scholarly journals Insulin increases sympathetic nerve activity in part by suppression of tonic inhibitory neuropeptide Y inputs into the paraventricular nucleus in female rats

2016 ◽  
Vol 311 (1) ◽  
pp. R97-R103 ◽  
Author(s):  
Priscila A. Cassaglia ◽  
Zhigang Shi ◽  
Virginia L. Brooks
Keyword(s):  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Female Rats ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Melanocyte Stimulating Hormone ◽  
Y1 Receptors ◽  
Type 3

Following binding to receptors in the arcuate nucleus (ArcN), insulin increases sympathetic nerve activity (SNA) and baroreflex control of SNA via a pathway that includes the paraventricular nucleus of the hypothalamus (PVN). Previous studies in males indicate that the sympathoexcitatory response is mediated by α-melanocyte stimulating hormone (α-MSH), which binds to PVN melanocortin type 3/4 receptors (MC3/4R). The present study was conducted in α-chloralose-anesthetized female rats to test the hypothesis that suppression of inhibitory neuropeptide Y (NPY) inputs to the PVN is also involved. In support of this, blockade of PVN NPY Y1 receptors with BIBO 3304 (NPY1x), ArcN insulin nanoinjections, and PVN NPY1x followed by ArcN insulin each increased lumbar SNA (LSNA) and its baroreflex regulation similarly. Moreover, prior PVN injections of NPY blocked the sympathoexcitatory effects of ArcN insulin. Finally, PVN nanoinjections of the MC3/4R inhibitor SHU9119 prevented both the acute (15 min) and longer, more slowly developing (60 min), increases in LSNA in response to ArcN insulin. In conclusion, in females, ArcN insulin increases LSNA, in part, by suppressing tonic PVN NPY inhibition, which unmasks excitatory α-MSH drive of LSNA. Moreover, the steadily increasing rise in LSNA induced by ArcN insulin is also dependent on PVN MC3/4R.

scholarly journals Comparison of high-fat style diet-induced dysregulation of baroreflex control of renal sympathetic nerve activity in intact and ovariectomized female rats

2020 ◽  
Vol 245 (9) ◽  
pp. 761-776
Author(s):  
Yamuna Sucedaram ◽  
Edward James Johns ◽  
Ruby Husain ◽  
Munavvar Abdul Sattar ◽  
Mohammed Abdulla ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Ovarian Hormones ◽  
Female Rats ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The present study compared high-fat style diet (HFSD)-induced renal nerve-dependent dysregulation of the baroreflex control of renal sympathetic nerve activity (RSNA) in ovary-intact and ovariectomized (OVX) rats. Female rats received a normal diet (ND) or a HFSD for 10 weeks prior to the acute study. The rats were anesthetized; RSNA and heart rate (HR) were measured. Acute bilateral renal denervation was performed, and baroreflex gain curves were constructed from the baroreflex changes in RSNA to vasopressor and vasodepressor drugs. Cardiopulmonary baroreflex control of RSNA was assessed by acute saline volume expansion (VE). Mean blood pressure was elevated in the OVX-HFSD rats compared to the HFSD group reaching significance on week 6 of the experimental study (P < 0.01). Adiposity index and creatinine clearance were significantly greater in all HFSD rats compared to their ND counterparts. Fractional excretion of sodium rose initially in all HFSD rats but was normalized towards the end of the study although absolute sodium excretion remained high. In the acute study, baroreflex gain curve sensitivity (A2) of RSNA was similarly decreased in both the HFSD and OVX-HFSD rats by 88% (P < 0.005) and 94% (P < 0.001) respectively compared to their control counterparts, but was normalized following bilateral renal denervation. VE-reduced RSNA in ND and OVX-ND rats by 55% and 52% (both P < 0.001) respectively, but did not alter RSNA in both HFSD and OVX-HFSD female rats. Following bilateral renal denervation, HFSD and OVX-HFSD rats exhibited 37% (P < 0.01) and 24% (P < 0.01) reduction in RSNA respectively. These findings demonstrate that although obesity-induced impairment of baroreflex control of RSNA occurred similarly in HFSD and OVX-HFSD rats, mean blood pressure was increased only in the ovarian hormones deprived-group suggesting that ovarian hormones could have modulatory role on other mechanisms that regulate blood pressure in female obesity. Impact statement Over activation of renal sensory nerve in obesity blunts the normal regulation of renal sympathetic nerve activity. To date, there is no investigation that has been carried out on baroreflex regulation of renal sympathetic nerve activity in obese ovarian hormones deprived rat model, and the effect of renal denervation on the baroreflex regulation of renal sympathetic nerve activity. Thus, we investigated the role of renal innervation on baroreflex regulation of renal sympathetic nerve activity in obese intact and ovariectomized female rats. Our data demonstrated that in obese states, the impaired baroreflex control is indistinguishable between ovarian hormones deprived and non-deprived states. This study will be of substantial interest to researchers working on the impact of diet-induced hypertension in pre- and postmenopausal women. This study provides insight into health risks amongst obese women regardless of their ovarian hormonal status and may be integrated in preventive health strategies.

scholarly journals Neuropeptide Y acts in the paraventricular nucleus to suppress sympathetic nerve activity and its baroreflex regulation

2014 ◽  
Vol 592 (7) ◽  
pp. 1655-1675 ◽  
Author(s):  
Priscila A. Cassaglia ◽  
Zhigang Shi ◽  
Baoxin Li ◽  
Wagner L. Reis ◽  
Nicholas M. Clute-Reinig ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity
Sign in / Sign up

Export Citation Format

Share Document