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.

Effect of endotoxin on kidney function and renal hemodynamics in the dog

1961 ◽  
Vol 201 (1) ◽  
pp. 144-148 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Wesley W. Spink ◽  
James A. Vick ◽  
Edmund Mallet ◽  
Joanne Finstad
Keyword(s):  
Kidney Function ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Temporary Increase ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Sublethal Doses ◽  
Renal Tubular ◽  
Lethal Doses ◽  
Logical Extension

The effect of endotoxin on kidney function and renal hemodynamics in the intact dog has not been reported. The present study is a logical extension of previous work completed in eviscerated dogs and its purpose was to study the effects of lethal and sublethal injections of endotoxin on the kidney of the intact dog. PAH and creatinine clearance procedures were carried out in adult anesthetized animals. Findings show that administration of lethal doses of endotoxin results in impaired renal function which may be attributed to the effects of systemic hypotension, renal vasoconstriction, and a possible action of endotoxin on renal tubular activity. However, with sublethal doses of endotoxin, in which the systemic arterial blood pressure does not fall to hypotensive levels, a temporary increase in renal plasma flow may be observed which appears to be due to an effect of endotoxin on the kidney or to extrarenal influences.

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.

Systemic and renal haemodynamic changes in renal schemia/reperfusion injury: impact of erythropoietin

2012 ◽  
Vol 90 (11) ◽  
pp. 1535-1543 ◽  
Author(s):  
Abdel-Aziz M. Hussein ◽  
Nashwa Barakat ◽  
Amira Awadalla ◽  
Ahmed A. Shokeir
Keyword(s):  
Renal Function ◽  
Renal Plasma Flow ◽  
Treated Group ◽  
Significant Rise ◽  
Control Group ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Group I ◽  
Haemodynamic Changes ◽  
Renal Vascular

The objective of this study was to investigate the effects of erythropoietin (EPO) on systemic and renal hemodynamics in a rat model of renal ischemic/reperfusion (I/R) injury. We used 30 male Sprague–Dawley rats distributed among the following 3 groups (10 rats per group): (i) the sham-operated group, (ii) the control group (I/R injury only), and (iii) the EPO-treated group (I/R injury with 1500 U EPO·(kg body mass)–1 on day 0, and 500 U·kg–1 on days 2 and 4 after ischemia). Renal function, arterial blood pressure (ABP), renal plasma flow (RPF), renal blood flow (RBF), and renal vascular resistance (RVR) were measured on days 1, 2, and 7 after ischemia. The expression of endothelial NO synthase (eNOS) and histopathology of kidney were evaluated on day 7. The contractility of aortic strips was recorded from the different groups. The results show that renal function and histopathology were significantly improved after treatment with EPO. Compared with the control group, the EPO-treated group showed a significant increase in RPF, RBF, haematocrite, ABP, eNOS expression, and a decrease in RVR (p < 0.05).The response of aortic strips to the relaxant effect of acetylcholine was improved in the EPO-treated group. In conclusion, treatment with EPO improves renal function and renal haemodynamics in renal I/R injury, and causes significant rise of ABP and haematocrite value.

Increased spillover of dopa into arterial blood during dietary salt loading

1990 ◽  
Vol 78 (4) ◽  
pp. 423-429 ◽  
Author(s):  
Ehud Grossman ◽  
Aaron Hoffman ◽  
Peter C. Chang ◽  
Harry R. Keiser ◽  
David S. Goldstein
Keyword(s):  
Steady State ◽  
Urinary Excretion ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Dietary Salt ◽  
Rat Strains ◽  
Salt Loading ◽  
Arterial Blood ◽  
Daily Excretion ◽  
Excretion Rates

1. We measured urinary excretion rates of dopamine (3,4-dihydroxyphenethylamine) and dopa (3,4-dihydroxyphenylalanine) and the spillover rate of dopa into arterial blood during dietary salt loading in conscious Dahl salt-sensitive and salt-resistant rats with intact or denervated kidneys. 2. Dopa spillover was calculated from the steady-state clearance of intravenously infused l-[3H]dopa and arterial levels of endogenous dopa. 3. Daily excretion rates of dopa and dopamine increased by about sixfold during salt loading in both rat strains. Bilateral renal denervation delayed these increases and the natriuretic responses. 4. During dietary salt loading, dopa spillover increased to approximately the same extent as simultaneously measured dopamine excretion. 5. The results suggest that increases in urinary excretion of dopamine during dietary salt loading can be accounted for by increases in the release of dopa into the bloodstream and that the renal nerves contribute to the dopa and dopamine excretory responses.

