Regulation of renal sympathetic nerve activity at birth

1996 ◽  
Vol 270 (1) ◽  
pp. R86-R93 ◽  
Author(s):  
J. E. Mazursky ◽  
J. L. Segar ◽  
A. M. Nuyt ◽  
B. A. Smith ◽  
J. E. Robillard
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
In Utero ◽  
Nerve Activity ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Series Of Experiments ◽  
Renal Sympathetic

The present studies were designed to assess the contribution of onset of respiration, separation from the placenta, and a decrease in environmental temperature on the increase in renal sympathetic nerve activity (RSNA) that occurs at birth. In the first series of experiments, heart rate (HR), mean arterial blood pressure (MABP), and RSNA were recorded in chronically instrumented near-term fetal sheep (n = 12) before and during in utero ventilation (V), V + oxygenation (V + O), and V + O + umbilical cord occlusion (V + O + CO). RSNA increased by 49 +/- 16% during V alone (P < 0.05), whereas no additional changes were seen with V + O or V + O + CO. HR and MABP did not change with any intervention. In a second series of experiments (n = 10), changes in fetal HR, MABP, and RSNA in response to in utero cooling were recorded. Cooling of the fetal core temperature by -3.1 +/- 0.2 degree C produced a rapid and sustained increase in RSNA (330 +/- 155%), HR (25 +/- 11%), and MABP (10 +/- 2%) consistent with generalized sympathoexcitation. In a third series of studies (n = 3), we found that brain stem transection between the rostral pons and posterior hypothalamus abolishes the increases in RSNA seen at birth. These results suggest that cooling is a major contributor to the postnatal rise in RSNA and that brain centers at the level of or above the hypothalamus are involved in mediating sympathoexcitation at birth.

Renal sympathetic nerve activity during asphyxia in fetal sheep

2012 ◽  
Vol 303 (1) ◽  
pp. R30-R38 ◽  
Author(s):  
Lindsea C. Booth ◽  
Simon C. Malpas ◽  
Carolyn J. Barrett ◽  
Sarah-Jane Guild ◽  
Alistair J. Gunn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Near Term ◽  
Renal Sympathetic

The sympathetic nervous system (SNS) is an important mediator of fetal adaptation to life-threatening in utero challenges, such as asphyxia. Although the SNS is active well before term, SNS responses mature significantly over the last third of gestation, and its functional contribution to adaptation to asphyxia over this critical period of life remains unclear. Therefore, we examined the hypotheses that increased renal sympathetic nerve activity (RSNA) is the primary mediator of decreased renal vascular conductance (RVC) during complete umbilical cord occlusion in preterm fetal sheep (101 ± 1 days; term 147 days) and that near-term fetuses (119 ± 0 days) would have a more rapid initial vasomotor response, with a greater increase in RSNA. Causality of the relationship of RSNA and RVC was investigated using surgical (preterm) and chemical (near-term) denervation. All fetal sheep showed a significant increase in RSNA with occlusion, which was more sustained but not significantly greater near-term. The initial fall in RVC was more rapid in near-term than preterm fetal sheep and preceded the large increase in RSNA. These data suggest that although RSNA can increase as early as 0.7 gestation, it is not the primary determinant of RVC. This finding was supported by denervation studies. Interestingly, chemical denervation in near-term fetal sheep was associated with an initial fall in blood pressure, suggesting that by 0.8 gestation sympathetic innervation of nonrenal vascular beds is critical to maintain arterial blood pressure during the rapid initial adaptation to asphyxia.

