Feeding-induced increase in urinary dopamine excretion is independent of renal innervation and sodium intake

1994 ◽  
Vol 266 (4) ◽  
pp. F563-F567
Author(s):  
B. Muhlbauer ◽  
H. Osswald
Keyword(s):  
Time Course ◽  
Sodium Intake ◽  
Tap Water ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Urinary Dopamine ◽  
Renal Innervation

Food intake increases urinary dopamine excretion. To investigate the role of renal nerve activity in this renal response to feeding, we studied urinary dopamine excretion after chronic bilateral renal denervation (DNX, n = 8) in male Sprague-Dawley rats. Controls were sham operated (CON, n = 6). In a paired crossover design, animals were studied both in fed and fasted state. Time course measurements of renal tissue norepinephrine (NE) content in a third group of DNX rats showed a decrease by 90% not earlier than 18 h post-DNX, remaining to be reduced to this level until day 11. Renal NE content in DNX animals was measured at the end of the study to confirm complete denervation. In 24-h urine, collected from fed and fasted conscious CON and DNX rats in metabolic cages, concentrations of dopamine and sodium were measured during two different sodium intake regimens, i.e., tap water and 1 g/dl NaCl as drinking water. No influence of renal innervation on urinary dopamine could be observed in fed and fasted animals. The marked changes in urinary volume and sodium output due to the different sodium regimens were not paralleled by urinary dopamine excretion. However, urinary dopamine was increased 2.1- to 2.4-fold (P < 0.01) because of feeding in all groups, independent of sodium balance and renal innervation. We conclude that in conscious rats both basal urinary dopamine excretion and its marked increase in response to feeding are independent of sodium balance and of renal nerve activity.

Neurogenic regulation of proximal bicarbonate and chloride reabsorption

1986 ◽  
Vol 250 (1) ◽  
pp. F22-F26 ◽  
Author(s):  
M. G. Cogan
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Sprague Dawley ◽  
Electrolyte Excretion ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Single Nephron ◽  
Renal Nerve Activity ◽  
Chloride Excretion

Although a change in renal nerve activity is known to alter proximal reabsorption, it is unclear whether reabsorption of NaHCO3 or NaCl or both are affected. Sprague-Dawley rats (n = 10) were studied using free-flow micropuncture techniques during euvolemia and following acute ipsilateral denervation. Glomerular filtration rate and single nephron glomerular filtration rate were stable. Absolute proximal bicarbonate reabsorption fell following denervation (933 +/- 40 to 817 +/- 30 pmol/min) with a parallel reduction in chloride reabsorption (1,643 +/- 116 to 1,341 +/- 129 peq/min). Urinary sodium, potassium, bicarbonate, and chloride excretion all increased significantly. To further assess the physiological significance of neurogenic modulation of proximal transport, other rats (n = 6) were subjected to acute unilateral nephrectomy (AUN). There is evidence that AUN induces a contralateral natriuresis (renorenal reflex) at least partially by causing inhibition of efferent renal nerve traffic. AUN caused significant changes in proximal NaHCO3 and NaCl reabsorption as well as in whole kidney electrolyte excretion in the same pattern as had denervation. Prior denervation of the remaining kidney prevented the proximal and whole kidney response to AUN (n = 6). In conclusion, depression of renal nerve activity inhibits both NaHCO3 and NaCl reabsorption in the rat superficial proximal convoluted tubule. The data are consistent with the hypothesis that changes in renal nerve activity modify whole kidney electrolyte excretion under physiological conditions at least partially by regulating proximal transport.

beta-Adrenoceptor modulation of renin response to short-term reductions in pressure in young SHR

1992 ◽  
Vol 263 (2) ◽  
pp. R405-R411
Author(s):  
J. P. Porter
Keyword(s):  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sprague Dawley ◽  
Short Term ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Beta Adrenoceptor ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Renal Nerve Activity

