scholarly journals Afferent renal denervation impairs baroreflex control of efferent renal sympathetic nerve activity

2008 ◽  
Vol 295 (6) ◽  
pp. R1882-R1890 ◽  
Author(s):  
Ulla C. Kopp ◽  
Susan Y. Jones ◽  
Gerald F. DiBona
Keyword(s):  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
High Sodium ◽  
Sodium Diet ◽  
Baroreflex Function ◽  
Transfer Function Gain ◽  
High Sodium Diet ◽  
Renal Sympathetic

Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which decreases ERSNA to prevent sodium retention. High-sodium diet enhances ARNA, suggesting an important role for ARNA in suppressing ERSNA during excess sodium intake. Mean arterial pressure (MAP) is elevated in afferent renal denervated by dorsal rhizotomy (DRX) rats fed high-sodium diet. We examined whether the increased MAP in DRX is due to impaired arterial baroreflex function. In DRX and sham DRX rats fed high-sodium diet, arterial baroreflex function was determined in conscious rats by intravenous nitroprusside and phenylephrine or calculation of transfer function gain from arterial pressure to ERSNA (spontaneous baroreflex sensitivity). Increasing MAP did not suppress ERSNA to the same extent in DRX as in sham DRX, −60 ± 4 vs. −77 ± 6%. Maximum gain, −4.22 ± 0.45 vs. −6.04 ± 0.90% ΔERSNA/mmHg, and the maximum value of instantaneous gain, −4.19 ± 0.45 vs. −6.04 ± 0.81% ΔERSNA/mmHg, were less in DRX than in sham DRX. Likewise, transfer function gain was lower in DRX than in sham DRX, 3.9 ± 0.2 vs. 6.1 ± 0.5 NU/mmHg. Air jet stress produced greater increases in ERSNA in DRX than in sham DRX, 35,000 ± 4,900 vs. 20,900 ± 3,410%·s (area under the curve). Likewise, the ERSNA responses to thermal cutaneous stimulation were greater in DRX than in sham DRX. These studies suggest impaired arterial baroreflex suppression of ERSNA in DRX fed high-sodium diet. There were no differences in arterial baroreflex function in DRX and sham DRX fed normal-sodium diet. Impaired arterial baroreflex function contributes to increased ERSNA, which would eventually lead to sodium retention and increased MAP in DRX rats fed high-sodium diet.

Effect of endogenous angiotensin II on renal nerve activity and its arterial baroreflex regulation

1996 ◽  
Vol 271 (2) ◽  
pp. R361-R367 ◽  
Author(s):  
G. F. DiBona ◽  
S. Y. Jones ◽  
L. L. Sawin
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
High Sodium ◽  
Sodium Diet ◽  
Renal Sympathetic Nerve ◽  
High Sodium Diet ◽  
Renal Sympathetic

To determine the effects of physiological alterations in endogenous angiotensin II (ANG II) activity on basal renal sympathetic nerve activity and its arterial baroreflex regulation, the effect of ANG II receptor (AT1) blockade with losartan was examined in conscious rats consuming low, normal, or high sodium diet that were instrumented for the simultaneous measurement of arterial pressure and renal sympathetic nerve activity. Intravenous losartan decreased arterial pressure in low (-27 +/- 4 mmHg) and normal (-15 +/- 2 mmHg) but not in high sodium diet rats (-5 +/- 2 mmHg). When arterial pressure had been restored to the prelosartan value with methoxamine infusion, renal sympathetic nerve activity was decreased in low (-27 +/- 4%) and normal (-20 +/- 3%) but not in high sodium diet rats (-5 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-8 +/- 2 mmHg) and normal (-7 +/- 2 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). Intracerebroventricular losartan did not significantly decrease arterial pressure but decreased renal sympathetic nerve activity in low (-28 +/- 5%) and normal (-20 +/- 4%) but not in high sodium diet rats (-2 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-7 +/- 2 mmHg) and normal (-5 +/- 1 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). These results indicate that physiological alterations in endogenous ANG II activity tonically influence basal levels of renal sympathetic nerve activity and its arterial baroreflex regulation.