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.

1196Transvascular pace-capture of aorticorenal ganglia provides a testable procedural endpoint for transcatheter renal artery denervation and identifies a novel therapeutic ablation target for denervation

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
P C Qian ◽  
M A Barry ◽  
J Lu ◽  
J Pouliopoulos ◽  
A Mina ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Sympathetic Nerve ◽  
Renal Denervation ◽  
Vena Cava ◽  
Renal Sympathetic Denervation ◽  
Local Health ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Renal Sympathetic

Abstract Background Transcatheter renal denervation procedures often produces incomplete renal denervation and inconsistent antihypertensive effect. The lack of an intraprocedural method for renal sympathetic nerve function assessment has precluded a rational and physiologically based approach to ensure adequate denervation has been achieved at the time of the procedure. Purpose To demonstrate that it is possible to localise aorticorenal ganglia via transvascular pacing to provide: 1) a testable procedural endpoint for transcatheter renal denervation and, 2) a novel ablation target for renal denervation. Methods High frequency pacing in the inferior vena cava and aorta, invasive blood pressure measurements and renal angiography was performed in sheep (N=19) to identify ARG pace-capture sites by concurrent hypertensive and renal vasoconstrictive responses. Group A (N=5) underwent ink injection labelling at the ARG pace-capture site for histological verification; Group B (N=6) received unilateral irrigated radiofrequency ablation of ARG pace-capture sites and assessment of renal innervation at 1week post-procedure; and Group C (N=8) had ARG pacing performed prior to and 2–3 weeks after unilateral transcatheter microwave renal denervation. Results ARG pace-capture responses were observed at paired discrete sites in the posterior IVC and anterolateral aorta approximately 40mm above the ipsilateral renal artery. Pacing elicited a mean arterial blood pressure change of 22.2 [IQR 15.5–34.3] mmHg, p<0.001, together with ipsilateral renal vasoconstriction with main renal artery calibre change of −0.42mm [IQR −0.64mm to −0.24mm] measured with quantitative coronary analysis (QCA), p<0.0001, and branch renal artery median pixel density index change −10.4% [IQR −22.7% to −3.0%], p=0.003. Contralateral renal arterial vasoconstriction was not observed consistently at either the main or branch renal artery level. Sympathetic ganglionic tissue was observed at ARG pace-capture sites, and ganglion ablation caused significant ipsilateral renal denervation with a median hilar functional sympathetic nerve area reduction of 51% [IQR 24%–52%], p=0.043, and renal cortical norepinephrine reduction of 54% [IQR 36%–59%], p=0.043. Circumferential renal denervation resulted in immediate and sustained abolition of ARP pacing induced renal vasoconstriction and significant ipsilateral renal denervation. Conclusion Localisation of ARG using transvascular pacing is feasible with pace-capture demonstrated by concurrent hypertensive and ipsilateral renal arterial vasoconstrictive responses. Abolition of ARG pacing induced renal arterial vasoconstriction may indicate successful renal sympathetic denervation, providing a physiological procedural endpoint to guide transcatheter renal denervation. Additionally, ablation of ARG could provide an alternative or adjunctive method for renal denervation. Acknowledgement/Funding University of Sydney; Western Sydney Local health District; National Health and Medical Research Council of Australia; National Heart Foundation (Au)

