Selective efferent chemical sympathectomy of rat kidneys

1985 ◽  
Vol 249 (4) ◽  
pp. R496-R501
Author(s):  
L. M. LeNoble ◽  
R. W. Lappe ◽  
M. J. Brody ◽  
H. A. Struyker Boudier ◽  
J. F. Smits
Keyword(s):  
Blood Pressure ◽  
Renal Denervation ◽  
Left Kidney ◽  
Posterior Hypothalamus ◽  
Renal Nerves ◽  
Chemical Sympathectomy ◽  
Arterial Blood ◽  
6 Hydroxydopamine ◽  
The Right ◽  
And Control

Surgical denervation of kidneys results in interruption of both afferent and efferent renal nerves. We attempted selective efferent renal denervation in rats by slow infusions of 6-hydroxydopamine (6-OHDA) into the right renal artery. Integrity of efferent renal nerves was assessed by chemical and physiological methods and by measuring responses of mean arterial blood pressure (MAP) and heart rate (HR) to intrarenal (ir) infusion of bradykinin in conscious rats. Results were compared with those in surgically denervated and ir saline-infused rats. Surgical denervation of left kidney reduced renal norepinephrine (NE) to 58 and 14% of control levels at 1 and 7 days, respectively, after surgery. Increase in left renal resistance during posterior hypothalamus (PH) stimulation was only 70 +/- 28% (n = 5) compared with 289 +/- 69% (n = 6) in control animals. Response in opposite kidney was unchanged. Although 0.1 mg 6-OHDA ir caused considerable reduction of NE levels in both kidneys, responses to PH stimulation were unchanged. 6-OHDA (1 mg) reduced NE levels in infused and control kidney and atria. Functional evidence for denervation was only obtained in the kidney infused with 6-OHDA. Responses of MAP and HR to ir bradykinin were unchanged 7 days after 1 mg 6-OHDA. The data suggest that ir 6-OHDA results in functional efferent sympathectomy without affecting afferent renal nerves.

Renal hemodynamic changes during serial seizures in rats

1991 ◽  
Vol 261 (5) ◽  
pp. H1508-H1513
Author(s):  
R. M. Zweifler ◽  
E. M. Slaven ◽  
L. L. Rihn ◽  
J. C. Magee ◽  
N. R. Kreisman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Status Epilepticus ◽  
Mean Arterial Blood Pressure ◽  
Renal Denervation ◽  
Adrenal Glands ◽  
Renal Nerves ◽  
Hemodynamic Changes ◽  
Arterial Blood ◽  
Early Seizures

Renal blood flow (RBF) and mean arterial blood pressure (MABP) were measured during serially induced seizures in anesthetized paralyzed rats to investigate possible alterations in hemodynamic responses during experimental status epilepticus. During initial seizures, MABP increased from 143 to 193 mmHg, and RBF decreased from 4.8 to 1.5 ml/min. In contrast, MABP fell from 124 to 100 mmHg and RBF dropped from 3.6 to 2.8 ml/min during late seizures. The large decreases in RBF during initial seizures were blocked by renal denervation or bilateral adrenalectomy. During the period of late seizures, both the increase in MABP and the decrease in RBF in response to intravenous boluses of norepinephrine fell to 55% of the preseizure value. Our data indicate that the marked decreases in RBF during early seizures can be mediated by either the renal nerves or the adrenal glands. Furthermore, decreased sensitivity of the vasculature to norepinephrine likely contributes to the diminution of both MABP and RBF responses during later seizures.

The kidney and control of blood pressure

2015 ◽  
Author(s):  
Olga Gonzalez-Albarrán ◽  
Luis M. Ruilope
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Renal Nerves ◽  
Renal Ischaemia ◽  
Arterial Blood ◽  
Gene Defects ◽  
And Control ◽  
Transplantation Experiments ◽  
Primary Gene

The kidneys can be at the root of the development of arterial hypertension or they can participate in the maintenance of hypertension and its sequels. Renal alterations interfering with the regulation of sodium homeostasis or facilitating the generation of vasoconstrictors, particularly angiotensin II, are involved in the dysregulation of arterial blood pressure that underlies the development of arterial hypertension. The biology of angiotensin is described in detail.The kidneys are also the mediator of hypertension in such examples as renal ischaemia and hyperaldosteronism. The role of renal nerves, and renal depressor substances, are also described.Transplantation experiments in animals and observations in human transplantation, as well as some primary gene defects, show the importance of renal mechanisms in hypertension. Once kidneys have been damaged, they often contribute to an increase in arterial pressure. Salt sensitivity is probably a major part of the mechanism, but it is mediated by multiple pathways.