The increase in renin secretion in response to short-term (5 min) reductions in arterial pressure has recently been shown to be similar in young spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) animals. This was puzzling, since tonic renal nerve activity is thought to be elevated in the young SHR, and this has the potential to enhance the renin response. The purpose of the present investigation was to determine whether beta-adrenoceptor modulation of pressure-dependent renin release is diminished in the SHR. In conscious, age-matched SHR, WKY, and Sprague-Dawley rats, the effect on arterial plasma renin activity of 5-min reductions in renal perfusion pressure to 90 and 50 mmHg was determined before and during beta-adrenoceptor activation with isoproterenol or beta-adrenoceptor blockade with propranolol. Isoproterenol augmented the renin response at 50 mmHg in all three strains, with the greatest effect occurring in the Sprague-Dawley rats. The response at 90 mmHg was also enhanced in the SHR and Sprague-Dawley rats, but not the WKY rats. Propranolol had no effect in the SHR and WKY animals, but significantly reduced the renin response at 50 mmHg in the Sprague-Dawley rats. Thus, under the conditions of the present investigation (i.e., short-term reductions in pressure), tonic renal nerve activity does not affect pressure-dependent renin release through a beta-adrenergic receptor mechanism in either the SHR or WKY rats. However, under conditions of acute beta-adrenoceptor activation, the renin response is enhanced at a higher renal perfusion pressure in the SHR than in the WKY rat.

scholarly journals Dietary sodium modulates the interaction between efferent and afferent renal nerve activity by altering activation of α2-adrenoceptors on renal sensory nerves

2011 ◽  
Vol 300 (2) ◽  
pp. R298-R310 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Lori A. Smith ◽  
Saku Ruohonen ◽  
Mika Scheinin ◽  
...  
Keyword(s):  
Substance P ◽  
Sodium Intake ◽  
Sensory Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium ◽  
Renal Nerve Activity ◽  
High Sodium Diet

Activation of efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which then reflexively decreases ERSNA via activation of the renorenal reflexes to maintain low ERSNA. The ERSNA-ARNA interaction is mediated by norepinephrine (NE) that increases and decreases ARNA by activation of renal α1-and α2-adrenoceptors (AR), respectively. The ERSNA-induced increases in ARNA are suppressed during a low-sodium (2,470 ± 770% s) and enhanced during a high-sodium diet (5,670 ± 1,260% s). We examined the role of α2-AR in modulating the responsiveness of renal sensory nerves during low- and high-sodium diets. Immunohistochemical analysis suggested the presence of α2A-AR and α2C-AR subtypes on renal sensory nerves. During the low-sodium diet, renal pelvic administration of the α2-AR antagonist rauwolscine or the AT1 receptor antagonist losartan alone failed to alter the ARNA responses to reflex increases in ERSNA. Likewise, renal pelvic release of substance P produced by 250 pM NE (from 8.0 ± 1.3 to 8.5 ± 1.6 pg/min) was not affected by rauwolscine or losartan alone. However, rauwolscine+losartan enhanced the ARNA responses to reflex increases in ERSNA (4,680 ± 1,240%·s), and renal pelvic release of substance P by 250 pM NE, from 8.3 ± 0.6 to 14.2 ± 0.8 pg/min. During a high-sodium diet, rauwolscine had no effect on the ARNA response to reflex increases in ERSNA or renal pelvic release of substance P produced by NE. Losartan was not examined because of low endogenous ANG II levels in renal pelvic tissue during a high-sodium diet. Increased activation of α2-AR contributes to the reduced interaction between ERSNA and ARNA during low-sodium intake, whereas no/minimal activation of α2-AR contributes to the enhanced ERSNA-ARNA interaction under conditions of high sodium intake.

scholarly journals Afferent renal innervation in anti-Thy1.1 nephritis in rats

2020 ◽  
Vol 319 (5) ◽  
pp. F822-F832
Author(s):  
Kristina Rodionova ◽  
Roland Veelken ◽  
Karl F. Hilgers ◽  
Eva-Maria Paulus ◽  
Peter Linz ◽  
...  
Keyword(s):  
Renal Tissue ◽  
In Vitro Assays ◽  
Renal Nerves ◽  
Dual Function ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Cgrp Release ◽  
Renal Nerve Activity

