scholarly journals Blunted natriuretic response to saline loading in sheep with hypertensive kidney disease following radiofrequency catheter-based renal denervation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Reetu R. Singh ◽  
Zoe McArdle ◽  
Harshil Singh ◽  
Lindsea C. Booth ◽  
Clive N. May ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Disease ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Sympathetic Nerves ◽  
Excretory Function ◽  
Load Following ◽  
Saline Loading ◽  
Renal Sympathetic

AbstractRenal sympathetic nerves contribute to renal excretory function during volume expansion. We hypothesized that intact renal innervation is required for excretion of a fluid/electrolyte load in hypertensive chronic kidney disease (CKD) and normotensive healthy settings. Blood pressure, kidney hemodynamic and excretory response to 180 min of isotonic saline loading (0.13 ml/kg/min) were examined in female normotensive (control) and hypertensive CKD sheep at 2 and 11 months after sham (control-intact, CKD-intact) or radiofrequency catheter-based RDN (control-RDN, CKD-RDN) procedure. Basal blood pressure was ~ 7 to 9 mmHg lower at 2, and 11 months in CKD-RDN compared with CKD-intact sheep. Saline loading did not alter glomerular filtration rate in any group. At 2 months, in response to saline loading, total urine and sodium excretion were ~ 40 to 50% less, in control-RDN and CKD-RDN than intact groups. At 11 months, the natriuretic and diuretic response to saline loading were similar between control-intact, control-RDN and CKD-intact groups but sodium excretion was ~ 42% less in CKD-RDN compared with CKD-intact at this time-point. These findings indicate that chronic withdrawal of basal renal sympathetic activity impairs fluid/electrolyte excretion during volume expansion. Clinically, a reduced ability to excrete a saline load following RDN may contribute to disturbances in body fluid balance in hypertensive CKD.

Reduced renal sympathoinhibition in response to acute volume expansion in diabetic rats

1994 ◽  
Vol 267 (2) ◽  
pp. R372-R379 ◽  
Author(s):  
K. P. Patel ◽  
P. L. Zhang
Keyword(s):  
Sympathetic Nerve ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Diabetic Rats ◽  
Urine Flow ◽  
Control Group ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

To determine whether the renal sympathetic nerve responses to acute volume expansion (VE) are altered in the diabetic state, we measured the acute VE-induced renal sympathoinhibition in streptozotocin (STZ)-induced diabetic rats. Urine flow, sodium excretion, and integrated renal sympathetic nerve activity were measured before and during an acute graded VE (with isotonic saline) in anesthetized (Inactin; 0.1 g/kg ip) control rats (vehicle; n = 7), diabetic rats (Sprague-Dawley rats injected with STZ 65 mg/kg ip 2 wk before experiment; n = 7), and diabetic rats treated with insulin (2 U/day sc; n = 6). Blood glucose levels were significantly elevated in the diabetic group (370 +/- 8 mg/dl) compared with the control group (104 +/- 3 mg/dl). Acute graded VE with isotonic saline produced a significantly blunted renal sympathoinhibition (50% of control by 10% VE), diuresis (19% of control by 10% VE), and natriuresis (24% of control by 10% VE) in the diabetic rats compared with control rats. Treatment with insulin for 2 wk to restore normoglycemia in diabetic rats (third group; 93 +/- 9 mg/dl) resulted in reversal of the blunted urine flow, sodium excretion, and renal sympathoinhibition in response to acute VE. However, acute (a few hours before VE challenge) reduction of hyperglycemia in the diabetic rats (125 +/- 18 mg/dl) did not correct the blunted renal sympathoinhibition. The second goal of this study was to determine if enalapril treatment (10 mg/day by mouth) for 2 wk corrects the blunted volume reflex in diabetic rats. Enalapril did not correct the blunted renal excretory and renal nerve responses to acute VE in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

The Potential Role of Catheter-Based Renal Sympathetic Denervation in Chronic and End-Stage Kidney Disease

2016 ◽  
Vol 21 (4) ◽  
pp. 344-352 ◽  
Author(s):  
Yusuke Sata ◽  
Markus P. Schlaich
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Kidney Disease ◽  
End Stage Renal Disease ◽  
Renal Denervation ◽  
Potential Role ◽  
Stage Renal Disease ◽  
End Stage ◽  
Renal Sympathetic

Sympathetic activation is a hallmark of chronic and end-stage renal disease and adversely affects cardiovascular prognosis. Hypertension is present in the vast majority of these patients and plays a key role in the progressive deterioration of renal function and the high rate of cardiovascular events in this patient cohort. Augmentation of renin release, tubular sodium reabsorption, and renal vascular resistance are direct consequences of efferent renal sympathetic nerve stimulation and the major components of neural regulation of renal function. Renal afferent nerve activity directly influences sympathetic outflow to the kidneys and other highly innervated organs involved in blood pressure control via hypothalamic integration. Renal denervation of the kidney has been shown to reduce blood pressure in many experimental models of hypertension. Targeting the renal nerves directly may therefore be specifically useful in patients with chronic and end-stage renal disease. In this review, we will discuss the potential role of catheter-based renal denervation in patients with impaired kidney function and also reflect on the potential impact on other cardiovascular conditions commonly associated with chronic kidney disease such as heart failure and arrhythmias.