Increased circulating plasma catecholamines and plasma renin activity in dogs after chemical sympathectomy with 6-hydroxydopamine

1977 ◽  
Vol 55 (3) ◽  
pp. 724-733 ◽  
Author(s):  
Gérald A. Porlier ◽  
Réginald A. Nadeau ◽  
Jacques de Champlain ◽  
Daniel G. Bichet
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Mean Arterial Blood Pressure ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Renin Activity ◽  
Chemical Sympathectomy ◽  
Arterial Blood ◽  
6 Hydroxydopamine

Circulating plasma catecholamines, plasma renin activity, and other variables were measured in unanesthetized dogs before and after chemical sympathectomy with 6-hydroxydopamine (6-OHDA, 50 mg/kg). Chemical sympathectomy resulted in an immediate fall in mean arterial blood pressure and a delayed reduction in heart rate. Significant increases in plasma glucose and lactate concentrations, circulating plasma catecholamines, and plasma renin activity were found 24 h after 6-OHDA treatment. Circulating catecholamine levels decreased rapidly as time elapsed after sympathectomy and were half the initial values after 2 weeks. Plasma renin activity remained elevated during the 1st week after 6-OHDA treatment and returned to control levels during the 2nd week. Significant correlations were found between circulating catecholamines and heart rate mean arterial pressure, and plasma glucose and lactate concentrations. A significant correlation was also found between plasma renin activity and the mean arterial blood pressure. These results confirm that the adrenal medulla increases its catecholamine secretion rate into the circulation to compensate for the loss of adrenergic innervation after 6-OHDA treatment. They also indicate that the rennin–angiotensin system represents another important compensatory mechanism for circulatory homeostasis in sympathec-tomized animals.

Intravenous 6-hydroxydopamine attenuates vasopressin and oxytocin secretion stimulated by hemorrhage and hypotension but not hyperosmolality in rats

2006 ◽  
Vol 291 (1) ◽  
pp. R59-R67 ◽  
Author(s):  
Sean D. Stocker ◽  
Melinda E. Wilson ◽  
Christopher J. Madden ◽  
Usman Lone ◽  
Alan F. Sved
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Substantial Effect ◽  
Posterior Pituitary ◽  
Marked Contrast ◽  
Arterial Blood ◽  
Chemical Destruction ◽  
6 Hydroxydopamine ◽  
And Control ◽  
Supraoptic Nuclei

The present study sought to determine whether chemical destruction of peripheral catecholaminergic fibers with 6-hydroxydopamine (6OHDA) attenuates vasopressin (VP) and oxytocin (OT) secretion stimulated by hemorrhage, hypotension, and hyperosmolality. Rats received 6OHDA (100 mg/kg iv) or vehicle (1 ml/kg iv) on days 1 and 7, and experiments were performed on day 8. Serial hemorrhage (4 samples of 2 ml per 300 g body wt at 10-min intervals) increased plasma VP and OT levels in both groups; however, the increase in plasma VP and OT levels was significantly attenuated in 6OHDA-treated vs. control rats despite a significantly lower mean arterial blood pressure. Similarly, the increase in plasma VP and OT levels in response to hypotension produced by the selective arteriolar vasodilator diazoxide was significantly attenuated in 6OHDA-treated rats. In marked contrast to hemorrhage and hypotension, hyperosmolality produced by an infusion of 1 M NaCl (2 ml/h iv) stimulated increases in plasma VP and OT levels that were not different between 6OHDA-treated and control rats. In a parallel set of experiments, intravenous 6OHDA treatment reduced dopamine-β-hydroxylase immunoreactivity in the posterior pituitary but had no substantial effect in the hypothalamic paraventricular and supraoptic nuclei. In each experiment, the pressor response to tyramine (250 μg/kg iv) was significantly attenuated in 6OHDA-treated rats, thereby confirming that 6OHDA treatment destroyed sympathetic catecholaminergic fibers. Collectively, these findings suggest that catecholaminergic fibers located outside the blood-brain barrier contribute to VP and OT secretion during hemorrhage and arterial hypotension.

scholarly journals Hypertension in an experimental model of systemic lupus erythematosus occurs independently of the renal nerves

2013 ◽  
Vol 305 (7) ◽  
pp. R711-R719 ◽  
Author(s):  
Keisa W. Mathis ◽  
Marcia Venegas-Pont ◽  
Elizabeth R. Flynn ◽  
Jan Michael Williams ◽  
Christine Maric-Bilkan ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Blood Pressure ◽  
Lupus Erythematosus ◽  
Renal Injury ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Inflammatory Disorder ◽  
Systemic Lupus ◽  
Chronic Inflammatory Disorder ◽  
And Control