Evidence that dopamine-2 mechanisms control renal function

1990 ◽  
Vol 259 (5) ◽  
pp. F793-F800 ◽  
Author(s):  
H. M. Siragy ◽  
R. A. Felder ◽  
N. L. Howell ◽  
R. L. Chevalier ◽  
M. J. Peach ◽  
...  
Keyword(s):  
Renal Function ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Urinary Flow ◽  
Plasma Aldosterone Concentration ◽  
Arterial Blood ◽  
Ly 171555 ◽  
Renal Vascular ◽  
Dose Dependent

Dopamine is synthesized by the kidney, and dopamine-2 (DA2) receptors are present in the renal glomerulus. However, no role for DA2 receptors in the kidney has been defined. We investigated the possible role of DA2 receptors in control of renal function by intrarenal infusion of a highly specific DA2 antagonist YM-09151 (YM), in conscious uninephrectomized dogs (n = 5) in metabolic balance at Na intake 40 meq/day. YM infused at 0.01 pmol.kg-1.min-1 did not cause any changes in urinary flow rate or Na excretion. Administration of YM (infusions from 0.1 to 10.0 pmol.kg-1.min-1) caused a significant dose-dependent diuresis (F = 20.3; P less than 0.001) and natriuresis (F = 35.2; P less than 0.0001) and an increase in glomerular filtration rate (F = 45.4; P less than 0.0001), renal plasma flow (F = 209.3; P less than 0.0001), and filtration fraction (F = 11.2; P less than 0.0001). No significant changes in plasma renin activity, plasma aldosterone concentration, or mean arterial blood pressure occurred with any of the doses of YM infused into the renal artery. Coinfusion of LY-171555, a specific DA2 agonist, at a dose that itself did not affect renal function, completely abrogated the renal hemodynamic and excretory changes induced by YM. The data suggest that dopamine produced intrarenally may act at renal vascular and/or glomerular DA2 receptors to control renal function.

Renal nerves and experimental hypertension: evidence and controversy

1987 ◽  
Vol 65 (8) ◽  
pp. 1540-1547 ◽  
Author(s):  
Robert L. Kline
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Renal Denervation ◽  
Spontaneously Hypertensive Rat ◽  
Sodium Intake ◽  
Renal Nerves ◽  
Experimental Hypertension ◽  
Renal Nerve ◽  
Spontaneously Hypertensive ◽  
Hemodynamic Variables

Noradrenergic fibers innervate various parts of the nephron and can contribute to sodium and water homeostasis by influencing hemodynamic variables, tubular reabsorptive mechanisms, and renin release. As renal function is considered to be a primary determinant of arterial pressure, efferent renal nerves may be an important link between the central nervous system and the kidney in the development and maintenance of hypertension. Little is known about the relative importance of renal nerves and their interactions with other factors in influencing renal function chronically. There is disagreement about the evidence for enhanced noradrenergic drive to the kidney in hypertensive rats, as the renal nerve firing rate, neurotransmitter release and metabolism, and receptor properties are generally not studied in association with measurements of renal function. However, chronic renal denervation has been shown to significantly affect arterial pressure in diverse forms of experimental hypertension in rats, including genetic models, as well as renovascular, mineralocorticoid, neurogenic, and angiotensin II hypertension. The actual mechanisms responsible for this effect of renal denervation are not clear, but presumably reflect changes in the arterial pressure – urinary sodium output relationship. On the whole, there is reasonable correlation between neurophysiological, biochemical, and renal denervation studies in the spontaneously hypertensive rat, suggesting that renal nerves do play a role in the onset of hypertension in these animals. The effect of renal denervation in other models of hypertension seems less clear, with recent reports showing that renal denervation does not alter the hypertensive process in renovascular, mineralocorticoid, and salt-related hypertension. These contradictory findings are not easily explained, but there is some indication that elevated sodium intake may alter the response to renal denervation. Resolution of these controversies must await a better understanding of the influence of renal nerves on renal function and arterial pressure in normal and hypertensive animals.