scholarly journals Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 569 ◽  
Author(s):  
Dragana Komnenov ◽  
Peter Levanovich ◽  
Noreen Rossi
Keyword(s):  
Blood Pressure ◽  
Chronic Renal Disease ◽  
Sympathetic Nerves ◽  
Renal Nerve ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Salt Consumption ◽  
High Fructose ◽  
Salt Sensitive Hypertension ◽  
Renal Sympathetic

Hypertension is a leading cause of cardiovascular and chronic renal disease. Despite multiple important strides that have been made in our understanding of the etiology of hypertension, the mechanisms remain complex due to multiple factors, including the environment, heredity and diet. This review focuses on dietary contributions, providing evidence for the involvement of elevated fructose and salt consumption that parallels the increased incidence of hypertension worldwide. High fructose loads potentiate salt reabsorption by the kidney, leading to elevation in blood pressure. Several transporters, such as NHE3 and PAT1 are modulated in this milieu and play a crucial role in salt-sensitivity. High fructose ingestion also modulates the renin-angiotensin-aldosterone system. Recent attention has been shifted towards the contribution of the sympathetic nervous system, as clinical trials demonstrated significant reductions in blood pressure following renal sympathetic nerve ablation. New preclinical data demonstrates the activation of the renal sympathetic nerves in fructose-induced salt-sensitive hypertension, and reductions of blood pressure after renal nerve ablation. This review further demonstrates the interplay between sodium handling by the kidney, the renin-angiotensin-aldosterone system, and activation of the renal sympathetic nerves as important mechanisms in fructose and salt-induced hypertension.

Central sympathoinhibition and peripheral neuronal uptake blockade after desipramine in rabbits

1991 ◽  
Vol 260 (4) ◽  
pp. R824-R832 ◽  
Author(s):  
G. Eisenhofer ◽  
T. Saigusa ◽  
M. D. Esler ◽  
H. S. Cox ◽  
J. A. Angus ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Nerves ◽  
Neuronal Uptake ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Mediated Effects ◽  
Before And After ◽  
Peripheral Effect ◽  
Renal Sympathetic

Peripheral- and central nervous system (CNS)-mediated effects of desipramine (Des) on sympathetic nerves and the contribution of alpha 2-adrenoceptors to these effects were studied in conscious rabbits. Blood pressure, renal sympathetic nerve activity (SNA), and norepinephrine (NE) reuptake and spillover into plasma were measured before and after intracisternal (ic) or intravenous (i.v.) administration of Des. In other animals, NE spillover responses to i.v. Des were examined before and after alpha 2-adrenoceptor blockade with i.v. idazoxan. Treatment with i.v. Des blocked neuronal reuptake and decreased renal SNA but did not alter blood pressure or NE spillover. Decreased NE release by sympathetic nerves after i.v. Des was reflected by a decrease in the combined rate of NE reuptake and spillover. Treatment with ic Des (at 1.7% of the i.v. dose) decreased blood pressure and renal SNA and produced equivalent falls in NE reuptake and spillover, indicating little peripheral effect of centrally administered Des on the efficiency of neuronal reuptake. Thus Des had two distinct actions: the drug blocked neuronal reuptake by direct actions on nerve endings and reduced SNA by actions within the CNS. After ic Des, decreased SNA produced parallel falls in NE reuptake, spillover, and blood pressure. After i.v. Des, blockade of neurotransmitter reuptake increased NE concentrations at sympathoeffector junctions offsetting the fall in SNA, so that there was little change in NE spillover or blood pressure. However, after alpha 2-adrenoceptor blockade with i.v. idazoxan, NE spillover increased in response to i.v. Des. Thus the Des-induced decrease in NE release was partly mediated by an action of raised intrasynaptic NE concentrations on inhibitory alpha 2-adrenoceptors.

