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 corticospinal tract stimulation on renal sympathetic nerve activity in rats with intact and chronically lesioned spinal cords

2007 ◽  
Vol 293 (1) ◽  
pp. R178-R184 ◽  
Author(s):  
Baohan Pan ◽  
Matthew R. Zahner ◽  
Ewa Kulikowicz ◽  
Lawrence P. Schramm
Keyword(s):  
Spinal Cord ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Corticospinal Tract ◽  
Sympathetic Neurons ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic ◽  
Stimulation Of

Sympathetic preganglionic neurons and interneurons are closely apposed (presumably synapsed upon) by corticospinal tract (CST) axons. Sprouting of the thoracic CST rostral to lumbar spinal cord injuries (SCI) substantially increases the incidence of these appositions. To test our hypothesis that these additional synapses would increase CST control of sympathetic activity after SCI, we measured the effects of electrical stimulation of the CST on renal sympathetic nerve activity (RSNA) and arterial pressure (AP) in α-chloralose-anesthetized rats with either chronically intact or chronically lesioned spinal cords. Stimuli were delivered to the CST at intensities between 25–150 μA and frequencies between 25 and 75 Hz. Stimulation of the CST at the midcervical level decreased RSNA and AP. These decreases were not mediated by direct projections of the CST to the thoracic spinal cord because we could still elicit them by midcervical stimulation after acute lesions of the CST at caudal cervical levels. In contrast, caudal thoracic CST stimulation increased RSNA and AP. Neither the responses to cervical nor thoracic stimulation were affected by chronic lumbar SCI. These data show that the CST mediates decreases in RSNA via a cervical spinal system but excites spinal sympathetic neurons at caudal thoracic levels. Because chronic lumber spinal cord injury affected responses evoked from neither the cervical nor thoracic CST, we conclude that lesion-induced or regeneration-induced formation of new synapses between the CST and sympathetic neurons may not affect cardiovascular regulation.

A highly selective cardiorenal serotonergic 5-HT3-mediated reflex in rats

1993 ◽  
Vol 264 (6) ◽  
pp. H1871-H1877 ◽  
Author(s):  
R. Veelken ◽  
K. F. Hilgers ◽  
M. Leonard ◽  
K. Scrogin ◽  
J. Ruhe ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Receptor Agonist ◽  
Sympathetic Nerve Activity ◽  
Short Term ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Prolonged Stimulation ◽  
Saline Loading ◽  
Renal Sympathetic ◽  
Stimulation Of

To elucidate whether prolonged stimulation of cardiopulmonary serotonergic (5-HT3) receptors could play a role in the control of renal sympathetic nerve activity (RSNA), we compared 15-min intravenous infusions to bolus administrations of the 5-HT3 receptor agonist phenyl biguanide (PBG) and to a 0.9% saline load (5% body wt) in rats. Short-term and prolonged stimulation of 5-HT3-sensitive cardiopulmonary reflexes caused dose-related decreases in RSNA but not in lumbar sympathetic nerve activity (LSNA); only short-term stimulation caused decreases in blood pressure (BP) and heart rate (HR). Saline loading lowered RSNA but not LSNA, BP, or HR. Baroreceptor denervation did not influence any of these responses. Scopolamine attenuated BP and HR but not RSNA responses to bolus PBG. Pretreatment with a 5-HT3 receptor antagonist inhibited responses to PBG but not to saline. Vagotomy abolished all responses to all interventions. Thus 1) the prolonged stimulation of cardiopulmonary 5-HT3 receptors caused sustained suppression of RSNA, 2) decreased BP and HR were manifest only during short-term stimulation (3 min), and 3) blockade of 5-HT3 receptors did not influence responses to cardiopulmonary mechanoreceptor stimulation.

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.

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.

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