Effects of renal denervation on cardiovascular response to furosemide in conscious lambs

1995 ◽  
Vol 269 (1) ◽  
pp. H149-H152 ◽  
Author(s):  
F. G. Smith ◽  
A. M. Strack
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Renal Denervation ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Before And After ◽  
Renal Sympathetic

The cardiovascular response to furosemide in the newborn and the role of renal sympathetic nerves in influencing this response have not been investigated. We hypothesized that in conscious lambs, furosemide would decrease blood pressure, the response being accentuated in the absence of renal sympathetic nerves. Pulsatile pressures and heart rates were measured before and after furosemide (2 mg/kg) administration to chronically instrumented lambs with either bilateral renal denervation (denervated, n = 8) or renal nerves intact (intact, n = 6). In intact lambs, mean arterial pressure remained constant after furosemide; in denervated lambs there was an increase in arterial pressure 20 min after furosemide (P < 0.001), and control levels were reached by 100 min. Basal heart rate was higher in denervated than in intact lambs (P = 0.009). In both groups of lambs, heart rate increased 40 min after furosemide and remained elevated. These data provide new information that, in conscious newborn animals, renal sympathetic nerves influence the blood pressure response to furosemide, as well as basal control of heart rate.

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.

Contribution of renal nerves to renal blood flow variability during hemorrhage

1998 ◽  
Vol 274 (5) ◽  
pp. R1283-R1294 ◽  
Author(s):  
Simon C. Malpas ◽  
Roger G. Evans ◽  
Geoff A. Head ◽  
Elena V. Lukoshkova
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Spectral Power ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Similar Frequency ◽  
Blood Withdrawal ◽  
Conscious Rabbits ◽  
Renal Sympathetic

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml ⋅ min−1 ⋅ kg−1for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 ± 1 vs. 31 ± 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of the oscillations in each variable. Before hemorrhage, a rhythm at ∼0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (<0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies >0.25 Hz was significantly less in intact than denervated rabbits (0.83 ± 0.12 vs. 1.19 ± 0.10 ml ⋅ min−1 ⋅ mmHg−1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These were accompanied by increases in the spectral power of RBF at the same frequency. As arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this is myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.

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.

scholarly journals Renal Denervation and Celiac Ganglionectomy Decrease Mean Arterial Pressure Similarly in Genetically Hypertensive Schlager (BPH/2J) Mice

Hypertension ◽  
2021 ◽  
Author(s):  
Ninitha Asirvatham-Jeyaraj ◽  
Madeline M. Gauthier ◽  
Christopher T. Banek ◽  
Abhismitha Ramesh ◽  
Hannah Garver ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Denervation ◽  
Before And After ◽  
Pressor Activity ◽  
Celiac Ganglionectomy ◽  
Surgical Treatments ◽  
Tissue Norepinephrine ◽  
Genetically Hypertensive

Renal denervation (RDNX) lowers mean arterial pressure (MAP) in patients with resistant hypertension. Less well studied is the effect of celiac ganglionectomy (CGX), a procedure which involves the removal of the nerves innervating the splanchnic vascular bed. We hypothesized that RDNX and CGX would both lower MAP in genetically hypertensive Schlager (BPH/2J) mice through a reduction in sympathetic tone. Telemeters were implanted into the femoral artery in mice to monitor MAP before and after RDNX (n=5), CGX (n=6), or SHAM (n=6). MAP, systolic blood pressure, diastolic blood pressure, and heart rate were recorded for 14 days postoperatively. The MAP response to hexamethonium (10 mg/kg, IP) was measured on control day 3 and postoperative day 10 as a measure of global neurogenic pressor activity. The efficacy of denervation was assessed by measurement of tissue norepinephrine. Control MAP was similar among the 3 groups before surgical treatments (≈130 mm Hg). On postoperative day 14, MAP was significantly lower in RDNX (−11±2 mm Hg) and CGX (−11±1 mm Hg) groups compared with their predenervation values. This was not the case in SHAM mice (−5±3 mm Hg). The depressor response to hexamethonium in the RDNX group was significantly smaller on postoperative day 10 (−10±5 mm Hg) compared with baseline control (−25±10 mm Hg). This was not the case in mice in the SHAM (day 10; −28±5 mm Hg) or CGX (day 10; −34±7 mm Hg) group. In conclusion, both renal and splanchnic nerves contribute to hypertension in BPH/2J mice, but likely through different mechanisms.

