Glucocorticoids reduce responses to AMPA receptor activation and blockade in nucleus tractus solitarius

2003 ◽  
Vol 284 (5) ◽  
pp. H1751-H1761 ◽  
Author(s):  
Sylvan S. Shank ◽  
Deborah A. Scheuer
Keyword(s):  
Arterial Pressure ◽  
Ampa Receptors ◽  
Sympathetic Nerve Activity ◽  
Nucleus Tractus Solitarius ◽  
Receptor Activation ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Sprague Dawley Rats ◽  
Renal Sympathetic

We tested the hypothesis that glucocorticoids attenuate changes in arterial pressure and renal sympathetic nerve activity (RSNA) in response to activation and blockade of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors within the nucleus of the solitary tract (NTS). Experiments were performed in Inactin-anesthetized male Sprague-Dawley rats treated for 7 ± 1 days with a subcutaneous corticosterone (Cort) pellet or in control rats. Baseline mean arterial pressure (MAP) was significantly higher in Cort-treated rats (109 ± 2 mmHg, n = 39) than in control rats (101 ± 1 mmHg, n = 48, P < 0.05). In control rats, microinjection of AMPA (0.03, 0.1, and 0.3 pmol/100 nl) into the NTS significantly decreased MAP at all doses and decreased RSNA at 0.1 and 0.3 pmol/100 nl. Responses to AMPA in Cort-treated rats were attenuated at all doses of AMPA ( P < 0.05). Responses to the AMPA-kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) were also significantly reduced in Cort-treated rats relative to control rats. Blockade of glucocorticoid type II receptors with mifepristone significantly enhanced responses to CNQX in both control and Cort rats. We conclude that glucocorticoids attenuate MAP and RSNA responses to activation and blockade of AMPA receptors in the NTS.

Transfer function analysis between arterial pressure and renal sympathetic nerve activity at cardiac pacing frequencies in the rat

2007 ◽  
Vol 102 (3) ◽  
pp. 1034-1040 ◽  
Author(s):  
Valérie Oréa ◽  
Roy Kanbar ◽  
Bruno Chapuis ◽  
Christian Barrès ◽  
Claude Julien
Keyword(s):  
Transfer Function ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiac Pacing ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Baseline Conditions ◽  
Renal Sympathetic

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.

Cardiovascular and neurohormonal effects of intravenous adrenomedullin in conscious rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1289-R1293 ◽  
Author(s):  
M. Fukuhara ◽  
T. Tsuchihashi ◽  
I. Abe ◽  
M. Fujishima
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Conscious Rabbits ◽  
Renal Sympathetic

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.

AT1-receptor blockade in the hypothalamic PVN reduces central hyperosmolality-induced renal sympathoexcitation

2001 ◽  
Vol 281 (6) ◽  
pp. R1844-R1853 ◽  
Author(s):  
Qing Hui Chen ◽  
Glenn M. Toney
Keyword(s):  
Sympathetic Nerve Activity ◽  
Internal Carotid ◽  
Receptor Activation ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Autonomic Neurons ◽  
Osmotic Challenge ◽  
Renal Sympathetic

Autonomic neurons in the hypothalamic paraventricular nucleus (PVN) are innervated by osmotic-sensitive regions of the lamina terminalis, receive input from ANG II-containing cells, and express AT1 ANG II receptors. Therefore, we hypothesized that ANG II actions within the PVN could underlie hyperosmolality-induced increases in renal sympathetic nerve activity (RSNA). In anesthetized baroreceptor-denervated rats, graded concentrations of NaCl (0.30, 0.9, 1.5, and 2.1 osmol/l) were injected (300 μl) centrally via the internal carotid artery (ICA) and produced corresponding increases in mean arterial pressure (MAP) and RSNA. In addition, equivalent hyperosmotic loads (1.5 osmol/l) of NaCl, glucose, and mannitol each significantly ( P < 0.05) increased MAP and RSNA. The same stimuli had no effect when administered intravenously. Bilateral PVN microinjections (100 nl) of the AT1-receptor antagonist losartan (80 nmol) before osmotic challenge had no effect on resting RSNA but significantly ( P < 0.05) reduced RSNA responses to hyperosmotic NaCl ( n = 7), glucose ( n = 6), and mannitol ( n = 6). Increases in RSNA evoked by hyperosmotic NaCl were significantly ( P < 0.05) attenuated ∼20 min after losartan injection and recovered within 60–120 min. In contrast, losartan outside the PVN as well as vehicle (saline) within the PVN failed to alter RSNA responses to ICA hyperosmotic NaCl. Results suggest that elevated RSNA after central sodium/osmotic activation is mediated, at least in part, by a synaptic mechanism involving AT1-receptor activation within the PVN.