Cardiac sympathetic afferent stimulation impairs baroreflex control of renal sympathetic nerve activity in rats

2004 ◽  
Vol 286 (5) ◽  
pp. H1706-H1711 ◽  
Author(s):  
Lie Gao ◽  
Zhen Zhu ◽  
Irving H. Zucker ◽  
Wei Wang
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Maximum Slope ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Renal Sympathetic ◽  
Stimulation Of

It is well known that cardiac sympathetic afferent reflexes contribute to increases in sympathetic outflow and that sympathetic activity can antagonize arterial baroreflex function. In this study, we tested the hypothesis that in normal rats, chemical and electrical stimulation of cardiac sympathetic afferents results in a decrease in the arterial baroreflex function by increasing sympathetic nerve activity. Under α-chloralose (40 mg/kg) and urethane (800 mg/kg ip) anesthesia, renal sympathetic nerve activity, mean arterial pressure, and heart rate were recorded. The arterial baroreceptor reflex was evaluated by infusion of nitroglycerin (25 μg iv) and phenylephrine (10 μg iv). Left ventricular epicardial application of capsaicin (0.4 μg in 2 μl) blunted arterial baroreflex function by 46% (maximum slope 3.5 ± 0.3 to 1.9 ± 0.2%/mmHg, P < 0.01). When the central end of the left cardiac sympathetic nerve was electrically stimulated (7 V, 1 ms, 20 Hz), the sensitivity of the arterial baroreflex was similarly decreased by 42% (maximum slope 3.2 ± 0.3 to 1.9 ± 0.4%/mmHg; P < 0.05). Pretreatment with intracerebroventricular injection of losartan (500 nmol in 1 μl of artificial cerebrospinal fluid) completely prevented the impairment of arterial baroreflex function induced by electrical stimulation of the central end of the left cardiac sympathetic nerve (maximum slope 3.6 ± 0.4 to 3.1 ± 0.5%/mmHg). These results suggest that the both chemical and electrical stimulation of the cardiac sympathetic afferents reduces arterial baroreflex sensitivity and the impairment of arterial baroreflex function induced by cardiac sympathetic afferent stimulation is mediated by central angiotensin type 1 receptors.

Effects of pregnancy and progesterone metabolites on arterial baroreflex in conscious rats

1997 ◽  
Vol 272 (3) ◽  
pp. R924-R934 ◽  
Author(s):  
S. Masilamani ◽  
C. M. Heesch
Keyword(s):  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Progesterone Metabolites ◽  
Progesterone Metabolite ◽  
In Pregnancy ◽  
Renal Sympathetic

Previous experiments in anesthetized rats suggested that sympathoexcitatory responses were attenuated in pregnant (P) rats. The major progesterone metabolite, 3alpha-hydroxy-dihydroprogesterone (3alpha-OH-DHP), is elevated in pregnancy and reportedly potentiates central gamma-aminobutyric acidergic mechanisms, whereas the 3beta-isomer (3beta-OH-DHP) is inactive. This study obtained baroreflex curves in conscious rats by recording reflex changes in renal sympathetic nerve activity (RSNA) and heart rate (HR) due to perturbations in mean arterial pressure (MAP) [i.v. phenylephrine (PE) and nitroprusside (NTP)] in P rats and in virgin (V) rats before (control) and 15 min after infusion (i.v.) of 3alpha-OH-DHP or 3beta-OH-DHP. Baseline MAP was lower in P rats (P = 102 +/- 2 vs. V = 124 +/- 3 mmHg). Compared with V rats, P rats exhibited less "sympathetic reserve" to respond to a hypotensive challenge, as evidenced by decreased maximum NA and decreased slope of RSNA baroreflex responses to NTP. However, HR baroreflex curves were similar in P and V rats. Acute intravenous administration of 3alpha-OH-DHP to conscious V rats mimicked the effects of pregnancy. Baroreflex sympathoexcitatory responses were decreased, whereas baroreflex control of HR was unaffected. The 3beta-isomer of DHP had no effect on NA or HR baroreflex responses. These results suggest that pregnancy may have differential effects on baroreflex control of sympathetic outflow and HR, and the major metabolite of progesterone, 3alpha-OH-DHP, may contribute to this adaptation of pregnancy.

