scholarly journals Neonatal programming by immunological challenge: effects on ovarian function in the adult rat

Reproduction ◽  
2011 ◽  
Vol 141 (2) ◽  
pp. 241-248 ◽  
Author(s):  
Xue-Qing Wu ◽  
Xiao-Feng Li ◽  
Bilu Ye ◽  
Neha Popat ◽  
Stuart R Milligan ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ovarian Function ◽  
Pulse Generator ◽  
Female Rats ◽  
Neonatal Exposure ◽  
Inhibitory Influence ◽  
Nerve Activity ◽  
Adult Rats ◽  
Theca Interna

Neonatal exposure to an immunological challenge (lipopolysaccharide, LPS) increases the activity of hypothalamo-pituitary–adrenal axis and sensitises the GNRH pulse generator to the inhibitory influence of stress in adult rats. We investigated the effects of neonatal exposure to LPS on various reproductive parameters during puberty and into adulthood in female rats. LPS (50 μg/kg, i.p.) or saline was administered on postnatal days 3 and 5. Vaginal opening was recorded, and oestrous cyclicity was monitored immediately post puberty and again at 8–9 weeks of age. At 10 weeks of age, the ovaries were removed and the number of follicles was counted, together with the thickness of the theca interna of the largest antral follicles. Ovarian sympathetic nerve activity was assessed immunohistochemically by measurement of the levels of ovarian low-affinity receptor of nerve growth factor (p75NGFR). In rats exposed to LPS in early life, there was a significant delay in puberty and disruption of oestrous cyclicity immediately post puberty, which persisted into adulthood. The follicle reserve was decreased, the thickness of the theca interna increased and the expression profile of ovarian p75NGFR increased in the neonatal LPS-treated animals. These data suggest that exposure to LPS during early neonatal life can have long-term dysfunctional effects on the female reproductive system, which might involve, at least in part, increased ovarian sympathetic nerve activity.

Effect of vasopressin on baroreflex control of lumbar sympathetic nerve activity and hindquarter resistance

1996 ◽  
Vol 270 (6) ◽  
pp. H1963-H1971 ◽  
Author(s):  
D. A. Scheuer ◽  
V. S. Bishop
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Area Postrema ◽  
Resistance Index ◽  
Inhibitory Influence ◽  
Nerve Activity ◽  
Baroreflex Control

Arginine vasopressin (AVP) has been shown to increase the inhibitory influence of the baroreflex on sympathetic nerve activity by a mechanism involving receptors located in the area postrema. The purpose of these experiments was to study the functional effect of this action of AVP by testing the hypothesis that AVP can buffer its own vasoconstrictor effect by facilitating baroreflex-mediated withdrawal of sympathetic nerve activity. Specifically, we determined 1) if AVP can attenuate increases in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine, and 2) whether the effects of AVP on vascular resistance are associated with appropriate corresponding changes in lumbar sympathetic nerve activity (LSNA). In pentobarbital-anesthetized New Zealand White rabbits the baroreflex was stimulated by phenylephrine-induced elevations in arterial pressure. Baroreflex-mediated changes in heart rate (HR), calculated hindquarter vascular resistance index (R), and LSNA were determined during the simultaneous intravertebral infusion of AVP (0, 0.5, or 1.0 ng.kg-1, min-1). Intravertebral infusion of AVP alone had no effect on resting mean arterial pressure (MAP) but reduced baseline values for LSNA and HR. Intravenous infusion of phenylephrine alone produced dose-dependent increases in MAP and R and decreases in LSNA and HR. The simultaneous infusion of AVP (0.5 or 1.0 ng.kg-1 min-1) and phenylephrine (1.25, 2.5, 5.0, 7.5, and 10.0 micrograms.kg-1.min-1) had no effect on the increase in MAP but attenuated the increases in R and facilitated the reductions in LSNA at all doses of phenylephrine. The higher dose of AVP also enhanced the phenylephrine-induced reductions in HR. In contrast, the intravenous infusion of AVP (1.0 ng.kg-1.min-1) did not alter baroreflex-mediated changes in R, LSNA, or HR. Therefore, we conclude that the action of AVP to increase baroreflex-mediated sympathoinhibition results in an attenuated rise in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine.

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.

