Effect of mesenteric vascular congestion on reflex control of renal blood flow

2007 ◽  
Vol 293 (5) ◽  
pp. R1917-R1922 ◽  
Author(s):  
Shereen M. Hamza ◽  
Susan Kaufman
Keyword(s):  
Blood Flow ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Vascular Congestion ◽  
Reflex Control ◽  
Celiac Ganglionectomy ◽  
Renal Sympathetic

Portal hypertension initiates a splenorenal reflex, whereby increases in splenic afferent nerve activity and renal sympathetic nerve activity cause a decrease in renal blood flow (RBF). We postulated that mesenteric vascular congestion similarly compromises renal function through an intestinal-renal reflex. The portal vein was partially occluded in anesthetized rats, either rostral or caudal to the junction with the splenic vein. Portal venous pressure increased (6.5 ± 0.1 to 13.2 ± 0.1 mmHg; n = 78) and mesenteric venous outflow was equally obstructed in both cases. However, only rostral occlusion increased splenic venous pressure. Rostral occlusion caused a fall in RBF (−1.2 ± 0.2 ml/min; n = 9) that was attenuated by renal denervation (−0.5 ± 0.1 ml/min; n = 6), splenic denervation (−0.2 ± 0.1 ml/min; n = 11), celiac ganglionectomy (−0.3 ± 0.1 ml/min; n = 9), and splenectomy (−0.5 ± 0.1 ml/min; n = 6). Caudal occlusion induced a significantly smaller fall in RBF (−0.5 ± 0.1 ml/min; n = 9), which was not influenced by renal denervation (−0.2 ± 0.2 ml/min; n = 6), splenic denervation (−0.1 ± 0.1 ml/min; n = 7), celiac ganglionectomy (−0.1 ± 0.3 ml/min; n = 8), or splenectomy (−0.3 ± 0.1 ml/min; n = 7). Renal arterial conductance fell only in intact animals subjected to rostral occlusion (−0.007 ± 0.002 ml·min−1·mmHg−1). This was accompanied by increases in splenic afferent nerve activity (15.0 ± 3.5 to 32.6 ± 6.2 spikes/s; n = 7) and renal efferent nerve activity (32.7 ± 5.2 to 39.3 ± 6.0 spikes/s; n = 10). In animals subjected to caudal occlusion, there were no such changes in renal arterial conductance or splenic afferent/renal sympathetic nerve activity. We conclude that the portal hypertension-induced fall in RBF is initiated by increased splenic, but not mesenteric, venous pressure, i.e., we did not find evidence for intestinal-renal reflex control of the kidneys.

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.

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.

scholarly journals Role of the heart in blood pressure lowering during chronic baroreflex activation: insight from an in silico analysis

2018 ◽  
Vol 315 (5) ◽  
pp. H1368-H1382 ◽  
Author(s):  
John S. Clemmer ◽  
W. Andrew Pruett ◽  
Robert L. Hester ◽  
Radu Iliescu ◽  
Thomas E. Lohmeier
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Blood Pressure Lowering ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Pressure Lowering ◽  
Renal Sympathetic ◽  
Stimulation Of

Electrical stimulation of the baroreflex chronically suppresses sympathetic activity and arterial pressure and is currently being evaluated for the treatment of resistant hypertension. The antihypertensive effects of baroreflex activation are often attributed to renal sympathoinhibition. However, baroreflex activation also decreases heart rate, and robust blood pressure lowering occurs even after renal denervation. Because controlling renal sympathetic nerve activity (RSNA) and cardiac autonomic activity cannot be achieved experimentally, we used an established mathematical model of human physiology (HumMod) to provide mechanistic insights into their relative and combined contributions to the cardiovascular responses during baroreflex activation. Three-week responses to baroreflex activation closely mimicked experimental observations in dogs including decreases in blood pressure, heart rate, and plasma norepinephrine and increases in plasma atrial natriuretic peptide (ANP), providing validation of the model. Simulations showed that baroreflex-induced alterations in cardiac sympathetic and parasympathetic activity lead to a sustained depression of cardiac function and increased secretion of ANP. Increased ANP and suppression of RSNA both enhanced renal excretory function and accounted for most of the chronic blood pressure lowering during baroreflex activation. However, when suppression of RSNA was blocked, the blood pressure response to baroreflex activation was not appreciably impaired due to inordinate fluid accumulation and further increases in atrial pressure and ANP secretion. These simulations provide a mechanistic understanding of experimental and clinical observations showing that baroreflex activation effectively lowers blood pressure in subjects with previous renal denervation. NEW & NOTEWORTHY Both experimental and clinical studies have shown that the presence of renal nerves is not an obligate requirement for sustained reductions in blood pressure during chronic electrical stimulation of the carotid baroreflex. Simulations using HumMod, a mathematical model of integrative human physiology, indicated that both increased secretion of atrial natriuretic peptide and suppressed renal sympathetic nerve activity play key roles in mediating long-term reductions in blood pressure during chronic baroreflex activation.