Afferent renal nerves exhibit a dual function controlling central sympathetic outflow via afferent electrical activity and influencing intrarenal immunological processes by releasing peptides such as calcitonin gene-related peptide (CGRP). We tested the hypothesis that increased afferent and efferent renal nerve activity occur with augmented release of CGRP in anti-Thy1.1 nephritis, in which enhanced CGRP release exacerbates inflammation. Nephritis was induced in Sprague-Dawley rats by intravenous injection of OX-7 antibody (1.75 mg/kg), and animals were investigated neurophysiologically, electrophysiologically, and pathomorphologically 6 days later. Nephritic rats exhibited proteinuria (169.3 ± 10.2 mg/24 h) with increased efferent renal nerve activity (14.7 ± 0.9 bursts/s vs. control 11.5 ± 0.9 bursts/s, n = 11, P < 0.05). However, afferent renal nerve activity (in spikes/s) decreased in nephritis (8.0 ± 1.8 Hz vs. control 27.4 ± 4.1 Hz, n = 11, P < 0.05). In patch-clamp recordings, neurons with renal afferents from nephritic rats showed a lower frequency of high activity following electrical stimulation (43.4% vs. 66.4% in controls, P < 0.05). In vitro assays showed that renal tissue from nephritic rats exhibited increased CGRP release via spontaneous (14 ± 3 pg/mL vs. 6.8 ± 2.8 pg/ml in controls, n = 7, P < 0.05) and stimulated mechanisms. In nephritic animals, marked infiltration of macrophages in the interstitium (26 ± 4 cells/mm2) and glomeruli (3.7 ± 0.6 cells/glomerular cross-section) occurred. Pretreatment with the CGRP receptor antagonist CGRP8–37 reduced proteinuria, infiltration, and proliferation. In nephritic rats, it can be speculated that afferent renal nerves lose their ability to properly control efferent sympathetic nerve activity while influencing renal inflammation through increased CGRP release.

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.

Abstract 121: Afferent Renal Nerve Chemo- and Mechanosensitive Responses and the Modulation of Sodium Homeostasis and Blood Pressure

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Alissa A Frame ◽  
Casey Y Carmichael ◽  
Kathryn R Walsh ◽  
Richard D Wainford
Keyword(s):  
Blood Pressure ◽  
Constant Infusion ◽  
Renal Nerves ◽  
Neuronal Activation ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Sodium Homeostasis ◽  
Sd Rats ◽  
Renal Nerve Activity

Aim: We hypothesize that challenges to sodium homeostasis differentially activate chemo- vs. mechanosensitive afferent renal nerves to evoke sympathoinhibition, sodium homeostasis and normotension in the Sprague-Dawley (SD) rat. Methods: Conscious SD rats, post sham (S) or afferent renal nerve ablation (Renal-CAP; capsaicin 33 mM) underwent IV volume expansion (VE; 5% BW) or IV sodium loading (1M NaCl Infusion – constant infusion volume) and HR, MAP, natriuresis and PVN neuronal activation (c-Fos expression) were assessed (N=4/gp). Naïve SD rats were fed a 0.6% (NS) or 4% NaCl (HS) diet for 21 days and afferent renal nerve activity was assessed as norepinephrine (NE) (1250 pmol) and NaCl-evoked (450mM) substance P (SP) release in a renal pelvic assay (N=4/gp). Radiotelemetered SD rats post S or Renal-CAP immediately prior a 0.6% (NS) or 4% NaCl (HS) diet underwent continuous MAP monitoring. On day-21 plasma and renal NE content was assessed (N=5/group). Results: Renal-CAP attenuated the natriuretic and PVN parvocellular responses to IV VE (peak UNaV [μeq/min]; S 43±4 vs Renal-CAP 26±6, P<0.05, PVN Medial Parvocellular neuronal activation [c-fos positive cells]; S 49±6 vs Renal-CAP 22±5 P<0.05) and evoked increased MAP (MAP 90min post-VE [mmHg] S 118±3 vs Renal-CAP 132±4, P<0.05). In contrast Renal-CAP did not alter the natriuresis to IV 1M NaCl (UNaV [μeq/min]; S 21±4 vs Renal-CAP 21±3) or increase MAP. In naïve SD rats HS-intake did not alter MAP and suppressed plasma and renal NE (P<0.05). HS intake increased NE, but not NaCl, mediated afferent renal nerve activity (NE-evoked peak ΔSP [ng/ml); NS 14±2, HS 22±3, P<0.05, NaCl-evoked peak ΔSP [ng/ml]; NS 17±3, HS 16±2). Renal-CAP immediately prior to a HS-intake persistently increased MAP (Day 21 MAP [mmHg] S HS 106±4, Renal-CAP HS 123±5, P<0.05) and attenuated HS-evoked global and renal sympathoinhibition (P<0.05). Conclusion: The mechanosensitive afferent renal nerves mediate acute natriuresis and blood pressure regulation via activation of PVN sympathoinhibitory neurons. During HS intake the afferent renal nerves counter the development of salt-sensitive hypertension via a mechanism involving increased mechano but not chemosensitive afferent nerve responsiveness to potentiate sympathoinhibition.

