scholarly journals Chronic AT1Receptor Blockade Alters Aortic Nerve Activity in Hypertension

Hypertension ◽  
1998 ◽  
Vol 31 (4) ◽  
pp. 973-977 ◽  
Author(s):  
Claudia M. dos Santos ◽  
Edson D. Moreira ◽  
Eduardo M. Krieger ◽  
Lisete C. Michelini
Keyword(s):  
1992 ◽  
Vol 262 (2) ◽  
pp. H503-H510 ◽  
Author(s):  
C. M. Heesch ◽  
K. W. Barron

This study was designed to evaluate a possible central nervous system (CNS) component to acute baroreflex resetting. In nine arterial baroreceptor-denervated, chloralose-urethan-anesthetized rats, a control (C) aortic nerve stimulation curve (3-5 V, 1 ms, 0-64 Hz) was obtained. Next, a constant "baroreceptor" input was delivered to the CNS (left aortic nerve stimulation, 10 min, 10.2 +/- 1.5 Hz). Within the first 13 s of aortic nerve stimulation, maximum inhibition of lumbar sympathetic nerve activity (LSNA) was 60 +/- 7.8% of baseline and at 1 min it increased to 68 +/- 5.6% of baseline. At the end of the 10-min aortic nerve stimulation, LSNA was not different from the response at 1 min (68 +/- 5.6% = 74 +/- 4.1%). Immediately after the constant stimulation (within 30 s), a test or reset (RS) curve was obtained (0-64 Hz). A recovery (RC) curve was obtained 10-20 min later. The slope of the linear portion of the curve and the stimulation frequency that produced 50% maximum inhibition (ES50) were compared among the three baroreflex curves (C, RS, RC,) and no significant differences were found. Thus, although a CNS component to baroreflex adaptation was evident during the first minute of aortic nerve stimulation, a longer term acute resetting of the baroreflex curve did not occur.


1984 ◽  
Vol 246 (2) ◽  
pp. H302-H305 ◽  
Author(s):  
K. P. Undesser ◽  
M. P. Lynn ◽  
V. S. Bishop

The effect of increased arterial pressure on aortic depressor nerve activity was studied in the conscious rabbit. Aortic baroreceptor resetting was observed following 15 min of sustained pressure elevation. At 15 min, there was a significant increase in the threshold arterial pressure for aortic nerve activity, but peak nerve activity did not change. This resulted in an increase in the slope of the pressure-nerve activity relationship. Therefore, except for peak nerve activity, aortic nerve activity was reduced at all pressures following 15 min of sustained pressure elevation. At 30 min, peak nerve activity also increased, resulting in a parallel shift in the pressure-activity curve. The early increase in slope of the pressure-activity relationship may be due to an early resetting of low threshold fibers with a high pressure differential between their threshold pressure and the sustained pressure elevation used to induce resetting. A late resetting of high threshold fibers with a low pressure differential between their threshold pressures and the pressure used to cause resetting of baroreceptors results in a parallel shift in the curve observed at 30 min. These data obtained from multiunit recordings provide unexpected evidence about baroreceptor resetting, which is not apparent from single-unit recordings.


1989 ◽  
Vol 28 (3) ◽  
pp. 227-232 ◽  
Author(s):  
Małgorzata Tafil-Klawe ◽  
Jacek Klawe ◽  
Stanisław Majcherczyk ◽  
Andrzej Trzebski

1976 ◽  
Vol 41 (1) ◽  
pp. 111-114 ◽  
Author(s):  
I. Ninomiya ◽  
Y. Yonezawa ◽  
M. F. Wilson

An implantable electrode assembly consisting of collagen and metallic electrodes was constructed to measure simultaneously neural signals from the intact nerve and bioelectrical noises in awake animals. Mechanical artifacts, due to bodily movement, were negligibly small. The impedance of the collagen electrodes, measured in awake cats 6-7 days after implantation surgery, ranged from 39.8-11.5 komega at a frequency range of 20-5 kHz. Aortic nerve activity and renal nerve activity, measured in awake conditions using the collagen electrode, showed grouped activity synchronous with the cardiac cycle. Results indicate that most of the remal nerve activity was from postganglionic sympathetic fibers and was inhibited by the baroceptor reflex inthe same cardiac cycle.


2001 ◽  
Vol 304 (1-2) ◽  
pp. 33-36 ◽  
Author(s):  
Hironobu Morita ◽  
You Tsuchiya ◽  
Taro Miyahara ◽  
Kunihiko Tanaka ◽  
Nobuhiro Fujiki

1984 ◽  
Vol 246 (6) ◽  
pp. H843-H850 ◽  
Author(s):  
M. D. Thames ◽  
B. N. Gupta ◽  
B. J. Ballon

The purpose of our study was to determine if there is a central abnormality in the arterial baroreceptor reflex control of renal nerve activity in renal hypertension. We recorded simultaneously the changes in aortic (input) and renal (output) nerve traffic during phenylephrine-induced increases in arterial pressure in 14 normotensive and 11 hypertensive rabbits [mean arterial pressure (+/- SE) in conscious state 106 +/- 2 and 141 +/- 6 mmHg, respectively]. Changes in aortic nerve traffic were considered representative of changes in total arterial baroreceptor input to the central nervous system. Renal nerve traffic was inhibited by 5.2 +/- 0.5% per mmHg rise in arterial pressure in normotensive rabbits but by only 2.5 +/- 0.3% per mmHg in hypertensive rabbits (P less than 0.05). Increases of aortic nerve traffic during increases in arterial pressure were similar in the two groups. These data suggest that there is a central abnormality in the baroreflex control of renal nerve activity in renal hypertensive rabbits. This hypothesis was tested further by sectioning vagal, carotid, and aortic nerves and stimulating electrically the left aortic depressor nerve while recording changes in blood pressure and renal sympathetic nerve traffic. Decreases of renal traffic during stimulation of myelinated fibers alone were strikingly impaired (P less than 0.001) at all frequencies in hypertensive rabbits. Responses were not impaired significantly during stimulation of myelinated plus nonmyelinated fibers. Arterial pressure decreases were not different during stimulation of myelinated fibers or of both myelinated and nonmyelinated fibers.(ABSTRACT TRUNCATED AT 250 WORDS)


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