scholarly journals Activation of P2X‐purinergic receptors in the lateral parabrachial nucleus increases renal sympathetic nerve discharge and mean arterial pressure in anesthetized rats (686.13)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Miguel Menezes ◽  
Michele Favero ◽  
Kenta Yamamoto ◽  
Jose Menani ◽  
Patricia Paula ◽  
...  
1995 ◽  
Vol 269 (5) ◽  
pp. R1289-R1293 ◽  
Author(s):  
M. Fukuhara ◽  
T. Tsuchihashi ◽  
I. Abe ◽  
M. Fujishima

Adrenomedullin is a vasodilative peptide and shows slight homology with calcitonin gene-related peptide. In the present study, we investigated the effects of adrenomedullin on cardiovascular and neurohormonal responses in 13 conscious rabbits. The animals were chronically instrumented with bipolar electrodes on the left renal sympathetic nerve. Intravenous administration of human adrenomedullin (10, 100, 1,000, and 3,000 pmol/kg, n = 6) caused a dose-dependent reduction in mean arterial pressure (0 +/- 2, -1 +/- 2, -19 +/- 2, and -29 +/- 4 mmHg, respectively) concomitant with increases in heart rate, renal sympathetic nerve activity, plasma renin activity, and plasma norepinephrine. The significant reduction in mean arterial pressure induced by 1,000 pmol/kg of adrenomedullin occurred within 1 min after injection and lasted for 15 min (n = 7). In contrast, the significant increases in heart rate and renal sympathetic nerve activity lasted for more than 50 min. When mean arterial pressure was decreased by 15 mmHg by adrenomedullin, the increases in heart rate and renal sympathetic nerve activity were 53 +/- 8 beats/min and 78 +/- 13%, respectively, which were significantly smaller than those induced by intravenous injection of sodium nitroprusside (102 +/- 14 beats/min and 155 +/- 34%, respectively). These results suggest that intravenous adrenomedullin exerts a hypotensive action that is associated with the attenuated reflex-mediated sympathetic activation.


1986 ◽  
Vol 251 (2) ◽  
pp. R289-R294 ◽  
Author(s):  
J. P. Koepke ◽  
S. Jones ◽  
G. F. DiBona

The effects of a stressful environmental stimulus (air stress) on mean arterial pressure, heart rate, renal sympathetic nerve activity, and renal function were studied in conscious deoxycorticosterone acetate-sodium chloride (DOCA-NaCl) hypertensive rats, sham DOCA-NaCl normotensive rats, and DOCA-NaCl rats with renal denervation. In conscious DOCA-NaCl hypertensive rats, air stress decreased urine flow rate [36% from 17.9 +/- 3.0 microliter X min-1 X 100 g body wt-1 (BW)], urinary sodium excretion (39% from 3.1 +/- 0.5 microeq X min-1 X 100 g BW-1), fractional water excretion (24% from 4.72 +/- 1.00%), and fractional sodium excretion (28% from 5.72 +/- 1.08%) and increased renal sympathetic nerve activity (94% from 8.3 +/- 0.6 integrator resets/min), but no changes occurred in glomerular filtration rate (-15% from 0.40 +/- 0.06 ml X min-1 X 100 g BW-1) or effective renal plasma flow (-7% from 2.50 +/- 0.53 ml X min-1 X 100 g BW-1). Air stress had no effect on these measures in conscious sham DOCA-NaCl normotensive rats or DOCA-NaCl rats with renal denervation. Mean arterial pressure and heart rate were unaffected by air stress in these three groups. Renal denervation lowered base-line mean arterial pressure in DOCA-NaCl rats. Thus DOCA-NaCl hypertensive rats respond to environmental stress with increased renal sympathetic nerve activity and, consequently, antidiuresis and antinatriuresis.


1995 ◽  
Vol 5 (12) ◽  
pp. 2082-2086
Author(s):  
J C Neahring ◽  
S Y Jones ◽  
G F DiBona