Effect of acute adrenalectomy on sympathetic responses to peripheral lipopolysaccharide or central PGE2

2000 ◽  
Vol 278 (5) ◽  
pp. R1321-R1328 ◽  
Author(s):  
B. J. MacNeil ◽  
A. H. Jansen ◽  
A. H. Greenberg ◽  
D. M. Nance
Keyword(s):  
Plasma Corticosterone ◽  
Renal Nerves ◽  
Onset Latency ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Enhanced Sensitivity ◽  
Electrophysiological Recordings ◽  
Renal Nerve Activity ◽  
The Impact

The impact of plasma corticosterone levels on the sympathetic nervous system (SNS) response to intravenous lipopolysaccharide (LPS) or intracerebroventricular injections of PG was studied in anesthetized (urethan-chloralose) male Sprague-Dawley rats. For this, electrophysiological recordings of splenic and renal nerves were completed in control or adrenalectomized (ADX) rats. LPS (10 μg iv) similarly increased splenic and renal nerve activity in control rats with a shorter onset latency for the splenic nerve. Acute ADX enhanced the response of both nerves to LPS ( P < 0.005) and reduced the onset latency of the renal nerve ( P < 0.05). PGE2 (2 μg icv) rapidly increased the activity of both nerves but preferentially (magnitude and onset latency) stimulated the renal nerve ( P < 0.05). The magnitude of the splenic nerve response to PGE2 was unaffected by ADX. Unexpectedly, PGE2 was less effective at stimulating renal nerve activity in ADX animals relative to intact controls ( P < 0.05). Pretreatment of ADX rats with a CRF antagonist {[d-Phe12, Nle21,38, Cα-MeLeu37]CRF-(12—41)} reversed this effect such that the renal nerve responded to central PGE2 to a greater extent than the splenic nerve ( P< 0.05), as was the case in non-ADX rats. These data indicate that enhanced sensitivity of central sympathetic pathways does not account for the enhanced SNS responses to LPS in ADX rats. Also, a CRF-related process appears to diminish renal sympathetic outflow in ADX rats.

Renal nerve activity in conscious rats during volume expansion and depletion

1985 ◽  
Vol 248 (1) ◽  
pp. F15-F23 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Volume Expansion ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Right Atrial ◽  
Renal Nerves ◽  
Volume Depletion ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Conscious Rats ◽  
Renal Nerve Activity

The role of renal nerve activity (RNA) in the renal response to isotonic saline volume expansion and furosemide-induced volume depletion was studied in conscious rats consuming a low (LNa), normal (NNa), or high (HNa) dietary sodium intake. In the control state, right atrial pressure (RAP) and UNa V were directly related and RNA was inversely related to dietary sodium intake, being 12.9 +/- 0.7, 10.9 +/- 1.1 and 8.7 +/- 0.6 units in LNa, NNa, and HNa rats, respectively. During volume expansion, RAP and UNa V increased and RNA decreased in all three dietary groups; however, the peak increase in UNa V was greater in the LNa (88 +/- 6 mueq/min) than NNa (34 +/- 9 mueq/min) or HNa (32 +/- 6 mueq/min) rats. The greater natriuresis in LNa was associated with a larger decrease in RNA in LNa (-6.1 +/- 0.5 units) than in NNa (-3.4 +/- 0.4 units). The greater contribution of inhibition of RNA to the increased natriuretic response to volume expansion in LNa compared with NNa rats was further examined in renal denervated animals. Bilateral renal denervation substantially reduced the natriuretic response to volume expansion in LNa rats (-70%) but had no significant effect in NNa rats (-15%). During volume depletion, RAP decreased, whereas UNa V and RNA increased in all three dietary groups. After the peak of the furosemide natriuresis, UNa V was lower in the LNa rats than in the NNa or HNa rats at any level of increased RNA, consistent with a role for the renal nerves in the normal renal adaptive response to sodium/volume depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Dietary salt loading produces baroreflex impairment and mild hypertension in rats

