Influence on renal blood flow in renal denervation procedures

2019 ◽  
Vol 37 (2) ◽  
pp. 453-454 ◽  
Author(s):  
Masayuki Tanemoto
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Denervation

Renal blood flow in dogs during diffusion respiration

1959 ◽  
Vol 14 (3) ◽  
pp. 405-410 ◽  
Author(s):  
Joseph E. Stone ◽  
Richard L. Irwin ◽  
Charles D. Wood ◽  
William B. Draper ◽  
Richard W. Whitehead
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Medical Research ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Respiratory Arrest ◽  
Renal Ischemia ◽  
Central Effects ◽  
Marked Decline ◽  
Series Of Experiments

Two series of experiments were performed with appropriate controls on dogs in which respiratory arrest was produced and maintained by the injection of an overdose of thiopental or by administration of decamethonium, respectively. Renal blood flow was measured by a modification of the method of Selkurt ( Methods in Medical Research, vol. 1). A marked fall in renal blood flow coincident with apnea and anuria was found to occur consistently with diffusion respiration under thiopental. Both the renal ischemia and the anuria were preventable by renal denervation (pharmacological block). During diffusion respiration experiments in which decamethonium was used to cause and maintain apnea, a marked decline in renal blood flow or urine secretion did not occur during the first 15 minutes of apnea. It is concluded that the prompt onset of anuria in diffusion respiration under thiopental is due to a central synergism between thiopental and endogenous carbon dioxide. Further, it is reasoned that the delayed fall in renal blood flow and attendant anuria which occurred under decamethonium represent the central effects of increasing concentrations of carbon dioxide in the absence of thiopental. Submitted on November 5, 1958

Renal intracortical blood flow during hemorrhage: role of adrenergic mechanisms

1975 ◽  
Vol 229 (1) ◽  
pp. 178-184 ◽  
Author(s):  
Hardaker WT ◽  
TC Graham ◽  
AS Wechsler
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Radioactive Microspheres ◽  
Adrenergic Mechanisms ◽  
Anesthetized Dogs ◽  
Intrarenal Blood Flow ◽  
Inner Cortex

Hemorrhagic hypotensin in anesthetized dogs produced a redistribution of renal blood flow from the outer to the inner cortex. The role of adrenergic mechanisms in this redistribution was studied in anesthetized dogs using a radioactive microspheres to determine intrarenal blood flow. Neither renal denervation, nor pretreatment with reserpine altered the characteristic redistribution of renal cortical flow during hemorrhage. These observations suggest that neither intact renal nerves nor circulating catecholamines are necessary for the redistribution of renal intracortical blood flow during hemorrhagic hypotension, and the role of myogenic autoregulation is emphasized.

Renal Denervation in Combination With Angiotensin Receptor Blockade Prolongs Blood Pressure Trough During Hemorrhage

Hypertension ◽  
2021 ◽  
Author(s):  
Reetu R. Singh ◽  
Zoe McArdle ◽  
Lindsea C. Booth ◽  
Clive N. May ◽  
Geoff A. Head ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Blood Loss ◽  
Renal Blood Flow ◽  
Blood Volume ◽  
Antihypertensive Medication ◽  
Renal Denervation ◽  
Organ Damage ◽  
Antihypertensive Medications ◽  
Hemodynamic Responses

Majority of patients with hypertension and chronic kidney disease (CKD) undergoing renal denervation (RDN) are maintained on antihypertensive medication. However, RDN may impair compensatory responses to hypotension induced by blood loss. Therefore, continuation of antihypertensive medications in denervated patients may exacerbate hypotensive episodes. This study examined whether antihypertensive medication compromised hemodynamic responses to blood loss in normotensive (control) sheep and in sheep with hypertensive CKD at 30 months after RDN (control-RDN, CKD-RDN) or sham (control-intact, CKD-intact) procedure. CKD-RDN sheep had lower basal blood pressure (BP; ≈9 mm Hg) and higher basal renal blood flow (≈38%) than CKD-intact. Candesartan lowered BP and increased renal blood flow in all groups. 10% loss of blood volume alone caused a modest fall in BP (≈6–8 mm Hg) in all groups but did not affect the recovery of BP. 10% loss of blood volume in the presence of candesartan prolonged the time at trough BP by 9 minutes and attenuated the fall in renal blood flow in the CKD-RDN group compared with CKD-intact. Candesartan in combination with RDN prolonged trough BP and attenuated renal hemodynamic responses to blood loss. To minimize the risk of hypotension-mediated organ damage, patients with RDN maintained on antihypertensive medications may require closer monitoring when undergoing surgery or experiencing traumatic blood loss.

