Reflex mechanisms for changes in renal nerve activity during positive end-expiratory pressure

1988 ◽  
Vol 65 (1) ◽  
pp. 109-115 ◽  
Author(s):  
M. Aibiki ◽  
S. Koyama ◽  
K. Ogli ◽  
Y. Shirakawa
Keyword(s):  
Carotid Sinus ◽  
Venous Pressure ◽  
Control Level ◽  
Vagal Afferents ◽  
Positive End Expiratory Pressure ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Cardiopulmonary Receptors

This study was designed to investigate the interaction between carotid sinus baroreceptors and cardiopulmonary receptors in the reflex control of renal nerve activity (RNA) during positive end-expiratory pressure (PEEP) in anesthetized dogs. PEEP at two different levels (10 and 20 cmH2O) was applied to the following groups: animals with neuraxis intact (I group, n = 12); vagal and aortic nerve denervated animals with carotid sinus nerves intact (V group, n = 6); carotid sinus denervated animals with vagal and aortic nerves intact (SD group, n = 6); and carotid sinus denervated animals also having severed vagal and aortic nerves (SAV group, n = 12). Mean blood pressure (MBP), central venous pressure, and mean airway pressure were also simultaneously measured. In the I group, no significant alterations in RNA occurred during PEEP at both levels, even when MBP fell significantly. Although the drop in MBP in the SD group was similar to that in the I group, RNA decreased significantly 10 s after intervention at both PEEP levels, followed by a recovery of RNA toward the control level. In contrast, a significant increase in RNA, which continued until the end of PEEP, appeared in the V group immediately after each intervention. In the SAV group, RNA responses to PEEP, which were observed in the other groups, were abolished. These results provide evidence that during PEEP, renal nerve activity is modified by an interaction between carotid sinus baroreceptors and cardiopulmonary receptors; excitatory effects occur via carotid sinus nerves and inhibitory effects occur via vagal afferents.

Role of vagal afferents in hypotension induced by venous air embolism

1994 ◽  
Vol 266 (3) ◽  
pp. R790-R795
Author(s):  
M. Aibiki ◽  
S. Ogura ◽  
K. Seki ◽  
K. Honda ◽  
O. Umegaki ◽  
...  
Keyword(s):  
Venous Pressure ◽  
Air Embolism ◽  
Air Injection ◽  
Vagal Afferents ◽  
Renal Nerve ◽  
Intact Group ◽  
Venous Air Embolism ◽  
Renal Nerve Activity ◽  
Cardiopulmonary Receptors

To evaluate the role of the autonomic nervous system in the development of hypotension during air embolism, we studied the effects of an intravenous bolus injection of air (0.5 ml/kg) on mean blood pressure (MBP), central venous pressure (CVP), and renal nerve activity (RNA) in urethan-anesthetized rabbits of three groups: animals with an intact neuraxis (intact group; n = 5), cervical-vagotomized animals (vagotomy group; n = 5), and sinoaortic-denervated animals (SAD group; n = 5). In the intact group, despite a significant decrease in MBP at 10 s after air injection, RNA did not increase from the preinjection level. This response of RNA was associated with a significant increase in CVP and lasted for 20 s after the injection. Vagotomized animals, however, exhibited a significant augmentation in RNA in response to a drop in MBP at 10 s after the injection. In the SAD group, profound declines in both MBP and RNA were observed at 10 s after the injection of air. Animals in these two groups showed remarkable increases in CVP. At 5 min after the air administration, MBP in the vagotomy group was significantly higher than that in the intact group. All animals in the SAD group died within 5 min of the injection. These results indicate that during hypotension induced by air injection, sympathetic activation through arterial baroreceptors may be depressed by vagal afferents emanating from cardiopulmonary receptors; the results also suggest that the arterial baroreceptor nerves may be required to overcome the lethal events that should occur during venous air embolism.

Atrial receptor modulation of renal nerve activity in the nonhuman primate

1982 ◽  
Vol 242 (6) ◽  
pp. F592-F598 ◽  
Author(s):  
J. P. Gilmore ◽  
S. Echtenkamp ◽  
C. R. Wesley ◽  
I. H. Zucker
Keyword(s):  
Significant Influence ◽  
Nonhuman Primate ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Balloon Inflation ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Receptor Modulation ◽  
Renal Nerve Activity ◽  
Cervical Vagotomy

Experiments were done in the nonhuman primate Macaca fascicularis to determine the extent to which low-pressure receptors modulate renal nerve activity (RNA). Left atrial pressure (LAP) was increased either by inflating a balloon in the left atrium or by intravascular volume expansion. Arterial pressure (AP) was increased by the administration of epinephrine. Balloon inflation produced variable changes in RNA when all reflexes were intact. In the bilateral vagotomized animal, balloon inflation significantly increased RNA. Compared with the intact state, neither carotid sinus denervation nor sinoaortic denervation had a significant influence on RNA during balloon inflation. The response of both baroreceptor-denervated groups, however, was significantly less than that of the vagotomized group. Vagotomy plus sinoaortic denervation essentially prevented any effect of balloon inflation on RNA. Volume expansion produced a greater inhibition of RNA per increase in AP than did epinephrine. However, this difference was abolished after bilateral cervical vagotomy. These experiments demonstrate a significant influence and interplay of low- and high-pressure receptors on RNA in the nonhuman primate.