Efferent renal sympathetic nerve activity is increased in experimental nephrotic syndrome and exhibits attenuated cardiopulmonary baroreflex inhibition during volume expansion in anesthetized rats. Additional studies were performed in conscious rats to avoid the potentially confounding influences of anesthesia; these studies used another more specific standardized stimulus for cardiopulmonary baroreflex activation. Sprague Dawley rats were studied 3 to 4 wk after adriamycin injection (3.5 mg/kg iv); all rats developed proteinuria. In sinoaortic denervated rats (anesthetized), graded frequency stimulation of the central end of the cut right vagus nerve produced frequency-dependent decreases in mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity. The decreases in mean arterial pressure and heart rate were similar in control and nephrotic rats, but efferent renal sympathetic nerve activity decreased significantly less in nephrotic than control rats over the entire frequency range (P < 0.02). In sinoaortic denervated rats (conscious), 10% body weight isotonic saline volume expansion decreased mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity. The decreases in mean arterial pressure and heart rate were similar in control and nephrotic rats, but efferent renal sympathetic nerve activity decreased significantly less in nephrotic than control rats over the entire period of volume expansion (P < 0.04). In nephrotic syndrome, the cardiopulmonary baroreflex inhibition of efferent renal sympathetic nerve activity is decreased; the defect lies in the central portion of the reflex. This may contribute to the observed increase in efferent renal sympathetic nerve activity in nephrotic syndrome.


2006 ◽  
Vol 231 (10) ◽  
pp. 1616-1625 ◽  
Author(s):  
Mamoru Tanida ◽  
Akira Niijima ◽  
Jiao Shen ◽  
Shigeru Yamada ◽  
Hajime Sawai ◽  
...  

2007 ◽  
Vol 102 (3) ◽  
pp. 1034-1040 ◽  
Author(s):  
Valérie Oréa ◽  
Roy Kanbar ◽  
Bruno Chapuis ◽  
Christian Barrès ◽  
Claude Julien

This study examined the possible influence of changes in heart rate (HR) on the gain of the transfer function relating renal sympathetic nerve activity (RSNA) to arterial pressure (AP) at HR frequency in rats. In seven urethane-anesthetized rats, AP and RSNA were recorded under baseline conditions (spontaneous HR = 338 ± 6 beats/min, i.e., 5.6 ± 0.1 Hz) and during 70-s periods of cardiac pacing at 6–9 Hz applied in random order. Cardiac pacing slightly increased mean AP (0.8 ± 0.2 mmHg/Hz) and decreased pulse pressure (−3.6 ± 0.3 mmHg/Hz) while leaving the mean level of RSNA essentially unaltered ( P = 0.680, repeated-measures ANOVA). The gain of the transfer function from AP to RSNA measured at HR frequency was always associated with a strong, significant coherence and was stable between 6 and 9 Hz ( P = 0.185). The transfer function gain measured under baseline conditions [2.44 ± 0.28 normalized units (NU)/mmHg] did not differ from that measured during cardiac pacing (2.46 ± 0.27 NU/mmHg). On the contrary, phase decreased linearly as a function of HR, which indicated the presence of a fixed time delay (97 ± 6 ms) between AP and RSNA. In conclusion, the dynamic properties of arterial baroreflex pathways do not affect the gain of the transfer function between AP and RSNA measured at HR frequency in the upper part of the physiological range of HR variations in the rat.


1997 ◽  
Vol 273 (3) ◽  
pp. H1606-H1610 ◽  
Author(s):  
S. E. DiCarlo ◽  
L. K. Stahl ◽  
V. S. Bishop

"Central command" may initiate the sympathoexcitatory responses at the onset of exercise by shifting the operating point of the arterial baroreflex toward higher pressures. Daily exercise (DE) attenuates the sympathoexcitatory responses to submaximal exercise. This DE-induced adaptation may be due, in part, to an enhanced inhibitory influence of cardiac afferents. This is suggested because cardiac afferents exert a tonic inhibitory influence on the arterial baroreflex which is enhanced by DE. Therefore, the influence of cardiac afferents on the regulation of renal sympathetic nerve activity (RSNA) during exercise was examined in a group of sedentary and age-matched DE rabbits. The rabbits were instrumented with a Silastic catheter inserted into the pericardial sac, electrodes around the renal sympathetic nerves, and catheters in the femoral artery and vein. In the sedentary rabbits, treadmill exercise (12 m/min, 20% grade) significantly increased mean arterial pressure (delta 18 +/- 3 mmHg), heart rate (delta 36 +/- 3 beats/min), and RSNA (delta 295 +/- 23%). More importantly, cardiac afferent blockade (2% intrapericardial procainamide) did not significantly alter the RSNA response to exercise in the sedentary rabbits. DE did not alter the mean arterial pressure (delta 15 +/- 1 mmHg) or heart rate (delta 55 +/- 8 beats/min) response to exercise; however, RSNA (delta 252 +/- 9%) was significantly reduced. In contrast to the sedentary rabbits, cardiac afferent blockade in the DE rabbits significantly increased the RSNA response to exercise (delta 417 +/- 30%). These results suggest that DE attenuates the RSNA response to dynamic exercise due, in part, to an enhanced inhibitory influence of cardiac afferents.


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