scholarly journals TCT-427 Second generation devices for renal denervation give better renal blood flow when compared with 1st generation catheters

2014 ◽  
Vol 64 (11) ◽  
pp. B125
Author(s):  
Waleed Kadro ◽  
Maya Turkmani ◽  
Hussam Rahim ◽  
Cathy John ◽  
Zaid Zaki ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Second Generation

scholarly journals Renal denervation modulates angiotensin receptor expression in the renal cortex of rabbits with chronic heart failure

2011 ◽  
Vol 300 (1) ◽  
pp. F31-F39 ◽  
Author(s):  
Sarah C. Clayton ◽  
Karla K. V. Haack ◽  
Irving H. Zucker
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Chronic Heart Failure ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

Excessive sympathetic drive is a hallmark of chronic heart failure (HF). Disease progression can be correlated with plasma norepinephrine concentration. Renal function is also correlated with disease progression and prognosis. Because both the renal nerves and renin-angiotensin II system are activated in chronic HF we hypothesized that excessive renal sympathetic nerve activity decreases renal blood flow in HF and is associated with changes in angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R) expression. The present study was carried out in conscious, chronically instrumented rabbits with pacing-induced HF. We found that rabbits with HF showed a decrease in mean renal blood flow (19.8 ± 1.6 in HF vs. 32.0 ± 2.5 ml/min from prepace levels; P < 0.05) and an increase in renal vascular resistance (3.26 ± 0.29 in HF vs. 2.21 ± 0.13 mmHg·ml−1·min in prepace normal rabbits; P < 0.05) while the blood flow and resistance was not changed in HF rabbits with the surgical renal denervation. Renal AT1R expression was increased by ∼67% and AT2R expression was decreased by ∼87% in rabbits with HF; however, kidneys from denervated rabbits with HF showed a near normalization in the expression of these receptors. These results suggest renal sympathetic nerve activity elicits a detrimental effect on renal blood flow and may be associated with alterations in the expression of angiotensin II receptors.

scholarly journals Renal nerves dynamically regulate renal blood flow in conscious, healthy rabbits

2016 ◽  
Vol 310 (2) ◽  
pp. R156-R166 ◽  
Author(s):  
Alicia M. Schiller ◽  
Peter R. Pellegrino ◽  
Irving H. Zucker
Keyword(s):  
Blood Flow ◽  
Phase Shift ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Function Analysis ◽  
Extracellular Fluid ◽  
Low Frequency ◽  
Renal Nerves ◽  
Physiological Regulation ◽  
Transfer Function Analysis

Despite significant clinical interest in renal denervation as a therapy, the role of the renal nerves in the physiological regulation of renal blood flow (RBF) remains debated. We hypothesized that the renal nerves physiologically regulate beat-to-beat RBF variability (RBFV). This was tested in chronically instrumented, healthy rabbits that underwent either bilateral surgical renal denervation (DDNx) or a sham denervation procedure (INV). Artifact-free segments of RBF and arterial pressure (AP) from calmly resting, conscious rabbits were used to extract RBFV and AP variability for time-domain, frequency-domain, and nonlinear analysis. Whereas steady-state measures of RBF, AP, and heart rate did not statistically differ between groups, DDNx rabbits had greater RBFV than INV rabbits. AP-RBF transfer function analysis showed greater admittance gain in DDNx rabbits than in INV rabbits, particularly in the low-frequency (LF) range where systemic sympathetic vasomotion gives rise to AP oscillations. In the LF range, INV rabbits exhibited a negative AP-RBF phase shift and low coherence, consistent with the presence of an active control system. Neither of these features were present in the LF range of DDNx rabbits, which showed no phase shift and high coherence, consistent with a passive, Ohm's law pressure-flow relationship. Renal denervation did not significantly affect nonlinear RBFV measures of chaos, self-affinity, or complexity, nor did it significantly affect glomerular filtration rate or extracellular fluid volume. Cumulatively, these data suggest that the renal nerves mediate LF renal sympathetic vasomotion, which buffers RBF from LF AP oscillations in conscious, healthy rabbits.