Renal Function in Saline-Loaded Dogs with Minimal Sodium Excretion

1973 ◽  
Vol 51 (2) ◽  
pp. 148-152 ◽  
Author(s):  
Mortimer Levy ◽  
Earle A. Lockhart
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Arterial Blood ◽  
Saline Loading ◽  
Blood Pressure Fall ◽  
Pressure Fall

In this laboratory, dogs acutely saline-loaded to 7–8% body weight and treated with large doses of antidiuretic hormone and deoxycorticosterone acetate will excrete on the average 400–700 μequiv/min of sodium. We have been able to study five dogs, similarly treated, which for no apparent cause showed a trivial natriuretic response following comparable volume expansion. Postexpansion sodium excretion varied from 30 to 150 μequiv/min. Glomerular filtration rate and arterial blood pressure remained constant, but in each case p-aminohippurate clearance rate (CPAH) fell in response to acute saline loading. Renal vasodilatation with acetylcholine and elevation of perfusion pressure with noradrenaline reversed the sodium retention. Fractional reabsorption in the proximal tubule was normal, and the loop of Henle appeared to be the major nephron site responsible for the augmented sodium reabsorption. Constancy of arterial blood pressure, fall in CPAH, and response to altered intrarenal hemodynamics seem to characterize these saline-loaded dogs with minimal sodium excretion as a unique population.

Role of renal sympathetic nerves in response of the ovine fetus to volume expansion

1990 ◽  
Vol 259 (5) ◽  
pp. R1050-R1055 ◽  
Author(s):  
F. G. Smith ◽  
T. Sato ◽  
O. J. McWeeny ◽  
J. M. Klinkefus ◽  
J. E. Robillard
Keyword(s):  
Volume Expansion ◽  
Renal Denervation ◽  
Sympathetic Nerves ◽  
Renal Hemodynamics ◽  
Fetal Life ◽  
Renal Nerve ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Renal Sympathetic

To investigate the role of renal sympathetic nerves in the fetal response to hypervolemia, studies were carried out in conscious, chronically instrumented fetal sheep aged 137-142 days of gestation. Bilateral renal denervation (n = 9) or sham surgery (n = 8) was carried out under halothane anesthesia 3-6 days before experiments. Bilateral renal denervation did not alter basal fetal renal hemodynamics, glomerular filtration rate (GFR), or Na+ excretion. Volume expansion with 6% Dextran 70 (18 ml/kg) was associated with a fall in fetal hematocrit, a sustained increase in mean arterial blood pressure, and a sustained diuresis and natriuresis. There was no significant change in GFR during fetal hypervolemia from control levels of 4.51 +/- 0.74 ml/min (intact) and 4.43 +/- 0.43 ml/min (denervated). Atrial natriuretic factor increased from 144 +/- 34 to 464 +/- 134 pg/ml, and plasma renin activity decreased from 5.15 +/- 1.7 to 3.04 +/- 1.0 ng.ml-1.h-1 in intact animals, within 30 min of completion of the dextran infusion. Similar changes occurred in denervated fetuses. Plasma aldosterone levels remained constant in intact and denervated fetuses during hypervolemia at control levels of 40.8 +/- 5.4 and 59.3 +/- 8.4 pg/ml, respectively. These findings suggest that renal sympathetic nerves do not influence basal renal hemodynamics or function and do not appear to play an important role in the natriuretic response to volume expansion during fetal life. This can be explained by a low tonic renal nerve activity before birth.

Attenuated pressure natriuresis in the early phases of two-kidney Goldblatt hypertension

1984 ◽  
Vol 246 (5) ◽  
pp. F691-F699
Author(s):  
S. G. Rostand ◽  
K. A. Kirk
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Adrenal Glands ◽  
Perfusion Pressure ◽  
Hypertensive Rats ◽  
Excretory Function ◽  
Perfusate Flow ◽  
Pressure Natriuresis ◽  
Early Phases ◽  
Intact Rats

We studied the effect of changing perfusion pressure on the excretory function of isolated perfused nonclipped kidneys from the two-kidney Goldblatt hypertensive rat ( GHR ). Kidneys were studied from newly hypertensive rats about 8 days after contralateral renal artery clipping [blood pressure (BP) 138 +/- 4.3 mmHg] and before onset of hypertension 3 days following surgery (BP 111 +/- 1.9 mmHg). In addition, nonclipped kidneys from adrenalectomized Goldblatt rats were also examined approximately 9 days following surgery (BP 114 +/- 4.7 mmHg). Kidneys from sham-operated rats served as controls. We noted no differences in GFR in kidneys from newly hypertensive rats and sham controls above a perfusion pressure of 120 mmHg. In response to increasing perfusing pressure, perfusate flow and fractional sodium excretion were significantly lower in newly hypertensive rats than in sham-operated controls. No differences in glomerular filtration rate, perfusate flow, or sodium excretion were noted in kidneys from sham-operated rats or Goldblatt rats 3 days following surgery. After clipping, adrenalectomized (ADX) Goldblatt rats had less of a rise in blood pressure than did rats with intact adrenal glands. No attenuation of natriuresis was noted in the ADX-clipped group in response to increasing perfusion pressure. Isolated perfused kidneys from ADX rats had greater sodium excretion at all levels of pressure than kidneys from rats with intact adrenal glands. Deoxycorticosterone acetate replacement returned sodium excretion to that approaching intact rats. We conclude that nonclipped kidneys of newly hypertensive Goldblatt rats exhibit blunted pressure natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

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