitric oxide [ 17 ], and possible activation of prostaglandin synthesis [ 19 ] have not been tested with GPR-54 or NPFF receptor antagonists.…”

Serotonin (5-HT) Activation of Immortalized Hypothalamic Neuronal Cells Through the 5-HT1B Serotonin Receptor

“…Interestingly, the mHypoA-2/30 neurons have also been shown to express receptors for ghrelin, NPY, and kisspeptin (24). In rodents, PVN administration of ghrelin and NPY elicits increases in food intake (59,60), whereas kisspeptin has been demonstrated to activate the HPA axis and control fluid metabolism in part through regulation of vasopressin expression and release in the PVN (61,62). Having established the mHypoA-2/30 cell line as a representative PVN model, these neurons can potentially be used to determine the cellular events underlying action of these neuropeptides in the PVN.…”