scholarly journals Effects of Renal Denervation from the Intima and the Adventitia of Renal Arteries on Renal Sympathetic Nerve Activity in Dogs: A Comparative Study

Cardiology ◽  
2015 ◽  
Vol 131 (3) ◽  
pp. 189-196 ◽  
Author(s):  
Minfu Bai ◽  
Chaokuan Yang ◽  
Chuanyu Gao ◽  
Xianpei Wang ◽  
Hongzhi Liu ◽  
...  
Keyword(s):  
Treatment Group ◽  
Renal Artery ◽  
Sympathetic Nerve ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Renal Arteries ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Objectives: This study was designed to observe the efficacy and safety of renal denervation from the inside and outside of renal arteries. Methods: Fourteen beagles were randomly divided into a control group (n = 4) and treatment group (n = 10). One renal artery in every beagle of the treatment group was randomly assigned to an intimal group (10 renal arteries) which underwent percutaneous renal denervation from the inside, and another renal artery was assigned to an adventitial group (10 renal arteries) which underwent renal denervation from the outside by laparotomy. Results: Compared with the intimal group, the renal norepinephrine (NE) concentration in the adventitial group had significantly decreased (p = 0.003) at 3 months postsurgery. Renal artery HE staining showed that the perineurium from the adventitial group appeared thickened. Western blotting showed that renal tissue tyrosine hydroxylase (TH) protein expression in the adventitial group was significantly lower than that in the intimal group (p < 0.01) at 3 months postsurgery. There was a renal artery stenosis and a renal atrophy in the intimal group after 1 month of follow-up. Conclusion: The inhibitory effect on renal sympathetic nerve activity was more effective in the adventitial group than the intimal group, and renal denervation in the former group was safe.

Renal responses to acute reflex activation of renal sympathetic nerve activity and renal denervation in secondary hypertension

2007 ◽  
Vol 293 (3) ◽  
pp. R1247-R1256 ◽  
Author(s):  
Roger G. Evans ◽  
Sandra L. Burke ◽  
Gavin W. Lambert ◽  
Geoffrey A. Head
Keyword(s):  
Sympathetic Nerve ◽  
Neural Control ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Whole Body ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Norepinephrine Spillover ◽  
Renal Sympathetic

We tested whether the responsiveness of the kidney to basal renal sympathetic nerve activity (RSNA) or hypoxia-induced reflex increases in RSNA, is enhanced in angiotensin-dependent hypertension in rabbits. Mean arterial pressure, measured in conscious rabbits, was similarly increased (+16 ± 3 mmHg) 4 wk after clipping the left ( n = 6) or right ( n = 5) renal artery or commencing a subcutaneous ANG II infusion ( n = 9) but was not increased after sham surgery ( n = 10). Under pentobarbital sodium anesthesia, reflex increases in RSNA (51 ± 7%) and whole body norepinephrine spillover (90 ± 17%), and the reductions in glomerular filtration rate (−27 ± 5%), urine flow (−43 ± 7%), sodium excretion (−40 ± 7%), and renal cortical perfusion (−7 ± 3%) produced by hypoxia were similar in normotensive and hypertensive groups. Hypoxia-induced increases in renal norepinephrine spillover tended to be less in hypertensive (1.1 ± 0.5 ng/min) than normotensive (3.7 ± 1.2 ng/min) rabbits, but basal overflow of endogenous and exogenous dihydroxyphenolglycol was greater. Renal plasma renin activity (PRA) overflow increased less in hypertensive (22 ± 29 ng/min) than normotensive rabbits (253 ± 88 ng/min) during hypoxia. Acute renal denervation did not alter renal hemodynamics or excretory function but reduced renal PRA overflow. Renal vascular and excretory responses to reflex increases in RSNA induced by hypoxia are relatively normal in angiotensin-dependent hypertension, possibly due to the combined effects of reduced neural norepinephrine release and increased postjunctional reactivity. In contrast, neurally mediated renin release is attenuated. These findings do not support the hypothesis that enhanced neural control of renal function contributes to maintenance of hypertension associated with activation of the renin-angiotensin system.

scholarly journals Comparison of high-fat style diet-induced dysregulation of baroreflex control of renal sympathetic nerve activity in intact and ovariectomized female rats