Novel recordings of renal sympathetic nerve activity in conscious fetal sheep and newborn lambs

1990 ◽  
Vol 258 (1) ◽  
pp. F218-F221 ◽  
Author(s):  
F. G. Smith ◽  
J. M. Klinkefus ◽  
U. C. Kopp ◽  
J. E. Robillard
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Perinatal Period ◽  
Postnatal Period ◽  
Left Renal Artery ◽  
Nerve Activity ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

This study describes a technique for measuring efferent renal sympathetic nerve activity (RSNA) during the perinatal period. Experiments were carried out in four chronically instrumented fetal sheep (gestational age, 134–140 days) and 6 newborn lambs (postnatal age, 3–7 days). Surgery, performed under halothane anesthesia, consisted of routine catheter insertions and placement of a Doppler flow probe around the left renal artery. In addition, bipolar platinum electrodes were placed on a branch of the left renal postganglionic nerve. At least 24 h after surgery RSNA was measured in conscious fetal and newborn animals. RSNA was pulse synchronous, reduced with pressor agents, and completely inhibited during ganglionic blockade. Using this method, we have provided direct evidence of efferent renal sympathetic nerve traffic in utero and in the immediate postnatal period. This technique opens new avenues into the investigation of the role of the sympathetic nervous system during the perinatal period.

Effect of dynamic exercise on renal sympathetic nerve activity in conscious rabbits

1993 ◽  
Vol 74 (5) ◽  
pp. 2099-2104 ◽  
Author(s):  
K. P. O'Hagan ◽  
L. B. Bell ◽  
S. W. Mittelstadt ◽  
P. S. Clifford
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Treadmill Exercise ◽  
Dynamic Exercise ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Conscious Rabbits ◽  
Renal Sympathetic

Renal sympathetic nerve activity (RSNA) increases abruptly at the onset of treadmill exercise in conscious rabbits. This study investigated whether the rise in RSNA is related to the intensity of the exercise and whether an elevated level of RSNA is maintained during submaximal exercise. RSNA, arterial blood pressure (BP), and heart rate (HR) were recorded in 10 New Zealand White rabbits during two treadmill exercise protocols at 0% grade: 7 m/min for 5 min and 12 m/min for 2 min. Peak levels of RSNA were observed in the first 10 s of exercise at 7 and 12 m/min. Through 2 min of exercise, the rise in RSNA was greater (P < 0.05) at 12 m/min (delta 83 +/- 22%) compared with 7 m/min (delta 49 +/- 8%). At 7 m/min, HR and BP reached steady-state levels during the 2nd min of exercise. RSNA remained elevated at delta 43 +/- 10 to delta 54 +/- 13% over resting levels as exercise continued from the 2nd through the 5th min of exercise (P < 0.05). These data demonstrate that the RSNA response to exercise is intensity related and suggest that RSNA remains elevated and thus may contribute to the control of renal blood flow during submaximal dynamic exercise.

Angiotensin II acutely attenuates range of arterial baroreflex control of renal sympathetic nerve activity

2000 ◽  
Vol 279 (4) ◽  
pp. H1804-H1812 ◽  
Author(s):  
Max G. Sanderford ◽  
Vernon S. Bishop
Keyword(s):  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Renal Sympathetic

Acutely increasing peripheral angiotensin II (ANG II) reduces the maximum renal sympathetic nerve activity (RSNA) observed at low mean arterial blood pressures (MAPs). We postulated that this observation could be explained by the action of ANG II to acutely increase arterial blood pressure or increase circulating arginine vasopressin (AVP). Sustained increases in MAP and increases in circulating AVP have previously been shown to attenuate maximum RSNA at low MAP. In conscious rabbits pretreated with an AVP V1 receptor antagonist, 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 MAP and RSNA when the acute pressor action of ANG II was left unopposed with that when the acute pressor action of ANG II was opposed by a simultaneous infusion of sodium nitroprusside (SNP). Intravenous infusion of ANG II resulted in a dose-related attenuation of the maximum RSNA observed at low MAP. When the acute pressor action of ANG II was prevented by SNP, maximum RSNA at low MAP was attenuated, similar to that observed when ANG II acutely increased MAP. In contrast, intravertebral infusion of ANG II attenuated maximum RSNA at low MAP significantly more than when administered intravenously. The results of this study suggest that ANG II may act within the central nervous system to acutely attenuate the maximum RSNA observed at low MAP.