Excitation of cardiac sympathetic afferent nerves: effects on renal function

1981 ◽  
Vol 241 (5) ◽  
pp. R267-R270
Author(s):  
R. L. Meckler ◽  
L. J. Macklem ◽  
L. C. Weaver
Keyword(s):  
Renal Function ◽  
Chemical Stimulation ◽  
Afferent Neurons ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Afferent Nerves ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Stimulation Of

Cardiac sympathetic afferent nerves can reflexly alter renal efferent nerve activity during myocardial ischemia and in response to mechanical or chemical stimulation of cardiac receptors. They also may influence renal excretion of water and electrolytes; however, this potential influence on renal function has not been determined. Therefore, receptors of cardiac sympathetic afferent nerves were chemically stimulated by epicardial application of bradykinin to determine effects on renal function. Experiments were performed in anesthetized dogs in which cervical vagosympathetic trunks were severed and common carotid arteries were tied to diminish influences of arterial baroreceptors and vagal afferent nerves. Chemical stimulation of cardiac afferent neurons excited renal nerve activity and produced decreases in urine flow rate, glomerular filtration rate, and excretion of sodium and potassium. In contrast, no consistent changes in renal function were observed in control dogs, which did not undergo cardiac afferent stimulation. These data provide evidence that activation of cardiac sympathetic afferent neurons can lead to alterations in excretion of water and electrolytes as well as changes in renal nerve activity.

Renorenal reflexes: neural components of ipsilateral and contralateral renal responses

1985 ◽  
Vol 249 (4) ◽  
pp. F507-F517 ◽  
Author(s):  
U. C. Kopp ◽  
L. A. Smith ◽  
G. F. DiBona
Keyword(s):  
Spinal Cord ◽  
Venous Pressure ◽  
Urinary Sodium Excretion ◽  
Reflex Response ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Electrophysiological Responses ◽  
Renal Nerve Activity ◽  
Renal Vascular ◽  
Renal Responses

In anesthetized rats, stimulating renal mechanoreceptors (MR) by increasing renal venous pressure (RVP) 22 mmHg increased ipsilateral (ipsi) renal vascular resistance (RVR) from 23.5 to 31.3 mmHg/(ml X min-1 X g-1), ipsi urinary sodium excretion (UNaV) from 0.26 to 0.49 mumol X min-1 X g-1, contralateral (contra) urine flow rate (V) from 3.13 to 4.43 microliter X min-1 X g-1, and UNaV from 0.30 to 0.46 mumol X min-1 X g-1. Ipsi renal denervation (DNX) did not affect the increase in ipsi RVR but reduced the increase in ipsi UNaV. The increases in contra V and UNaV were abolished by either ipsi or contra renal DNX. Increases RVP increased ipsi afferent renal nerve activity (ARNA) 288 counts/10 s and decreased ipsi and contra efferent renal nerve activity (ERNA) 242 and 490 counts/10 s, respectively. Renal pelvic instillation of lidocaine (5 micrograms/ml) did not affect the renal functional or electrophysiological responses to increases RVP but abolished the increase in ipsi ARNA, the decrease in contra ERNA, and the increases in contra V and UNaV produced by increasing ureteral pressure (UP) or retrograde ureteropelvic perfusion with 0.9 M NaCl [chemoreceptor (CR) stimulation]. Chronic T6 spinal cord section abolished the increase in ipsi ARNA, the decrease in contra ERNA, and the increases in contra V and UNaV produced by renal MR (increases RVP, increases UP) and CR stimulation. We conclude increases that RVP results in an ipsi and contra inhibitory renorenal reflex. Differential blockade with pelvic lidocaine suggests that the sensory receptors activated by increases RVP are located in an anatomically different area than those activated by increases UP or retrograde ureteropelvic perfusion with 0.9 M NaCl. An intact spinal cord is required for the normal responsiveness of renal sensory neuroreceptor complexes to specific stimuli in the context of the complete renorenal reflex response.