2020 ◽  
Vol 245 (9) ◽  
pp. 761-776
Author(s):  
Yamuna Sucedaram ◽  
Edward James Johns ◽  
Ruby Husain ◽  
Munavvar Abdul Sattar ◽  
Mohammed Abdulla ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Ovarian Hormones ◽  
Female Rats ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The present study compared high-fat style diet (HFSD)-induced renal nerve-dependent dysregulation of the baroreflex control of renal sympathetic nerve activity (RSNA) in ovary-intact and ovariectomized (OVX) rats. Female rats received a normal diet (ND) or a HFSD for 10 weeks prior to the acute study. The rats were anesthetized; RSNA and heart rate (HR) were measured. Acute bilateral renal denervation was performed, and baroreflex gain curves were constructed from the baroreflex changes in RSNA to vasopressor and vasodepressor drugs. Cardiopulmonary baroreflex control of RSNA was assessed by acute saline volume expansion (VE). Mean blood pressure was elevated in the OVX-HFSD rats compared to the HFSD group reaching significance on week 6 of the experimental study (P < 0.01). Adiposity index and creatinine clearance were significantly greater in all HFSD rats compared to their ND counterparts. Fractional excretion of sodium rose initially in all HFSD rats but was normalized towards the end of the study although absolute sodium excretion remained high. In the acute study, baroreflex gain curve sensitivity (A2) of RSNA was similarly decreased in both the HFSD and OVX-HFSD rats by 88% (P < 0.005) and 94% (P < 0.001) respectively compared to their control counterparts, but was normalized following bilateral renal denervation. VE-reduced RSNA in ND and OVX-ND rats by 55% and 52% (both P < 0.001) respectively, but did not alter RSNA in both HFSD and OVX-HFSD female rats. Following bilateral renal denervation, HFSD and OVX-HFSD rats exhibited 37% (P < 0.01) and 24% (P < 0.01) reduction in RSNA respectively. These findings demonstrate that although obesity-induced impairment of baroreflex control of RSNA occurred similarly in HFSD and OVX-HFSD rats, mean blood pressure was increased only in the ovarian hormones deprived-group suggesting that ovarian hormones could have modulatory role on other mechanisms that regulate blood pressure in female obesity. Impact statement Over activation of renal sensory nerve in obesity blunts the normal regulation of renal sympathetic nerve activity. To date, there is no investigation that has been carried out on baroreflex regulation of renal sympathetic nerve activity in obese ovarian hormones deprived rat model, and the effect of renal denervation on the baroreflex regulation of renal sympathetic nerve activity. Thus, we investigated the role of renal innervation on baroreflex regulation of renal sympathetic nerve activity in obese intact and ovariectomized female rats. Our data demonstrated that in obese states, the impaired baroreflex control is indistinguishable between ovarian hormones deprived and non-deprived states. This study will be of substantial interest to researchers working on the impact of diet-induced hypertension in pre- and postmenopausal women. This study provides insight into health risks amongst obese women regardless of their ovarian hormonal status and may be integrated in preventive health strategies.

Effects of sympathetic nerves and angiotensin II on renal sodium and water handling in rats with common bile duct ligature

2005 ◽  
Vol 288 (6) ◽  
pp. F1267-F1275 ◽  
Author(s):  
Roland Veelken ◽  
Karl F. Hilgers ◽  
Markus Porst ◽  
Holger Krause ◽  
Andrea Hartner ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Volume Load ◽  
Volume Retention ◽  
Renal Sympathetic

We tested the hypothesis that angiotensin II is likely to be mandatory for the neurogenic sodium and volume retention in cirrhotic rats with common bile duct ligature (BDL) following an acute volume load. To assess the neural control of volume homeostasis, 21 days after common BDL rats underwent volume expansion (0.9% NaCL; 10% body wt over 30 min) to decrease renal sympathetic nerve activity. Untreated animals, rats with renal denervation or pretreated with a nonhypotensive dose of an angiotensin II type 1 receptor antagonist were studied. The renal renin-angiotensin system was assessed by immunohistochemistry and RT-PCR. Rats with BDL excreted only 71 ± 4% of the administered volume load. In cirrhotic rats pretreated with an angiotensin II AT1 inhibitor or after renal denervation, these values ranged significantly higher from 98 to 103% ( P < 0.05 for all comparisons). Renal sympathetic nerve activity decreases by volume expansion were impaired in BDL rats ( P < 0.05) but unaffected by angiotensin II receptor inhibition. In kidneys of BDL animals, renin mRNA was increased, and immunohistochemistry revealed increased staining for peritubular angiotensin II. Renal denervation in BDL animals reduced renin expression within 5 days to control levels. In conclusion, the impaired excretion of an acute volume load in rats with liver cirrhosis is due to effects of an increased renal sympathetic nerve activity that are likely to be dependent on intrarenal angiotensin II and renin. We speculate that similar changes may contribute to long-term volume retention in liver cirrhosis.

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