Effect of renal denervation on dynamic autoregulation of renal blood flow

2004 ◽  
Vol 286 (6) ◽  
pp. F1209-F1218 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sympathetic Nerve ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Vasoconstrictor intensities of renal sympathetic nerve stimulation elevate the renal arterial pressure threshold for steady-state stepwise autoregulation of renal blood flow. This study examined the tonic effect of basal renal sympathetic nerve activity on dynamic autoregulation of renal blood flow in rats with normal (Sprague-Dawley and Wistar-Kyoto) and increased levels of renal sympathetic nerve activity (congestive heart failure and spontaneously hypertensive rats). Steady-state values of arterial pressure and renal blood flow before and after acute renal denervation were subjected to transfer function analysis. Renal denervation increased basal renal blood flow in congestive heart failure (+35 ± 3%) and spontaneously hypertensive rats (+21 ± 3%) but not in Sprague-Dawley and Wistar-Kyoto rats. Renal denervation significantly decreased transfer function gain (i.e., improved autoregulation of renal blood flow) and increased coherence only in spontaneously hypertensive rats. Thus vasoconstrictor intensities of renal sympathetic nerve activity impaired the dynamic autoregulatory adjustments of the renal vasculature to oscillations in arterial pressure. Renal denervation increased renal blood flow variability in spontaneously hypertensive rats and congestive heart failure rats. The contribution of vasoconstrictor intensities of basal renal sympathetic nerve activity to limiting renal blood flow variability may be important in the stabilization of glomerular filtration rate.

Sympathetic nervous system in the loss of autoregulation in acute renal failure

1984 ◽  
Vol 246 (4) ◽  
pp. F379-F386 ◽  
Author(s):  
S. P. Kelleher ◽  
J. B. Robinette ◽  
J. D. Conger
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Nervous System ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Renal Blood Flow Autoregulation

The responsiveness of the renal vascular system was investigated in uninephrectomized Sprague-Dawley rats in which acute renal failure had been induced by norepinephrine. The animals were studied at 1' and 3 wk after norepinephrine infusion. Uninephrectomized littermates served as controls. Compared with controls, there was an absence of renal blood flow autoregulation in 1-wk acute renal failure that returned in part by 3 wk. In 1-wk rats there was a marked increase, rather than decrease, in renovascular resistance as renal perfusion pressure was decreased. The renal vasculature was significantly less responsive in 1-wk rats than in control or 3-wk animals when acetylcholine, angiotensin II, or norepinephrine was infused into the renal artery at minimal vasoactive doses (all P less than 0.01). Paradoxically, renal vasoconstriction in response to renal nerve stimulation was greater in 1-wk than in 3-wk and control rats (P less than 0.01) and was not inhibited by renal artery infusion of phenoxybenzamine. Renal denervation significantly improved renal blood flow autoregulation in 1-wk animals (P less than 0.001) and completely abolished the increase in renovascular resistance as renal perfusion pressure was lowered. No effects of renal denervation on renal blood flow autoregulation were seen in control and 3-wk rats. It is concluded that renovascular responses to neurohumoral stimuli are aberrant in acute renal failure. The loss of renal blood flow autoregulation is related to an increased renovascular resistance that is due to increased activity of non-alpha-adrenergic mechanisms of the autonomic nervous system.

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