scholarly journals Central effects of leptin on cardiovascular and neurohormonal responses in conscious rabbits

2000 ◽  
Vol 278 (5) ◽  
pp. R1314-R1320 ◽  
Author(s):  
Kiyoshi Matsumura ◽  
Isao Abe ◽  
Takuya Tsuchihashi ◽  
Masatoshi Fujishima
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Intracerebroventricular Injection ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Glucose Levels ◽  
Renal Sympathetic Nerve ◽  
Conscious Rabbits ◽  
Renal Sympathetic

We determined the cardiovascular and neurohormonal responses to intracerebroventricular injection of leptin in conscious rabbits. Intracerebroventricular injection of leptin elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity while producing no consistent, significant increases in heart rate. Peak values of mean arterial pressure and renal sympathetic nerve activity induced by intracerebroventricular injection of 50 μg of leptin (+17.3 ± 1.2 mmHg and +47.9 ± 12.0%) were obtained at 10 and 20 min after injection, respectively. Plasma catecholamine concentrations significantly increased at 60 min after intracerebroventricular injection of leptin (control vs. 60 min; epinephrine: 33 ± 12 vs. 97 ± 27 pg/ml, P < 0.05; norepinephrine: 298 ± 39 vs. 503 ± 86 pg/ml, P < 0.05). Intracerebroventricular injection of leptin also caused significant increases in plasma vasopressin and glucose levels. However, pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion blocking agent, abolished these cardiovascular and neurohormonal responses. On the other hand, intravenous injection of the same dose of leptin (50 μg) as used in the intracerebroventricular experiment failed to cause any cardiovascular and renal sympathetic nerve responses. These results suggest that intracerebroventricular leptin acts in the central nervous system and activates sympathoadrenal outflow, resulting in increases in arterial pressure and plasma glucose levels in conscious rabbits.

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.

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.

Effect of dynamic exercise on renal sympathetic nerve activity in conscious rabbits

1993 ◽  
Vol 74 (5) ◽  
pp. 2099-2104 ◽  
Author(s):  
K. P. O'Hagan ◽  
L. B. Bell ◽  
S. W. Mittelstadt ◽  
P. S. Clifford
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Treadmill Exercise ◽  
Dynamic Exercise ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Conscious Rabbits ◽  
Renal Sympathetic

Renal sympathetic nerve activity (RSNA) increases abruptly at the onset of treadmill exercise in conscious rabbits. This study investigated whether the rise in RSNA is related to the intensity of the exercise and whether an elevated level of RSNA is maintained during submaximal exercise. RSNA, arterial blood pressure (BP), and heart rate (HR) were recorded in 10 New Zealand White rabbits during two treadmill exercise protocols at 0% grade: 7 m/min for 5 min and 12 m/min for 2 min. Peak levels of RSNA were observed in the first 10 s of exercise at 7 and 12 m/min. Through 2 min of exercise, the rise in RSNA was greater (P < 0.05) at 12 m/min (delta 83 +/- 22%) compared with 7 m/min (delta 49 +/- 8%). At 7 m/min, HR and BP reached steady-state levels during the 2nd min of exercise. RSNA remained elevated at delta 43 +/- 10 to delta 54 +/- 13% over resting levels as exercise continued from the 2nd through the 5th min of exercise (P < 0.05). These data demonstrate that the RSNA response to exercise is intensity related and suggest that RSNA remains elevated and thus may contribute to the control of renal blood flow during submaximal dynamic exercise.

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.

Norepinephrine spillover faithfully reflects renal sympathetic nerve activity in conscious rabbits

1991 ◽  
Vol 261 (1) ◽  
pp. F44-F50 ◽  
Author(s):  
T. Noshiro ◽  
T. Saigusa ◽  
D. Way ◽  
P. K. Dorward ◽  
B. P. McGrath
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Relative Contribution ◽  
Conscious Rabbits ◽  
Phenylephrine Infusion ◽  
Norepinephrine Spillover ◽  
Renal Sympathetic

The relationship between directly recorded renal sympathetic nerve activity (RSNA) and simultaneous renal norepinephrine (NE) spillover rate across the kidney at rest and in response to changes in mean arterial pressure (MAP) was examined in six conscious rabbits. Integrated RSNA and renal NE spillover rate at rest were 5.1 +/- 1.1 microV/s and 20.8 +/- 3.0 ng/min, respectively. Sodium nitroprusside infusions at 10 and 20 microgram.kg-1.min-1 significantly increased RSNA by 42 +/- 14 and 84 +/- 14% and renal NE spillover rate 39 +/- 22 and 107 +/- 22% in response to falls in MAP of 15 +/- 2 and 21 +/- 2 mmHg (19 and 27%), respectively. During phenylephrine infusion at 8 micrograms.kg-1.min-1, RSNA and renal NE spillover rate significantly decreased by 65 +/- 14 and 67 +/- 16%, respectively, in response to a 15 +/- 2 mmHg (19%) rise in MAP. There was a highly significant positive correlation between changes in directly recorded RSNA and changes in renal NE spillover rate (r = 0.81, P less than 0.01). The ratio of renal to total NE spillover rate at rest was 0.44 +/- 0.06. This ratio was decreased during both sympathetic stimulation (0.30 +/- 0.04) and inhibition (0.26 +/- 0.06). This study indicates that the measurement of renal NE spillover rate is a useful reliable method for detecting the changes in RSNA and its relative contribution to overall sympathetic nerve activity in response to physiological stimuli in conscious rabbits.

Relationship between renal sympathetic nerve activity and arterial pressure during REM sleep in rats

2003 ◽  
Vol 284 (2) ◽  
pp. R467-R473 ◽  
Author(s):  
Kenju Miki ◽  
Makiko Kato ◽  
Suzuko Kajii
Keyword(s):  
Arterial Pressure ◽  
Rem Sleep ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Systemic Arterial Pressure ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Behavioral States ◽  
Renal Sympathetic

The relationship between renal sympathetic nerve activity (RSNA) and systemic arterial pressure obtained during rapid eye movement (REM) sleep was compared with that obtained in other sleep and awake states. Electrodes for the measurements of RSNA, electrocardiogram, electromyogram, and electroencephalogram and a catheter for the measurement of systemic arterial pressure were implanted while the animals were under aseptic conditions at least 5 days before the experiment. During the transition from non-REM (NREM) to REM sleep, RSNA and heart rate (HR) decreased immediately by 46 ± 2% ( P < 0.05) and 22 ± 3 beats/min ( P < 0.05), respectively, over 3 s after the onset of REM sleep. Meanwhile, systemic arterial pressure increased gradually after the onset of REM sleep, which was apparently independent of the changes in RSNA. During REM sleep, the relationships between RSNA/HR and systemic arterial pressure were dissociated compared with that obtained during the other behavioral states. These data indicate that the interdependency between systemic arterial pressure and RSNA during REM sleep is likely to be modified compared with other behavioral states.

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