Effect of sympathetic sensitization of baroreceptors on renal nerve activity

1987 ◽  
Vol 252 (2) ◽  
pp. R328-R335 ◽  
Author(s):  
J. L. Seagard ◽  
F. A. Hopp ◽  
J. P. Kampine
Keyword(s):  
Sympathetic Activity ◽  
Carotid Sinus ◽  
Baroreceptor Sensitivity ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Before And After ◽  
Renal Nerve Activity ◽  
Sinus Pressure ◽  
Renal Sympathetic

The role of sympathetic efferent innervation of the carotid sinus on the regulation of baroreceptor sensitivity was examined in thiopental-sodium anesthetized dogs (5 mg X kg-1 X h-1 infusion). Baroreflex sensitivity was defined as the slope of renal sympathetic efferent nerve activity vs. carotid sinus pressure in an isolated, perfused carotid sinus. Slopes were obtained before and after sinus sympathectomy performed by section of the cervical sympathetic trunk. There was no significant differences between baroreflex decreases in renal sympathetic activity due to increases in carotid sinus pressure before and after sympathectomy, but the responses to decreases in carotid sinus pressure after sympathectomy were significantly greater than control. Base-line level of renal sympathetic activity, obtained at a constant perfusion pressure of 115 mmHg, abruptly increased by 11% in response to sinus sympathectomy. The response of baroreceptors to sympathomimetic stimulation was examined by recording carotid baroreceptor afferent nerve activity during ramp changes in carotid sinus pressure after addition of epinephrine (10(-8) to 10(-6) M) to the perfusate of the sympathetically denervated sinus. The slopes of the sinus nerve activity vs. carotid sinus pressure were used as direct indexes of baroreceptor sensitivity. Lower levels of epinephrine (10(-8), 10(-7) M) increased the sensitivity of the baroreceptors and reduced renal nerve activity back toward presympathectomy levels. A higher dose of epinephrine (10(-6) M) did not significantly increase baroreceptor sensitivity. The results of this study suggest that sinus sympathetic fibers produce a tonic sensitization of the baroreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Disparity between renal venous norepinephrine and renin responses to sodium depletion

1988 ◽  
Vol 254 (5) ◽  
pp. F754-F761
Author(s):  
R. G. Carroll ◽  
T. E. Lohmeier ◽  
A. J. Brown
Keyword(s):  
Enzyme Inhibitor ◽  
Sodium Intake ◽  
Control Level ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Sodium Depletion ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Arterial Plasma

To evaluate the hypothesis that sodium depletion produces a chronic increase in renal nerve activity, arterial and renal venous plasma norepinephrine (NE) concentrations were measured in conscious dogs subjected to various degrees of sodium depletion. After 9 days of sodium depletion (LS), there was a net loss of 69 +/- 10 meq sodium, and mean arterial pressure (MAP) was reduced from 94 +/- 5 to 88 +/- 4 mmHg. At this time plasma renin activity (PRA) was increased from a control level (sodium intake = 45 meq/day) of 0.34 +/- 0.08 to 1.47 +/- 0.26 ng angiotensin I (ANG I).ml-1.h-1 in association with an approximately sixfold increase in the PRA gradient across the kidneys. Subsequently, when captopril was infused during an additional 7 days of sodium deprivation [(LS + converting enzyme inhibitor CEI)], there was further sodium depletion (31 +/- 11 meq) and hypotension (MAP = 65 +/- 6 mmHg) and PRA and the renal PRA gradient increased even further. In marked contrast, there were no significant changes in either arterial plasma NE concentration (control = 102 +/- 5 pg/ml) or the renal arteriovenous gradient of plasma NE concentration during either LS or LS + CEI. These experiments show a distinct disparity between changes in the PRA and the plasma NE concentration gradient across the kidneys during LS and fail to support the contention that increased renal nerve activity is an important long-term adaptive response to sodium depletion.

Somatosensory influences on renal sympathetic nerve activity in anesthetized Wistar and hypertensive rats

1997 ◽  
Vol 272 (3) ◽  
pp. R982-R990 ◽  
Author(s):  
T. Zhang ◽  
E. J. Johns
Keyword(s):  
Power Spectra ◽  
Total Power ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Somatosensory Stimulation ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Nerve Activity ◽  
Cardiopulmonary Receptors ◽  
Renal Sympathetic

This study compared the cardiovascular and renal nerve activity responses to somatosensory stimulation with capsaicin in normotensive and hypertensive rats. The importance of the cardiopulmonary receptors in these two states was examined with the use of phenylbiguanide (PBG) infusion. Subcutaneous capsaicin increased blood pressure (BP), heart rate (HR), and renal nerve activity (RNA) 6-35% (P < 0.01), and total power (TP) and %power at HR (%PHR) rose two- to threefold (P < 0.001). PBG reduced basal RNA, TP, and %PHR (20-70%, P < 0.05). PBG did not change the cardiovascular, but attenuated the TP and %PHR increases due to capsaicin (P < 0.001-0.01). PBG given to vagotomized normotensive rats normalized the cardiovascular and RNA responses to capsaicin. In hypertensive rats, capsaicin increased BP, HR, RNA(10-20%), TP, and %PHR (50-70%, P < 0.001). PBG infusion into hypertensive rats decreased RNA (20%, P < 0.01) and the capsaicin-dependent rise in RNA was smaller (P < 0.05). TP and %PHR were unchanged, except in vagotomized hypertensive rats given PBG, in which these responses were minimally affected. Somatosensory modulation of RNA power spectra was suppressed by the cardiopulmonary receptors in normotensive rats, but in hypertensive rats their impact was much smaller.