Arterial pressure lability and renal sympathetic nerve activity are dissociated in SAD rats

1992 ◽  
Vol 263 (3) ◽  
pp. R639-R646 ◽  
Author(s):  
C. Barres ◽  
S. J. Lewis ◽  
H. J. Jacob ◽  
M. J. Brody
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
High Variability ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

The purpose of this study was to determine whether the sympathetic nervous system drives the high variability of arterial pressure (AP) observed after sinoaortic denervation (SAD) in rats. One or fourteen days after SAD, rats were instrumented chronically to record mean AP (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) in the conscious unrestrained state. Acute SAD increased MAP, HR, RSNA, and variability of MAP and decreased variability of both HR and RSNA. In rats with chronic SAD, variability of MAP remained high, whereas MAP, HR, RSNA, and variability of HR and RSNA returned to normal levels. Correlation analysis showed that, in sham-operated rats, AP and RSNA were negatively correlated in 90% of cases. In contrast, rats with both acute and chronic SAD exhibited only 30% negative and 25% positive correlations. These results indicate that 1) low AP variability in intact rats results from baroreflex-mediated inversely related fluctuations in RSNA and HR and 2) high variability of AP after acute and chronic SAD is correlated infrequently with RSNA. Because lability is reduced by interventions that block the sympathetic nervous system, we conclude that lability of AP associated with SAD appears to be mediated largely by a permissive role of sympathetic activity.

Baroreflex dysfunction in diabetes mellitus. II. Site of baroreflex impairment in diabetic rabbits

1994 ◽  
Vol 266 (1) ◽  
pp. H244-H249 ◽  
Author(s):  
T. S. McDowell ◽  
G. Hajduczok ◽  
F. M. Abboud ◽  
M. W. Chapleau
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Companion Paper ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Diabetic Rabbits ◽  
The Right ◽  
Alpha Chloralose ◽  
Induced Changes ◽  
Renal Sympathetic

In our companion paper [T. S. McDowell, M. W. Chapleau, G. Hajduczok, and F. M. Abboud, Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H235-H243, 1994] we report that baroreflex-mediated bradycardia is impaired in diabetic rabbits. The purpose of the present study was to identify the site of impairment. Diabetes was induced in rabbits by alloxan (90–100 mg/kg iv; n = 7). Alloxan-treated rabbits that remained normoglycemic (n = 8) and rabbits given saline instead of alloxan (n = 4) served as controls. Twenty-four weeks after administration of alloxan or saline, rabbits were anesthetized with alpha-chloralose. Aortic baroreceptor and renal sympathetic nerve activity (RSNA) were recorded during phenylephrine- and nitroglycerin-induced changes in arterial pressure. The slope of the baroreceptor pressure-activity relation was not significantly different in diabetic rabbits (1.3 +/- 0.3%/mmHg, n = 7) compared with either alloxan-treated (1.3 +/- 0.1%/mmHg) or saline-treated normoglycemic rabbits (1.2 +/- 0.2%/mmHg). The slope of the arterial pressure-RSNA relation was not significantly different in diabetic rabbits (-3.5 +/- 0.3%/mmHg, n = 7) compared with the alloxan-treated normoglycemic rabbits (-3.0 +/- 0.4%/mmHg, n = 8) and was greater than that in saline-treated normoglycemic rabbits (-1.9 +/- 0.3%/mmHg, n = 4; P < 0.05). The decreases in heart rate in response to electrical stimulation (10 V, 2 ms, 0.5–16 Hz) of the cut peripheral end of the right cervical vagus were similar in diabetic and alloxan-treated normoglycemic rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Baroreflex control of sympathetic nerve activity after elevations of pressure in conscious rabbits

1985 ◽  
Vol 248 (6) ◽  
pp. H827-H834 ◽  
Author(s):  
K. P. Undesser ◽  
J. Y. Pan ◽  
M. P. Lynn ◽  
V. S. Bishop
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Afferent Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Pressure Stimulus ◽  
Renal Sympathetic

The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.

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