scholarly journals Alteration of Sympathetic Nerve Activity (SNA) with High Sodium Diet and Foot-Shock in Spontaneously Hypertensive Rat (SHR)

1988 ◽  
Vol 29 (4) ◽  
pp. 562-562
Author(s):  
Hiroaki Tomori ◽  
Hiroshi Kawamura ◽  
Masahiro Maki ◽  
Hideaki Higashi ◽  
Kazuyoshi Tsukamoto ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Spontaneously Hypertensive Rat ◽  
Nerve Activity ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
Sodium Diet ◽  
Hypertensive Rat ◽  
High Sodium Diet

Cardiopulmonary and arterial baroreflex responses to acute volume expansion during fetal and postnatal development

1994 ◽  
Vol 267 (4) ◽  
pp. H1467-H1475 ◽  
Author(s):  
D. C. Merrill ◽  
J. L. Segar ◽  
O. J. McWeeny ◽  
B. A. Smith ◽  
J. E. Robillard
Keyword(s):  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Arterial Baroreflex ◽  
Response Curves ◽  
Nerve Activity ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
The Right ◽  
Renal Sympathetic

Recent studies demonstrated that renal denervation had no effect on the natriuretic response to volume expansion (VE) in fetal sheep, suggesting that the sensitivity of the cardiopulmonary reflex in response to VE is impaired in the fetus. To test this hypothesis, we investigated the renal sympathetic nerve activity (RSNA) and heart rate (HR) responses to 20 and 50% intravascular VE in fetal (130-135 days gestation; term 145 days) (n = 7), newborn (n = 8), and 6- to 8-wk-old sheep (n = 9). Despite similar increases in right atrial pressure (RAP) in the three groups, 20% VE had no significant effect on RSNA and HR in fetal sheep but significantly decreased RSNA in newborn (-22.8 +/- 7.3%) and 6- to 8-wk-old sheep (-32.1 +/- 11.7%). Bradycardic responses to VE were also observed in both newborn (from 237 +/- 6 to 200 +/- 12 beats/min) and 6- to 8-wk-old sheep (from 170 +/- 9 to 140 +/- 9 beats/min). A 50% VE had no significant effect on fetal RSNA and HR, whereas it increased RAP by 6.8 +/- 0.9 mmHg. In addition, we tested the hypothesis that interactions between cardiopulmonary and arterial baroreflexes in response to VE change during development. We found that 20 and 50% VE shifted the RSNA and HR arterial baroreflex response curves to the right in the fetus but had no significant effects on the gain of the arterial baroreflex curves in either fetal, newborn, or 6- to 8-wk-old sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Central mechanisms of acute ANG II modulation of arterial baroreflex control of renal sympathetic nerve activity

2002 ◽  
Vol 282 (5) ◽  
pp. H1592-H1602 ◽  
Author(s):  
Max G. Sanderford ◽  
Vernon S. Bishop
Keyword(s):  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Short-term intravenous infusion of angiotensin II (ANG II) into conscious rabbits reduces the range of renal sympathetic nerve activity (RSNA) by attenuating reflex disinhibition of RSNA. This action of ANG II to attenuate the arterial baroreflex range is exaggerated when ANG II is directed into the vertebral circulation, which suggests a mechanism involving the central nervous system. Because an intact area postrema (AP) is required for ANG II to attenuate arterial baroreflex-mediated bradycardia and is also required for maintenance of ANG II-dependent hypertension, we hypothesized that attenuation of maximum RSNA during infusion of ANG II involves the AP. In conscious AP-lesioned (APX) and AP-intact rabbits, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng · kg−1 · min−1) on the relationship between mean arterial blood pressure (MAP) and RSNA. Intravenous infusion of ANG II into AP-intact rabbits resulted in a dose-related attenuation of maximum RSNA observed at low MAP. In contrast, ANG II had no effect on maximum RSNA in APX rabbits. To further localize the central site of ANG II action, its effect on the arterial baroreflex was assessed after a midcollicular decerebration. Decerebration did not alter arterial baroreflex control of RSNA compared with the control state, but as in APX, ANG II did not attenuate the maximum RSNA observed at low MAP. The results of this study indicate that central actions of peripheral ANG II to attenuate reflex disinhibition of RSNA not only involve the AP, but may also involve a neural interaction rostral to the level of decerebration.