Systemic lupus erythematosus (SLE) is a chronic inflammatory disorder with prevalent hypertension and renal injury. In this study, we tested whether the renal nerves contribute to the development of hypertension in an established mouse model of SLE ( NZBWF1). Female SLE and control ( NZW/LacJ) mice were subjected to either bilateral renal denervation or a sham procedure at 32 wk of age. Two weeks later, blood pressure was assessed in conscious mice using carotid artery catheters. Blood pressure was higher in SLE mice compared with controls, as previously reported; however, blood pressure was not altered in the denervated SLE or control mice. The development of albuminuria was markedly blunted in denervated SLE mice; however, glomerulosclerosis was increased. Renal denervation reduced renal cortical expression of monocyte-chemoattractant protein in SLE mice but did not significantly alter renal monocyte/macrophage infiltration. Renal cortical TNF-α expression was also increased in sham SLE mice, but this was not impacted by denervation. This study suggests that the renal nerves do not have a significant role in the pathogenesis of hypertension, but have a complex effect on the associated renal inflammation and renal injury.

scholarly journals Microdissection of the Human Renal Nervous System

Hypertension ◽  
2020 ◽  
Vol 76 (4) ◽  
pp. 1240-1246 ◽  
Author(s):  
Arturo García-Touchard ◽  
Eva Maranillo ◽  
Blanca Mompeo ◽  
José Ramón Sañudo
Keyword(s):  
Nervous System ◽  
Renal Artery ◽  
Renal Denervation ◽  
Left Kidney ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Main Renal Artery ◽  
Area Under Roc Curve ◽  
Human Cadavers ◽  
The Right

Despite the use of renal denervation to treat hypertension, the anatomy of the renal nervous system remains poorly understood. We performed a detailed quantitative analysis of the human renal nervous system anatomy with the goal of optimizing renal denervation procedural safety and efficacy. Sixty kidneys from 30 human cadavers were systematically microdissected to quantify anatomic variations in renal nerve patterns. Contrary to current clinical perception, not all renal innervation followed the main renal artery. A significant portion of the renal nerves (late arriving nerves) frequently reached the kidney (73% of the right kidney and 53% of the left kidney) bypassing the main renal artery. The ratio of the main renal artery length/aorta-renal hilar distance proved to be a useful variable to identify the presence/absence of these late arriving nerves (odds ratio, 0.001 (95% CI, 0.00002–0.0692; P : 0.001) with a cutoff of 0.75 (sensitivity: 0.68, specificity: 0.83, area under ROC curve at threshold: 0.76). When present, polar arteries were also highly associated with the presence of late arriving nerve. Finally, the perivascular space around the proximal main renal artery was frequently occupied by fused ganglia from the solar plexus (right kidney: 53%, left kidney: 83%) and/or by the lumbar sympathetic chain (right kidney: 63%, left kidney: 60%). Both carried innervation to the kidneys but importantly also to other abdominal and pelvic organs, which can be accidentally denervated if the proximal renal artery is targeted for ablation. These novel anatomic insights may help guide future procedural treatment recommendations to increase the likelihood of safely reaching and destroying targeted nerves during renal denervation procedures.

Renal denervation alters cardiovascular and endocrine responses to hemorrhage in conscious newborn lambs

1998 ◽  
Vol 275 (1) ◽  
pp. H285-H291 ◽  
Author(s):  
Francine G. Smith ◽  
Isam Abu-Amarah
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Elevated Plasma ◽  
Baseline Levels ◽  
Renal Sympathetic

To investigate the role of renal sympathetic nerves in modulating cardiovascular and endocrine responses to hemorrhage early in life, we carried out three experiments in conscious, chronically instrumented lambs with intact renal nerves (intact; n = 8) and with bilateral renal denervation (denervated; n = 5). Measurements were made 1 h before and 1 h after 0, 10, and 20% hemorrhage. Blood pressure decreased transiently after 20% hemorrhage in intact lambs and returned to control levels. In denervated lambs, however, blood pressure remained decreased after 60 min. After 20% hemorrhage, heart rate increased from 170 ± 16 to 207 ± 18 beats/min in intact lambs but not in denervated lambs, in which basal heart rates were already elevated to 202 ± 21 beats/min. Despite an elevated plasma renin activity (PRA) measured in denervated (12.0 ± 6.4 ng ANG I ⋅ ml−1 ⋅ h−1) compared with intact lambs (4.0 ± 1.1 ng ANG I ⋅ ml−1 ⋅ h−1), the increase in PRA in response to 20% hemorrhage was similar in both groups. Plasma levels of arginine vasopressin increased from 11 ± 8 to 197 ± 246 pg/ml after 20% hemorrhage in intact lambs but remained unaltered in denervated lambs from baseline levels of 15 ± 10 pg/ml. These observations provide evidence that in the newborn, renal sympathetic nerves modulate cardiovascular and endocrine responses to hemorrhage.