scholarly journals Renal Denervation in Hypertension

2021 ◽  
pp. 73-74
Author(s):  
Usman S Ansari ◽  
Benjamin J Lee
Keyword(s):  
Blood Pressure ◽  
Renal Denervation ◽  
Pressure Control ◽  
Renal Nerves ◽  
Radiofrequency Energy ◽  
Potential Treatment ◽  
Lifestyle Modifications ◽  
Potential Strategy ◽  
Maximal Medical Therapy ◽  
Renal Sympathetic

Hypertension is a significant cause of morbidity and mortality worldwide. However, many individuals fail to achieve proper blood pressure control despite lifestyle modifications and maximal medical therapy. Renal sympathetic overactivity has been proposed as a significant driver in such cases. One potential treatment is renal denervation (RDN), a minimally invasive catheter-based technology that uses radiofrequency energy to obliterate the renal nerves adjacent to the afferent and efferent renal arteries. While RDN was initially developed as a potential strategy to treat resistant hypertension, several studies have investigated its use as an adjunctive therapy for hypertension. The following are 10 points to remember about the use of RDN in hypertension.

Renal nerves in compensatory renal response to contralateral renal denervation

1980 ◽  
Vol 238 (1) ◽  
pp. F26-F30 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Rios
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Left Kidney ◽  
Fractional Excretion ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Renal Response ◽  
Fractional Sodium Excretion ◽  
Fractional Excretion Of Sodium ◽  
Renal Sympathetic

Acute unilateral renal denervation and the resultant antidiuresis and antinatriuresis are accompanied by a compensatory antidiuresis and antinatriuresis from the opposite kidney. The present study tested the hypothesis that the renal sympathetic nerves mediated this adaptive response. In the volume-expanded rat, acute left renal denervation increased left kidney fractional sodium excretion from 4.4 +/- 0.6 to 5.9 +/- 0.6%, while right kidney fractional sodium excretion decreased from 4.3 +/- 0.6 to 3.5 +/- 0.5%. Subsequent acute right renal denervation increased right kidney fractional sodium excretion from 3.5 +/- 0.5 to 4.7 +/- 0.6%. Measurement of efferent left renal sympathetic nerve activity before and after acute right renal denervation showed an increase from 10.9 +/- 0.8 to 16.0 +/- 1.4 Hz. When both kidneys were simultaneously subjected to acute renal denervation, fractional excretion of sodium increased bilaterally. In uninephrectomized rats subjected to acute denervation of the remaining kidney, fractional excretion of sodium increased. Glomerular filtration rate was unchanged throughout in all studies. These results demonstrate that the compensatory renal response to acute contralateral renal denervation is mediated by the efferent renal sympathetic nerves.

Abstract P149: Bilateral Renal Denervation Attenuates Hypertension in Male Rats Deficient of Functional Endothelin B Receptors but Does Not Affect Salt-Sensitivity

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Bryan K Becker ◽  
Amanda C Feagans ◽  
Chunhua Jin ◽  
David M Pollock
Keyword(s):  
Blood Pressure ◽  
Total Protein ◽  
Renal Denervation ◽  
High Salt ◽  
Male Rats ◽  
Renal Nerves ◽  
High Salt Diet ◽  
Salt Diet ◽  
Endothelin B ◽  
Renal Sympathetic

