scholarly journals Carotid body denervation reduces renal sympathetic nerve activity and fibrosis, and increases renal blood flow in congestive heart failure (875.14)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Noah Marcus ◽  
Rodrigo Del Rio ◽  
Harold Schultz
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Carotid Body ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

scholarly journals Angiotensin receptor antagonist improves cardiac reflex control of renal sodium handling in heart failure

1998 ◽  
Vol 274 (2) ◽  
pp. H636-H641 ◽  
Author(s):  
Gerald F. Dibona ◽  
Susan Y. Jones ◽  
Linda L. Sawin
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sodium Handling ◽  
Renal Sympathetic

In rats with congestive heart failure, type 1 angiotensin II receptor antagonist treatment (losartan) decreases basal renal sympathetic nerve activity and improves arterial baroreflex regulation of renal sympathetic nerve activity. This investigation examined the effect of losartan on cardiac baroreflex regulation of renal sympathetic nerve activity and renal sodium handling in rats with congestive heart failure. Losartan treatment decreased arterial pressure from 120 ± 3 to 93 ± 5 mmHg and increased the afferent (from 0.95 ± 0.21 to 2.22 ± 0.42% Δafferent vagal nerve activity/mmHg mean right atrial pressure, P < 0.05) and overall gain (from −1.14 ± 0.19 to −4.20 ± 0.39% Δrenal sympathetic nerve activity/mmHg mean right atrial pressure, P < 0.05) of the cardiac baroreflex. During isotonic saline volume loading, urinary sodium excretion increased from 2.4 ± 0.8 to 10.5 ± 1.3 μeq/min in vehicle-treated rats (excretion of 52 ± 3% of the load) and from 3.0 ± 1.0 to 15.1 ± 1.8 μeq/min in losartan-treated rats (excretion of 65 ± 4% of the load, P < 0.05). When rats were changed from a low- to a high-sodium diet, cumulative sodium balance over 5 days was 7.8 ± 0.6 meq in vehicle-treated rats and 4.2 ± 0.4 meq in losartan-treated rats ( P < 0.05). In congestive heart failure, losartan treatment improved cardiac baroreflex regulation of renal sympathetic nerve activity, which was associated with improved ability to excrete acute and chronic sodium loads.

scholarly journals Exercise training attenuates chemoreflex-mediated reductions of renal blood flow in heart failure

2015 ◽  
Vol 309 (2) ◽  
pp. H259-H266 ◽  
Author(s):  
Noah J. Marcus ◽  
Carolin Pügge ◽  
Jai Mediratta ◽  
Alicia M. Schiller ◽  
Rodrigo Del Rio ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Exercise Training ◽  
Renal Blood Flow ◽  
Carotid Body ◽  
Sympathetic Nerve Activity ◽  
Renal Perfusion ◽  
Renal Sympathetic Nerve Activity ◽  
Fractional Shortening ◽  
Renal Sympathetic

In chronic heart failure (CHF), carotid body chemoreceptor (CBC) activity is increased and contributes to increased tonic and hypoxia-evoked elevation in renal sympathetic nerve activity (RSNA). Elevated RSNA and reduced renal perfusion may contribute to development of the cardio-renal syndrome in CHF. Exercise training (EXT) has been shown to abrogate CBC-mediated increases in RSNA in experimental heart failure; however, the effect of EXT on CBC control of renal blood flow (RBF) is undetermined. We hypothesized that CBCs contribute to tonic reductions in RBF in CHF, that stimulation of the CBC with hypoxia would result in exaggerated reductions in RBF, and that these responses would be attenuated with EXT. RBF was measured in CHF-sedentary (SED), CHF-EXT, CHF-carotid body denervation (CBD), and CHF-renal denervation (RDNX) groups. We measured RBF at rest and in response to hypoxia (FiO2 10%). All animals exhibited similar reductions in ejection fraction and fractional shortening as well as increases in ventricular systolic and diastolic volumes. Resting RBF was lower in CHF-SED (29 ± 2 ml/min) than in CHF-EXT animals (46 ± 2 ml/min, P < 0.05) or in CHF-CBD animals (42 ± 6 ml/min, P < 0.05). In CHF-SED, RBF decreased during hypoxia, and this was prevented in CHF-EXT animals. Both CBD and RDNX abolished the RBF response to hypoxia in CHF. Mean arterial pressure increased in response to hypoxia in CHF-SED, but was prevented by EXT, CBD, and RDNX. EXT is effective in attenuating chemoreflex-mediated tonic and hypoxia-evoked reductions in RBF in CHF.

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 hypothalamic PVN in the regulation of renal sympathetic nerve activity and blood flow during hyperthermia and in heart failure

2010 ◽  
Vol 298 (4) ◽  
pp. F839-F846 ◽  
Author(s):  
Emilio Badoer
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The hypothalamic paraventricular nucleus is a key integrative area in the brain involved in influencing sympathetic nerve activity and in the release of hormones or releasing factors that contribute to regulating body fluid homeostasis and endocrine function. The endocrine and hormonal regulatory function of the paraventricular nucleus is well studied, but the regulation of sympathetic nerve activity and blood flow by this region is less clear. Here we review the critical role of the paraventricular nucleus in regulating renal blood blow during hyperthermia and the evidence pointing to an important pathophysiological role of the paraventricular nucleus in the elevated renal sympathetic nerve activity that is a characteristic of heart failure.

Relationship between renal sympathetic nerve activity and renal blood flow during natural behavior in rats

2004 ◽  
Vol 286 (5) ◽  
pp. R881-R887 ◽  
Author(s):  
Misa Yoshimoto ◽  
Tamaki Sakagami ◽  
Satsuki Nagura ◽  
Kenju Miki
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Rem Sleep ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nrem Sleep ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Behavioral Activities ◽  
Renal Sympathetic

The purpose of the present study was to determine the relationship between renal sympathetic nerve activity (RSNA) and renal blood flow (RBF) during normal daily activity in conscious, chronically instrumented Wistar rats ( n = 8). The animal's behavior was classified as rapid eye movement (REM) sleep, non-REM (NREM) sleep, quiet awake, moving, and grooming states. On average RSNA was lowest during REM sleep, which was decreased by 39.0 ± 3.2% ( P < 0.05) relative to NREM sleep, and rose linearly with an increase in activity level in the order of quiet awake (by 10.9 ± 1.8%, P < 0.05), moving (by 29.4 ± 2.9%, P < 0.05), and grooming (by 65.3 ± 3.9%, P < 0.05) relative to NREM sleep. By contrast, RBF was highest during REM sleep, which was increased by 4.8 ± 0.7% ( P < 0.05) relative to NREM sleep and decreased significantly ( P < 0.05) by 5.5 ± 0.6 and 6.6 ± 0.5% during moving and grooming states, respectively, relative to NREM sleep. There was a significant ( P < 0.05) inverse linear relationship between the percent changes in RSNA and RBF and between those in RSNA and renal vascular conductance. Furthermore, renal denervation ( n = 8) abolished the changes in RBF induced by different natural behavioral activities. These results suggest that the changes in RSNA induced by natural behavioral activities had a significant influence on RBF.

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