Response of Renal Blood Flow and Renal Sympathetic Nerve Activity to Baroreceptor and Emotional Stimuli in the Conscious Dog

1978 ◽  
pp. 203-208 ◽  
Author(s):  
H. R. Kirchheim ◽  
R. Gross
2004 ◽  
Vol 286 (6) ◽  
pp. F1209-F1218 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin

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.


Pharmacology ◽  
1997 ◽  
Vol 54 (5) ◽  
pp. 232-240 ◽  
Author(s):  
Masako Kiriyama ◽  
Akira Haji ◽  
Akira Masuda ◽  
Yusuke Ito ◽  
Ryuji Takeda

2003 ◽  
Vol 285 (5) ◽  
pp. R1135-R1144 ◽  
Author(s):  
Kathleen P. O'Hagan ◽  
Jennifer A. Alberts

The uterine artery blood flow (UtBF) and renal sympathetic nerve activity (SNA) responses to treadmill exercise were evaluated in 12 nonpregnant (NP) and 17 term pregnant (P) rabbits. UtBF was monitored continuously with a Transonic flowprobe. Rabbits underwent three exercise trials (5-min duration) that varied in absolute workload. The rise in renal SNA with exercise was intensity related. Pregnancy did not affect the average steady-state renal SNA response expressed relative to maximum activity (P 24 ± 1% vs. NP 23 ± 2% of maximum smoke-elicited activity) and increased the average renal SNA response expressed relative to resting activity (P +155 ± 19% vs. NP +84 ± 23% from rest, P = 0.03) At rest, UtBF (P 13 ± 3 vs. NP 1.9 ± 0.3 ml/min) and uterine artery conductance (UtC; P 22 ± 5 vs. NP 2.8 ± 0.5 ml · min-1·mmHg-1 × 10-2) were elevated in the P rabbits. The average exercise-related decreases in UtBF (P -16 ± 4% vs. NP -48 ± 4%) and UtC (P -27 ± 4% vs. NP -54 ± 4%) were attenuated in the P rabbits. Pregnancy does not impair the ability to raise renal SNA but attenuates the uterine artery constrictor response to moderate to heavy dynamic exercise in rabbits. Under normal conditions, the pregnant uterine circulatory bed may be relatively protected from exercise-related redistribution of blood flow.


2010 ◽  
Vol 298 (4) ◽  
pp. F839-F846 ◽  
Author(s):  
Emilio Badoer

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.


2004 ◽  
Vol 286 (5) ◽  
pp. R881-R887 ◽  
Author(s):  
Misa Yoshimoto ◽  
Tamaki Sakagami ◽  
Satsuki Nagura ◽  
Kenju Miki

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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