1985 ◽  
Vol 249 (2) ◽  
pp. H278-H284 ◽  
Author(s):  
E. Miyajima ◽  
R. D. Bunag
Keyword(s):  
Mild Hypertension ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Salt Loading ◽  
Sprague Dawley Rats ◽  
Direct Recording ◽  
Renal Nerve Activity ◽  
Underlying Mechanisms

Mild hypertension with reduced chronotropic baroreflex sensitivity to phenylephrine occurred in Sprague-Dawley rats fed a high-salt diet for 5 wk. Progressive elevation of systolic and mean pressures, detected initially by indirect tail-cuff measurement, was later verified by direct recording of phasic pressures from indwelling aortic catheters in the same rats. Reflex bradycardia during pressor responses to phenylephrine was consistently less pronounced in salt-loaded than in control rats, whether tested while rats were awake or anesthetized. However, attendant decreases in renal nerve activity were not appreciably altered. Neither central nor carotid baroreceptor mechanisms were considered likely but aortic baroreceptors must have somehow been depressed because increases in afferent aortic nerve activity elicited during intravenous infusion of phenylephrine were invariably smaller in salt-loaded than in control rats. Whatever the underlying mechanisms may be, our results show that when hypertension develops during dietary salt loading, baroreflex chronotropic responses are selectively inhibited while attendant decreases in renal nerve activity are preserved.

Neuronal regulation of renal function: A model system for nervous system interactions

1992 ◽  
Vol 70 (5) ◽  
pp. 733-734 ◽  
Author(s):  
J. Michael Wyss
Keyword(s):  
Nervous System ◽  
Renal Function ◽  
Renal Disease ◽  
Easy Access ◽  
Renal Nerves ◽  
Clinical Consequence ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity

The kidney is the most highly innervated peripheral organ, and both the excretory and endocrine functions of the kidney are regulated by renal nerve activity. The kidney plays a dominant role in body fluid homeostasis, blood ionic concentration, and pH and thereby contributes importantly to systemic blood pressure control. Early studies suggested that the neural-renal interactions were responsible only for short-term adjustments in renal function, but more recent studies indicate that the renal nerves may be a major contributor to chronic renal defects leading to established hypertension and (or) renal disease. The neural-renal interaction is also of considerable interest as a model to elucidate the interplay between the nervous system and peripheral organs, since there is abundant anatomical and physiological information characterizing the renal nerves. The investigator has easy access to the renal nerves and the neural influence on renal function is directly quantifiable both in vivo and in vitro. In this symposium that was presented at the 1990 annual convention of the Society for Neuroscience in St. Louis, Missouri, three prominent researchers evaluate the most recent progress in understanding the interplay between the nervous system and the kidney and explore how the results of these studies relate to the broader questions concerning the nervous system's interactions.First, Luciano Barajas examines the detailed anatomy of the intrarenal distribution of the efferent and afferent renal nerves along the nephron and vasculature, and he evaluates the physiological role of each of the discrete components of the innervation. His basic science orientation combined with his deep appreciation of the clinical consequence of the failure of neural-renal regulation enhances his discussion of the anatomy. Ulla C. Kopp discusses the role of the renorenal reflex, which alters renal responses following stimulation of the contralateral kidney. She also considers her recent findings that efferent renal nerve activity can directly modify sensory feedback to the spinal cord from the kidney. Finally, J. Michael Wyss examines the functional consequences of neural control of the kidney in health and disease. Although the nervous system has often been considered as only an acute regulator of visceral function, current studies into hypertension and renal disease suggest that neural-renal dysfunction may be an important contributor to chronic diseases.Together, these presentations examine most of the recent advances in the area of neural-renal interactions and point out how these data form a basis for future research into neuronal interactions with all visceral organs. The relative simplicity of the neural-renal interaction makes this system an important model with which to elucidate all neural-peripheral and neural-neural interactions.

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