Pulmonary serotonin 5-HT3-sensitive afferent fibers modulate renal sympathetic nerve activity in rats

1997 ◽  
Vol 272 (2) ◽  
pp. H979-H986 ◽  
Author(s):  
R. Veelken ◽  
M. Leonard ◽  
A. Stetter ◽  
K. F. Hilgers ◽  
J. F. Mann ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vagal Afferents ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Afferent Fibers ◽  
Renal Nerve Activity ◽  
Cardiac Afferents ◽  
Renal Sympathetic

Cardiopulmonary reflexes with vagal afferents may control volume homeostasis by influencing renal nerve activity. Such reflexes can be stimulated mechanically and chemically, e.g., by serotonin 5-HT). We have demonstrated that stimulation of epicardial 5-HT3 receptors inhibits renal sympathetic nerve activity (RSNA) by a cardiorenal reflex. We now tested the hypothesis that pulmonary 5-HT3-sensitive vagal afferent fibers participate in the control of renal nerve activity. Two sets of experiments were performed. First, the responses of multifiber RSNA, heart rate (HR), and blood pressure (BP) to the 5-HT3-receptor agonist phenylbiguanide (PBG; 10 microg iv) were recorded in the presence of intact pulmonary afferents. Abdominal afferents were removed by subdiaphragmatic vagotomy. Cardiac afferents were blocked by intrapericardial injection of 10% procaine. Second, the responses of 25 single vagal pulmonary afferent C fibers to PBG were assessed. PBG decreased BP, HR, and RSNA (-90 +/- 8%). When cardiac afferents were blocked by procaine, BP and HR failed to decrease in response to PBG; however, the RSNA decrease was still -48 +/- 8%. Single fibers generally responded to PBG by a slight increase in firing rate. A distinct subset of fibers (5 of 25) showed an activity increase of >15 Hz that preceded changes in BP and HR. The decreased RSNA in the absence of cardiac and abdominal vagal afferents and the strong response of 20% of pulmonary single fibers to intravenous PBG suggest that pulmonary fibers play a role in a 5-HT3 serotenergic reflex. Thus pulmonary serotonin could influence the neural control of renal function.

Renorenal reflexes: Interaction between efferent and afferent renal nerve activity

1992 ◽  
Vol 70 (5) ◽  
pp. 750-758 ◽  
Author(s):  
Ulla C. Kopp
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Vena Cava ◽  
Reflex Response ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Central Interaction ◽  
Renal Nerve Activity

In rats, stimulation of renal mechanoreceptors by increasing ureteral pressure results in a contralateral inhibitory renorenal reflex response consisting of increases in ipsilateral afferent renal nerve activity, decreases in contralateral efferent renal nerve activity, and increases in contralateral urine flow rate and urinary sodium excretion. Mean arterial pressure is unchanged. To study possible functional central interaction among the afferent renal nerves and the aortic and carotid sinus nerves, the responses to renal mechanoreceptor stimulation were compared in sinoaortic denervated rats and sham-denervated rats before and after vagotomy. In contrast to sham-denervated rats, there was an increase in mean arterial pressure in response to renal mechanoreceptor stimulation in sinoaortic-denervated rats. However, there were no differences in the renorenal reflex responses among the groups. Thus, our data failed to support a functional central interaction among the renal, carotid sinus, and aortic afferent nerves in the renorenal reflex response to renal mechanoreceptor stimulation. Studies to examine peripheral interaction between efferent and afferent renal nerves showed that marked reduction in efferent renal nerve activity produced by spinal cord section at T6, ganglionic blockade, volume expansion, or stretch of the junction of superior vena cava and right atrium abolished the responses in afferent renal nerve activity and contralateral renal function to renal mechanoreceptor stimulation. Conversely, increases in efferent renal nerve activity caused by thermal cutaneous stimulation increased basal afferent renal nerve activity and its responses to renal mechanoreceptor stimulation. These data suggest a facilitatory role of efferent renal nerves on renal sensory receptors.Key words: vagotomy, sinoaortic denervation, substance P, prostaglandins, mechanoreceptor stimulation.

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