Arterial baroreceptor reflex control of renal sympathetic nerve activity following chronic myocardial infarction in male, female, and ovariectomized female rats

2015 ◽  
Vol 309 (2) ◽  
pp. R169-R178 ◽  
Author(s):  
Maximilian I. Pinkham ◽  
Gillian A. Whalley ◽  
Sarah-Jane Guild ◽  
Simon C. Malpas ◽  
Carolyn J. Barrett
Keyword(s):  
Myocardial Infarction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sham Group ◽  
Chronic Myocardial Infarction ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

There is controversy regarding whether the arterial baroreflex control of renal sympathetic nerve activity (SNA) in heart failure is altered. We investigated the impact of sex and ovarian hormones on changes in the arterial baroreflex control of renal SNA following a chronic myocardial infarction (MI). Renal SNA and arterial pressure were recorded in chloralose-urethane anesthetized male, female, and ovariectomized female (OVX) Wistar rats 6–7 wk postsham or MI surgery. Animals were grouped according to MI size (sham, small and large MI). Ovary-intact females had a lower mortality rate post-MI (24%) compared with both males (38%) and OVX (50%) ( P < 0.05). Males and OVX with large MI, but not small MI, displayed an impaired ability of the arterial baroreflex to inhibit renal SNA. As a result, the male large MI group (49 ± 6 vs. 84 ± 5% in male sham group) and OVX large MI group (37 ± 3 vs. 75 ± 5% in OVX sham group) displayed significantly reduced arterial baroreflex range of control of normalized renal SNA ( P < 0.05). In ovary-intact females, arterial baroreflex control of normalized renal SNA was unchanged regardless of MI size. In males and OVX there was a significant, positive correlation between left ventricle (LV) ejection fraction and arterial baroreflex range of control of normalized renal SNA, but not absolute renal SNA, that was not evident in ovary-intact females. The current findings demonstrate that the arterial baroreflex control of renal SNA post-MI is preserved in ovary-intact females, and the state of left ventricular dysfunction significantly impacts on the changes in the arterial baroreflex post-MI.

scholarly journals Effect of endogenous angiotensin II on renal nerve activity and its cardiac baroreflex regulation.

1998 ◽  
Vol 9 (11) ◽  
pp. 1983-1989
Author(s):  
G F Dibona ◽  
S Y Jones ◽  
L L Sawin
Keyword(s):  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Sodium Diet ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The effects of physiologic alterations in endogenous angiotensin II activity on basal renal sympathetic nerve activity and its cardiac baroreflex regulation were studied. The effect of angiotensin II type 1 receptor blockade with intracerebroventricular losartan was examined in conscious rats consuming a low, normal, or high sodium diet that were instrumented for the simultaneous measurement of right atrial pressure and renal sympathetic nerve activity. The gain of cardiac baroreflex regulation of renal sympathetic nerve activity (% delta renal sympathetic nerve activity/mmHg mean right atrial pressure) was measured during isotonic saline volume loading. Intracerebroventricular losartan did not decrease arterial pressure but significantly decreased renal sympathetic nerve activity in low (-36+/-6%) and normal (-24+/-5%), but not in high (-2+/-3%) sodium diet rats. Compared with vehicle treatment, losartan treatment significantly increased cardiac baroreflex gain in low (-3.45+/-0.20 versus -2.89+/-0.17) and normal (-2.89+/-0.18 versus -2.54+/-0.14), but not in high (-2.27+/-0.15 versus -2.22+/-0.14) sodium diet rats. These results indicate that physiologic alterations in endogenous angiotensin II activity tonically influence basal levels of renal sympathetic nerve activity and its cardiac baroreflex regulation.

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