Renal sympathetic nerve activity and plasma catecholamines during eating in cats

1989 ◽  
Vol 257 (5) ◽  
pp. R1034-R1039 ◽  
Author(s):  
K. Matsukawa ◽  
T. Honda ◽  
I. Ninomiya
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Plasma Catecholamines ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Control Value ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Maximum Value ◽  
Renal Sympathetic

We measured renal sympathetic nerve activity (RNA) and arterial plasma concentration of norepinephrine (NE) and epinephrine (EPI) before, during, and after eating in six conscious cats. Eating continued for a period of 5 min. RNA, heart rate (HR), and arterial blood pressure (AP) increased almost simultaneously with the onset of eating and reached a maximum value of 192%, 221 beats/min, and 121 mmHg at 2.5-5 min after the onset of eating, respectively. The plasma NE level increased significantly (P less than 0.05) during eating from the control value of 0.56 ng/ml and reached a maximum value of 1.33 ng/ml at 4.5-5 min, whereas the plasma EPI level did not change significantly from the control value of 0.12 ng/ml. The plasma levels of NE and EPI were unaffected by the blood samplings. The relationship between the changes in RNA and the plasma NE level during eating had a significant (P less than 0.05) positive correlation (r = 0.52). The result suggests that plasma NE concentration tends to increase with the rise in RNA during eating.

Effects of anesthesia on cardiac and renal sympathetic nerve activities and plasma catecholamines

1993 ◽  
Vol 265 (4) ◽  
pp. R792-R797 ◽  
Author(s):  
K. Matsukawa ◽  
I. Ninomiya ◽  
N. Nishiura
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Plasma Catecholamines ◽  
Plasma Epinephrine ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Cardiac Sympathetic Nerve Activity ◽  
Renal Sympathetic

The effects of pentobarbital and chloralose on cardiac sympathetic nerve activity (CSNA), renal sympathetic nerve activity (RSNA), arterial pressure (AP), and heart rate (HR) were examined using conscious cats. Arterial blood was sampled intermittently to measure plasma epinephrine. Pentobarbital (25-30 mg/kg iv) decreased CSNA, RSNA, AP, and HR. The reduction of CSNA (71 +/- 7%) was larger and lasted longer than that of RSNA (33 +/- 12%). Chloralose (40-50 mg/kg iv) decreased CSNA 66 +/- 9% and HR, increased RSNA 127 +/- 122%, and did not affect AP. The baroreflex relationship between AP and CSNA was examined by increasing AP to 145 mmHg and decreasing AP to 55 mmHg. Both pentobarbital and chloralose shifted the AP-CSNA relationship curve downward and blunted the slope of the curve, indicating that both drugs attenuate tonic and baroreflex cardiac sympathetic outflow. Pentobarbital and chloralose reduced plasma epinephrine, suggesting a decrease in adrenal sympathetic nerve activity. It is concluded that pentobarbital or chloralose affects differentially sympathetic outflows to different organs such as the heart, kidney, and adrenal gland.

Effects of fetal behavioral states on renal sympathetic nerve activity and arterial pressure of unanesthetized fetal sheep

2003 ◽  
Vol 285 (4) ◽  
pp. R908-R916 ◽  
Author(s):  
Eugenie R. Lumbers ◽  
Ze-Yan Yu ◽  
Edward N. Crawford
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Fetal Breathing ◽  
Behavioral States ◽  
Renal Sympathetic