Gender difference in cardiopulmonary reflex inhibition of sympathetic nerve activity

1994 ◽  
Vol 267 (4) ◽  
pp. H1537-H1543 ◽  
Author(s):  
T. J. Scislo ◽  
S. E. DiCarlo
Keyword(s):  
Sympathetic Nerve ◽  
Left Atrial ◽  
Sympathetic Nerve Activity ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Female Rats ◽  
Reflex Inhibition ◽  
Nerve Activity ◽  
Cardiopulmonary Receptors ◽  
Alpha Chloralose

We tested the hypothesis that reflex responses to mechanical [increase in left atrial pressure (LAP) 0-25 mmHg] and chemical stimulation [left atrial injection of phenylbiguanide (PBG), 0.5-10 mg/kg] of cardiopulmonary receptors are greater in female (n = 9; 335 +/- 9 g) than in male (n = 10; 558 +/- 23 g) age-matched rats. Anesthetized (500 mg/kg urethan and 80 mg/kg alpha-chloralose), tracheotomized, and artificially ventilated (100% oxygen), sinoaortic-denervated animals were instrumented with left atrial, femoral venous, and arterial catheters and a Tygon occluder around the ascending aorta. Reflex inhibition of lumbar sympathetic nerve activity (LSNA) vs. LAP and dose PBG was higher in female rats. A two-way analysis of variance revealed a significant gender effect, males vs. females (P = 0.023), and a significant gender x dose interaction (P < 0.001) for LSNA vs. LAP. There was also a significant gender x dose interaction (P < 0.001) for LSNA vs. PBG. However, there was no influence of gender on the reflex inhibition of mean arterial pressure (P = 0.751) or heart rate (P = 0.561). These responses were associated with a higher left ventricular weight-to-body weight ratio in females (2.14 +/- 0.06 vs. 1.95 +/- 0.07 g/kg, P = 0.039).

scholarly journals Augmented Respiratory–Sympathetic Coupling and Hemodynamic Response to Acute Mild Hypoxia in Female Rodents With Chronic Kidney Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Manash Saha ◽  
Qi-Jian Sun ◽  
Cara M. Hildreth ◽  
Peter G. R. Burke ◽  
Jacqueline K. Phillips
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Area Under The Curve ◽  
Female Rats ◽  
Nerve Activity ◽  
Mild Hypoxia

Carotid body feedback and hypoxia may serve to enhance respiratory–sympathetic nerve coupling (respSNA) and act as a driver of increased blood pressure. Using the Lewis polycystic kidney (LPK) rat model of chronic kidney disease, we examined respSNA in adult female rodents with CKD and their response to acute hypoxia or hypercapnia compared to Lewis control animals. Under urethane anesthesia, phrenic nerve activity, splanchnic sympathetic nerve activity (sSNA), and renal sympathetic nerve activity (rSNA) were recorded under baseline conditions and during mild hypoxic or hypercapnic challenges. At baseline, tonic SNA and blood pressure were greater in female LPK rats versus Lewis rats (all P &lt; 0.05) and respSNA was at least two-fold larger [area under the curve (AUC), sSNA: 7.8 ± 1.1 vs. 3.4 ± 0.7 μV s, rSNA: 11.5 ± 3 vs. 4.8 ± 0.7 μV s, LPK vs. Lewis, both P &lt; 0.05]. Mild hypoxia produced a larger pressure response in LPK [Δ mean arterial pressure (MAP) 30 ± 6 vs. 12 ± 6 mmHg] and augmented respSNA (ΔAUC, sSNA: 8.9 ± 3.4 vs. 2 ± 0.7 μV s, rSNA: 6.1 ± 1.2 vs. 3.1 ± 0.7 μV s, LPK vs. Lewis, all P ≤ 0.05). In contrast, central chemoreceptor stimulation produced comparable changes in blood pressure and respSNA (ΔMAP 13 ± 3 vs. 9 ± 5 mmHg; respSNA ΔAUC, sSNA: 2.5 ± 1 vs. 1.3 ± 0.7 μV s, rSNA: 4.2 ± 0.9 vs. 3.5 ± 1.4 μV s, LPK vs. Lewis, all P &gt; 0.05). These results demonstrate that female rats with CKD exhibit heightened respSNA coupling at baseline that is further augmented by mild hypoxia, and not by hypercapnia. This mechanism may be a contributing driver of hypertension in this animal model of CKD.

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