Improvement in baroreflex control of renal sympathetic nerve activity in obese Sprague Dawley rats following immunosuppression

2017 ◽  
Vol 221 (4) ◽  
pp. 250-265 ◽  
Author(s):  
S. A. Khan ◽  
M. Z. A. Sattar ◽  
N. A. Abdullah ◽  
H. A. Rathore ◽  
A. Ahmad ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Sprague Dawley Rats ◽  
Renal Sympathetic

Glucocorticoids modulate baroreflex control of renal sympathetic nerve activity

2001 ◽  
Vol 280 (5) ◽  
pp. R1440-R1449 ◽  
Author(s):  
Deborah A. Scheuer ◽  
Steven W. Mifflin
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Gain Coefficient ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Baroreflex Function ◽  
Renal Sympathetic

Experiments were performed to determine the effects of glucocorticoids on arterial baroreceptor reflex control of renal sympathetic nerve activity (RSNA). Intravenous infusions of phenylephrine and nitroprusside were used to produce graded changes in arterial pressure (AP) in Inactin-anesthetized male Sprague-Dawley rats. Baroreflex control of RSNA was determined during a baseline period and 2 and 3 h after administration of the glucocorticoid type II receptor antagonist Mifepristone (30 mg/kg sc) or vehicle (oil). Corticosterone (cort) treatment (100 mg cort pellet sc for 2–3 wk) increased baseline AP from 115 ± 2 to 128 ± 1 mmHg. Cort treatment also decreased the gain coefficient and increased the midpoint of the baroreflex curve. Treatment of cort rats with Mifepristone decreased AP within 2 h and increased the gain coefficient and decreased the midpoint of the baroreflex function curve back toward values measured in control rats. Mifepristone altered the baroreflex function curve even when AP was maintained at baseline levels. Therefore, these data demonstrate for the first time that glucocorticoids can modulate baroreflex control of RSNA by a mechanism that is, in part, independent of changes in AP.

Baroreflex control of renal sympathetic nerve activity during air-jet stress in rats

2007 ◽  
Vol 292 (1) ◽  
pp. R362-R367 ◽  
Author(s):  
Roy Kanbar ◽  
Valérie Oréa ◽  
Christian Barrès ◽  
Claude Julien
Keyword(s):  
Emotional Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sigmoid Function ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Air Jet ◽  
Renal Sympathetic

The effects of acute emotional stress on the sympathetic component of the arterial baroreceptor reflex have not yet been described in conscious animals and humans. Arterial pressure (AP) and renal sympathetic nerve activity (RSNA) were simultaneously recorded in 11 conscious rats before and during exposure to a mild environmental stressor (jet of air). Baroreflex function curves relating AP and RSNA were constructed by fitting a sigmoid function to RSNA and AP measured during sequential nitroprusside and phenylephrine administrations. Stress increased mean AP from 112 ± 2 to 124 ± 2 mmHg, heart rate from 381 ± 10 to 438 ± 18 beats/min, and RSNA from 0.80 ± 0.14 to 1.49 ± 0.23 μV. The RSNA-AP relationship was shifted toward higher AP values, and its maximum gain was significantly ( P < 0.01) increased from 9.0 ± 1.3 to 16.2 ± 2.1 normalized units (NU)/mmHg. The latter effect was secondary to an increase ( P < 0.01) in the range of the RSNA variation from 285 ± 33 to 619 ± 59 NU. In addition, the operating range of the reflex was increased ( P < 0.01) from 34 ± 2 to 41 ± 3 mmHg. The present study indicates that in rats, the baroreflex control of RSNA is sensitized and operates over a larger range during emotional stress, which suggests that renal vascular tone, and possibly AP, are very efficiently controlled by the sympathetic nervous system under this condition.

scholarly journals Baroreflex control of renal sympathetic nerve activity in early heart failure assessed by the sequence method

2017 ◽  
Vol 595 (11) ◽  
pp. 3319-3330 ◽  
Author(s):  
Renata Maria Lataro ◽  
Luiz Eduardo Virgilio Silva ◽  
Carlos Alberto Aguiar Silva ◽  
Helio Cesar Salgado ◽  
Rubens Fazan
Keyword(s):  
Heart Failure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Sequence Method ◽  
Renal Sympathetic

Baroreflex control of sympathetic nerve activity after elevations of pressure in conscious rabbits

1985 ◽  
Vol 248 (6) ◽  
pp. H827-H834 ◽  
Author(s):  
K. P. Undesser ◽  
J. Y. Pan ◽  
M. P. Lynn ◽  
V. S. Bishop
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Afferent Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Pressure Stimulus ◽  
Renal Sympathetic

The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.

Baroreflex control of lumbar and renal sympathetic nerve activity in conscious rats

2008 ◽  
Vol 295 (1) ◽  
pp. R8-R14 ◽  
Author(s):  
Roy Kanbar ◽  
Bruno Chapuis ◽  
Valérie Oréa ◽  
Christian Barrès ◽  
Claude Julien
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Baseline Period ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Renal Sympathetic Nerve ◽  
Normalized Units ◽  
Renal Sympathetic

This study compared the baroreflex control of lumbar and renal sympathetic nerve activity (SNA) in conscious rats. Arterial pressure (AP) and lumbar and renal SNA were simultaneously recorded in six freely behaving rats. Pharmacological estimates of lumbar and renal sympathetic baroreflex sensitivity (BRS) were obtained by means of the sequential intravenous administration of sodium nitroprusside and phenylephrine. Sympathetic BRS was significantly ( P < 0.05) lower for lumbar [3.0 ± 0.4 normalized units (NU)/mmHg] than for renal (7.6 ± 0.6 NU/mmHg) SNA. During a 219-min baseline period, spontaneous lumbar and renal BRS were continuously assessed by computing the gain of the transfer function relating AP and SNA at heart rate frequency over consecutive 61.4-s periods. The transfer gain was considered only when coherence between AP and SNA significantly differed from zero, which was verified in 99 ± 1 and 96 ± 3% of cases for lumbar and renal SNA, respectively. When averaged over the entire baseline period, spontaneous BRS was significantly ( P < 0.05) lower for lumbar (1.3 ± 0.2 NU/mmHg) than for renal (2.3 ± 0.3 NU/mmHg) SNA. For both SNAs, spontaneous BRS showed marked fluctuations (variation coefficients were 26 ± 2 and 28 ± 2% for lumbar and renal SNA, respectively). These fluctuations were positively correlated in five of six rats ( R = 0.44 ± 0.06; n = 204 ± 8; P < 0.0001). We conclude that in conscious rats, the baroreflex control of lumbar and renal SNA shows quantitative differences but is modulated in a mostly coordinated way.

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.

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