Independent studies of renal sympathetic nerves and the endothelin (ET) system have demonstrated important contributions of each in the progression of hypertension. Very few studies, however, have investigated the interaction between the ET system and renal nerves in relation to blood pressure control and electrolyte homeostasis. Although endothelin B (ETB) receptors in the renal medulla promote natriuresis, ETB receptors on sympathetic neurons are thought to increase neuronal activity. We hypothesized that renal denervation reduces blood pressure in a salt-sensitive, hypertensive model of ET dysfunction, the ETB-deficient (ETB-def) rat, which lacks functional ETB receptors in all tissues except neurons. After bilateral renal sympathetic denervation (Dnx) or sham operation of ETB-def and transgenic control (TG) rats, baseline blood pressure was recorded via telemetry for 5 days on a normal salt (0.49% NaCl) diet followed by a high salt (4.0%) diet. At baseline, ETB-def Dnx rats had a lower 24-hr systolic blood pressure (SBP) (152.6 ± 3.6 mmHg) relative to ETB-def sham (167.8 ± 2.6 mmHg; p < 0.005; n = 7/group). Denervation did not significantly affect TG rats relative to sham on normal salt (138.8 ± 2.5 vs. 144.7 ± 0.5 mmHg respectively; p = 0.53; n = 6/group). Following 10 days of high salt diet, ETB-def sham rats had an increased 24-hr SBP (+10.59 ± 2.8 mmHg relative to baseline; p < 0.005). There was a similar increase in SBP in ETB-def Dnx rats (+10.03 ± 2.3 mmHg relative to baseline; p < 0.005), although the ETB-def Dnx group remained lower than ETB-def sham. High salt had no effect on TG sham or Dnx animals (-2.2 ± 1.3 and -0.6 ± 2.8 mmHg relative to baseline). Preliminary evidence from a subset of the animals in this experiment indicated a dramatically reduced inner medullary ET-1 content in ETB-def sham rats vs. TG sham (97.9 ± 15.4 vs. 327.0 ± 25.4 ng/mg total protein; p < 0.005; n = 3-4/group) in both ETB-def and TG groups, Dnx tended to increase inner medullary ET-1 content (181.8 ± 75.8 and 402.7 ± 19.6 ng/mg total protein respectively). We conclude that in a model of ET dysfunction, the renal nerves are integral mediators of hypertension during normal salt diet, but do not mediate the increase in pressure following high salt diet in this model of salt-sensitive hypertension.

Modulation of the baroreceptor reflex by the dorsomedial hypothalamic nucleus and perifornical area

2006 ◽  
Vol 290 (4) ◽  
pp. R1020-R1026 ◽  
Author(s):  
Lachlan M. McDowall ◽  
Jouji Horiuchi ◽  
Suzanne Killinger ◽  
Roger A. L. Dampney
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Psychological Stress ◽  
Cardiovascular Response ◽  
Baroreceptor Reflex ◽  
Hypothalamic Nucleus ◽  
Baroreflex Control ◽  
Dorsomedial Hypothalamic Nucleus ◽  
Renal Sympathetic

Neurons within the dorsomedial hypothalamic nucleus (DMH) and perifornical area (PeF), which lie within the classic hypothalamic defense area, subserve the cardiovascular response to psychological stress. Previous studies have shown that electrical stimulation of the hypothalamic defense area causes inhibition of the cardiac and (in some cases) sympathetic components of the baroreceptor reflex. In contrast, naturally evoked psychological stress does not appear to be associated with such inhibition. In this study, we tested the effect of specific activation of neurons within the DMH and PeF on the baroreflex control of renal sympathetic nerve activity and heart rate in urethane-anesthetized rats. Microinjection of bicuculline (a GABAA receptor antagonist) into the DMH caused dose-dependent increases in heart rate and renal sympathetic activity, shifted the baroreflex control of both variables to higher levels (i.e., increased the upper and lower plateaus of the baroreflex function curves, and increased the threshold, midpoint, and saturation levels of mean arterial pressure). The maximum gain of the sympathetic component of the baroreflex was also increased, while that of the cardiac component was not significantly changed. Increases in the midpoint were very similar in magnitude to the evoked increases in baseline mean arterial pressure. Microinjection of bicuculline into the PeF evoked very similar effects. The results indicate that disinhibition of neurons in the DMH/PeF region not only increases sympathetic vasomotor activity and heart rate but also resets the baroreceptor reflex such that it remains effective, without any decrease in sensitivity, over a higher operating range of arterial pressure.

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