Functional evidence for renorenal reflexes in the rat

1980 ◽  
Vol 239 (3) ◽  
pp. F265-F270 ◽  
Author(s):  
R. E. Colindres ◽  
W. S. Spielman ◽  
N. G. Moss ◽  
W. W. Harrington ◽  
C. W. Gottschalk
Keyword(s):  
Filtration Rate ◽  
Renal Denervation ◽  
Left Kidney ◽  
Mean Value ◽  
Urinary Volume ◽  
Hemodynamic Changes ◽  
Nerve Activity ◽  
Functional Changes ◽  
Simultaneous Decrease ◽  
The Right

Acute left renal denervation in anesthetized volume-expanded rats produced an ipsilateral diuresis and natriuresis in 19 animals. A simultaneous decrease of glomerular filtration rate, p-aminohippurate clearance, urinary volume (P < 0.002), and percentage of filtered sodium excreted (4.0 +/- 0.6 (SE) vs. 1.9 +/- 0.4%, P < 0.003) occurred in the right innervated kidney in 10 rats. Prior denervation of the right kidney in the other nine rats prevented the renal hemodynamic changes and the fall of urinary volume and of sodium excretion (3.9 +/- 0.6 vs. 4.3 +/- 0.5%) by the right kidney after left renal denervation. Nerve traffic to the right kidney was measured in six other animals after left renal denervation and was found to increase to a mean value 33.8 +/- 6.3% above control levels (P < 0.007) 0-30 min after denervation, with a further significant increase to 66.2 +/- 16.1% above control levels (P < 0.025) 30-60 min after denervation. These results indicate that the functional changes in the right kidney after contralateral renal denervation in volume-expanded rats are caused by a reflex increase in nerve traffic to the right kidney, possibly as a consequence of an interruption of afferent nerve activity originating in the left kidney.

Plasma renin activity responses to graded decreases in renal perfusion pressure in fetal and newborn lambs

1992 ◽  
Vol 262 (3) ◽  
pp. R524-R529 ◽  
Author(s):  
N. D. Binder ◽  
D. F. Anderson
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
The Right ◽  
The Relationship

We examined the relationship between acute reductions in renal perfusion pressure, as approximated by femoral arterial blood pressure, and plasma renin activity in the uninephrectomized fetal lamb. Renal perfusion pressure was reduced and maintained at a constant value by controlled partial occlusion of the aorta above the renal artery. After 15 min of reduced blood pressure, blood samples were taken for determination of plasma renin activity. This protocol was performed 22 times in 11 fetal lambs. Additionally, three of the fetuses were delivered by cesarean section and studied as newborns for the first week of life. In the fetus, there was a linear relationship between log plasma renin activity and femoral arterial blood pressure (P less than 0.01). After birth, the relationship still existed, although it was shifted to the right (P less than 0.0001). We conclude that there is a significant relationship between plasma renin activity and renal perfusion pressure in the fetal lamb, and as early as 1 day after birth, this relationship shifts to the right in the newborn lamb.

Effects of renal denervation on renal responses to hypoxemia in fetal lambs

1986 ◽  
Vol 250 (2) ◽  
pp. F294-F301 ◽  
Author(s):  
J. E. Robillard ◽  
K. T. Nakamura ◽  
G. F. DiBona
Keyword(s):  
Renal Function ◽  
Renal Denervation ◽  
Renal Hemodynamics ◽  
Significant Rise ◽  
Renal Nerves ◽  
Base Line ◽  
Urinary Flow ◽  
Renal Vasoconstriction ◽  
Physiological Conditions ◽  
Arterial Blood

The role of renal nerves in mediating renal hemodynamics and renal function during normal physiological conditions and following moderate hypoxemia was studied in chronically catheterized fetal lambs (125-141 days of gestation) following unilateral renal denervation. Base-line values for renal blood flow (RBF), renal vascular resistance (RVR), glomerular filtration rate (GFR), urinary flow rate (UFR), urinary electrolyte (Na+, K+, and Cl-) excretion rate, and urine osmolality (Uosm) were similar in both intact and denervated kidneys. Hypoxemia was associated with a significant rise in mean arterial blood pressure and a significant decrease in heart rate. Hypoxemia produced a similar decrease in GFR and similar increases in urinary Na+ and Cl- excretion rates in both intact and denervated kidneys. However, the effect of hypoxemia on renal hemodynamics differed between intact and denervated kidneys. Hypoxemia produced a continuous and progressive decrease in RBF and increase in RVR in the intact kidney. On the other hand, renal denervation was associated with an early renal vasodilation and attenuated the reduction in RBF and the rise in RVR during hypoxemia; this early renal vasodilation was blunted following prostaglandin synthesis inhibition. Taken together, these results suggest that fetal renal denervation is not associated with significant changes in renal hemodynamics or renal function during normal physiological conditions but that renal denervation partially inhibited the renal vasoconstriction associated with fetal hypoxemia. Finally, it was found that endogenous prostaglandins counteract the renal vasoconstriction associated with fetal hypoxemia.

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