Increasing oxidative stress with molsidomine increases blood pressure in genetically hypertensive rats but not normotensive controls

2005 ◽  
Vol 289 (3) ◽  
pp. R763-R770 ◽  
Author(s):  
Lourdes A. Fortepiani ◽  
Jane F. Reckelhoff
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Renal Hemodynamics ◽  
Hypertensive Rats ◽  
No Donor ◽  
Spontaneously Hypertensive ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Wistar Kyoto ◽  
Nitrate And Nitrite

Spontaneously hypertensive rats (SHR) have a higher level of oxidative stress and exhibit a greater depressor response to a superoxide scavenger, tempol, than normotensive Wistar-Kyoto rats (WKY). This study determined whether an increase in oxidative stress with a superoxide/NO donor, molsidomine, would amplify the blood pressure in SHR. Male SHR and WKY were given molsidomine (30 mg·kg−1·day−1) or vehicle (0.01% ethanol) for 1 wk, and blood pressure, renal hemodynamics, nitrate and nitrite excretion (NOx), renal superoxide production, and expression of renal antioxidant enzymes, Mn- and Cu,Zn-SOD, catalase, and glutathione peroxidase (GPx), were measured. Renal superoxide and NOx were higher in control SHR than in WKY. Molsidomine increased superoxide by ∼35% and NOx by 250% in both SHR and WKY. Mean arterial blood pressure (MAP) was also higher in control SHR than WKY. Molsidomine increased MAP by 14% and caused renal vasoconstriction in SHR but reduced MAP by 16%, with no effect on renal hemodynamics, in WKY. Renal expression of Mn- and Cu,Zn-SOD was not different between SHR and WKY, but expression of catalase and GPx were ∼30% lower in kidney of SHR than WKY. The levels of Mn- and Cu,Zn-SOD were not increased with molsidomine in either WKY or SHR. Renal catalase and GPx expression was increased by 300–400% with molsidomine in WKY, but there was no effect in SHR. Increasing oxidative stress elevated blood pressure further in SHR but not WKY. WKY are likely protected because of higher bioavailable levels of NO and the ability to upregulate catalase and GPx.

Renal responses to hypoxemia during renin-angiotensin system inhibition in fetal lambs

1985 ◽  
Vol 249 (1) ◽  
pp. R116-R124 ◽  
Author(s):  
K. T. Nakamura ◽  
N. A. Ayres ◽  
R. A. Gomez ◽  
J. E. Robillard
Keyword(s):  
Renin Angiotensin System ◽  
Base Line ◽  
Urinary Flow ◽  
Ang Ii ◽  
Functional Responses ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Renal Hemodynamic ◽  
Excretion Rates

The role of the renin-angiotensin system (RAS) in modulating the renal hemodynamic and functional responses to hypoxemia was studied in chronically catheterized fetal lambs (132-143 days gestation; term 145 days) before and during administration of either captopril or [Sar1-Gly8]ANG II. Base-line mean arterial blood pressure decreased significantly after administration of either captopril or [Sar1-Gly8]ANG II. This decrease was associated with a significant decline in renal vascular resistance (RVR) in captopril-treated fetuses, whereas no changes in RVR were observed in [Sar1-Gly8]ANG II-treated fetuses. However, the decline in renal blood flow (RBF) and the rise in RVR associated with hypoxemia in control fetuses were not attenuated significantly during inhibition of the RAS using either captopril or [Sar1-Gly8]ANG II. Moreover neither captopril nor [Sar1-Gly8]ANG II blunted the hypertensive response associated with fetal hypoxemia. The renal functional response to captopril was different from the response observed during infusion of [Sar1-Gly8]ANG II. Administration of [Sar1-Gly8]ANG II produced significant decreases in urinary flow rate (UFR), glomerular filtration rate (GFR), and urinary electrolyte (Na+, K+, Cl-) excretion rates, whereas no changes were observed during captopril infusion. The effects of hypoxemia on renal function were not modified after captopril. However, [Sar1-Gly8]ANG II tended to increase UFR and GFR, but these changes were pressure-dependent and not directly related to inhibition of the RAS. This study suggests that the RAS is not an important mediator of the fetal renal hemodynamic and functional responses to hypoxemia.

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