Fetal behavior, renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), and heart rate (HR) were studied 1-3 days after surgery in seven fetal sheep (aged 127-136 days). Five behavioral states were defined from chart recordings of electrocortical (electrocorticographic; ECoG) activity and eye, limb, and breathing movements. Most records were of high-voltage ECoG (HV) or low-voltage (LV) ECoG with breathing (LVB); 6.7 ± 1.7% were LV ECoG with no breathing (LV0). RSNA was lower in LV0 ( P < 0.001) and greater in LVB than in HV ( P < 0.05). MAP was lower in both LV states than in HV and when the fetuses went from LV to HV ( P < 0.001 to P < 0.03). HR was highest in HV ( P < 0.001). In HV and LVB and when the fetus went from LV to HV, MAP and HR were inversely related ( P = 0.012-0.003). In LVB and from LV to HV there were direct relationships between MAP and RSNA ( P = 0.0014, P = 0.08), and when the fetus went from LV to HV there was also an inverse relationship between HR and RSNA ( P = 0.02). Thus fetal RSNA, MAP, and HR are affected by behavioral state as is fetal cardiovascular control. The increase in RSNA during fetal breathing showed that there was an altered level of fetal RSNA associated with fetal breathing activity.

scholarly journals Renal sympathoinhibition mediated by 5-HT1Areceptors in the RVLM during severe hemorrhage in rats

2002 ◽  
Vol 282 (1) ◽  
pp. R122-R130 ◽  
Author(s):  
C. Dean ◽  
M. Bago
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Severe Hemorrhage ◽  
Renal Sympathetic

The role of 5-hydroxytryptamine type 1A (5-HT1A) receptors in the rostral ventrolateral medulla (RVLM) in the mediation of the sympathoinhibitory and hypotensive responses to severe hemorrhage was examined in pentobarbital sodium-anesthetized rats. The control response to hemorrhage (1 ml/min to 50 mmHg) consisted of a fall in arterial blood pressure and an initial baroreflex increase in renal sympathetic nerve activity followed after 2 min by a rapid decline in blood pressure accompanied by a decrease in renal sympathetic nerve activity. In response to hemorrhage in animals in which the specific 5-HT1A receptor antagonist WAY-100635 was microinjected into the pressor area of the RVLM, the fall in blood pressure was delayed and attenuated while renal sympathetic nerve activity was increased and maintained above baseline. In barodenervated animals with blockade of RVLM 5-HT1A receptors, there was no change in renal sympathetic nerve activity in response to hemorrhage. These data suggest that renal sympathoinhibition elicited in response to severe hemorrhage is mediated by 5-HT1A receptors in the RVLM.

Sympathoinhibition from ventrolateral periaqueductal gray mediated by the caudal midline medulla

2005 ◽  
Vol 289 (5) ◽  
pp. R1477-R1481 ◽  
Author(s):  
C. Dean
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Periaqueductal Gray ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Depressor Response ◽  
Arterial Blood ◽  
Renal Sympathetic

Activation of neurons in the ventrolateral region of the periaqueductal gray (vlPAG) can elicit a decrease in renal sympathetic nerve activity and blood pressure. The present study investigated whether the vlPAG-evoked sympathoinhibitory response depends on neurons in the caudal midline medulla (CMM). In pentobarbital-anesthetized rats, activation of neurons in the vlPAG evoked a decrease in renal sympathetic nerve activity to 29.4 ± 4.8% below baseline levels and arterial blood pressure fell 8.9 ± 1.6 mmHg ( n = 20). Microinjection of the GABA agonist muscimol into sympathoinhibitory regions of the CMM significantly attenuated the vlPAG-evoked sympathoinhibition to 17.9 ± 4.1% below baseline and the depressor response to 4.3 ± 1.2 mmHg. At 65% (13/20) of the sites examined, the vlPAG-evoked sympathoinhibition was responsive to CMM muscimol microinjection and attenuated from 34.2% to 11.5%, with the depressor response reduced from 14.8 to 3 mmHg. Microinjection of muscimol at the remaining 35% of the CMM sympathoinhibitory sites was ineffective on the vlPAG-evoked sympathoinhibition and depressor response. These data indicate that sympathoinhibitory and hypotensive responses elicited by activation of neurons in the vlPAG can be mediated by neurons in the sympathoinhibitory region of the CMM. The finding that the vlPAG-evoked response is not affected by muscimol at all CMM sympathoinhibitory sites also suggests that sympathoinhibitory sites in the CMM are not homogeneous and can mediate functionally different responses.

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