Baroreflex control of cardiac vagal efferent nerve activity in unanesthetized, decerebrate cats

1994 ◽  
Vol 1 ◽  
pp. 377
Author(s):  
K. Matsukawa ◽  
I. Ninomiya
Keyword(s):  
Nerve Activity ◽  
Baroreflex Control ◽  
Efferent Nerve ◽  
Decerebrate Cats ◽  
Vagal Efferent Nerve

Central command does not decrease cardiac parasympathetic efferent nerve activity during spontaneous fictive motor activity in decerebrate cats

2011 ◽  
Vol 300 (4) ◽  
pp. H1373-H1385 ◽  
Author(s):  
Akito Kadowaki ◽  
Kanji Matsukawa ◽  
Rie Wakasugi ◽  
Tomoko Nakamoto ◽  
Nan Liang
Keyword(s):  
Motor Activity ◽  
Time Course ◽  
Spontaneous Motor Activity ◽  
Initial Increase ◽  
Central Command ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Arterial Blood ◽  
Decerebrate Cats ◽  
Peak Increase

To examine whether withdrawal of cardiac vagal efferent nerve activity (CVNA) predominantly controls the tachycardia at the start of exercise, the responses of CVNA and cardiac sympathetic efferent nerve activity (CSNA) were directly assessed during fictive motor activity that occurred spontaneously in unanesthetized, decerebrate cats. CSNA abruptly increased by 71 ± 12% at the onset of the motor activity, preceding the tachycardia response. The increase in CSNA lasted for 4–5 s and returned to the baseline, even though the motor activity was not ended. The increase of 6 ± 1 beats/min in heart rate appeared with the same time course of the increase in CSNA. In contrast, CVNA never decreased but increased throughout the motor activity, in parallel with a rise in mean arterial blood pressure (MAP). The peak increase in CVNA was 37 ± 9% at 5 s after the motor onset. The rise in MAP gradually developed to 21 ± 2 mmHg and was sustained throughout the spontaneous motor activity. Partial sinoaortic denervation (SAD) blunted the baroreflex sensitivity of the MAP-CSNA and MAP-CVNA relationship to 22–33% of the control. Although partial SAD blunted the initial increase in CSNA to 53% of the control, the increase in CSNA was sustained throughout the motor activity. In contrast, partial SAD almost abolished the increase in CVNA during the motor activity, despite the augmented elevation of 31 ± 1 mmHg in MAP. Because afferent inputs from both muscle receptors and arterial baroreceptors were absent or greatly attenuated in the partial SAD condition, only central command was operating during spontaneous fictive motor activity in decerebrate cats. Therefore, it is likely that central command causes activation of cardiac sympathetic outflow but does not produce withdrawal of cardiac parasympathetic outflow during spontaneous motor activity.

Effects of CGRP on baroreflex control of heart rate and renal sympathetic nerve activity in rabbits

1992 ◽  
Vol 263 (4) ◽  
pp. R874-R879 ◽  
Author(s):  
H. Okamoto ◽  
S. Hoka ◽  
T. Kawasaki ◽  
M. Sato ◽  
J. Yoshitake
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Afferent Nerve ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Efferent Nerve ◽  
Induced Hypotension ◽  
Calcitonin Gene ◽  
Alpha Chloralose ◽  
Renal Sympathetic

We examined the effects of intravenous infusion of calcitonin gene-related peptide (CGRP) and sodium nitroprusside (SNP) on baroreceptor afferent nerve activity, renal sympathetic efferent nerve activity (RSNA), and heart rate in alpha-chloralose-anesthetized rabbits. Baroreceptor afferent nerve activity was measured from aortic nerves during CGRP- and SNP-induced hypotension. Decreases in aortic nerve activity in response to decreases in mean arterial pressure were not different during CGRP and SNP infusion. Progressive infusion of CGRP (12-120 pmol.kg-1.min-1) increased RNSA by 83 +/- 14 (mean +/- SE), 175 +/- 26, 246 +/- 36, and 343 +/- 41%, and heart rate by 8 +/- 2, 24 +/- 3, 37 +/- 4, and 47 +/- 6 beats/min during falls of blood pressure of 5, 10, 15, and 20 mmHg, respectively. These increases in RSNA and heart rate produced by CGRP were significantly greater than those produced by SNP. The alterations in heart rate and RSNA with CGRP were reversed by restoring blood pressure with phenylephrine HCl. In rabbits with sinoaortic and vagal deafferentation, the responses of heart rate and RSNA to a fall of blood pressure were abolished during both CGRP and SNP infusion. Therefore, it is suggested that the facilitated responses of heart rate and RSNA during CGRP infusion occurred by way of the arterial baroreflex arc.

scholarly journals Exogenous cholecystokinin-8 reduces vagal efferent nerve activity in rats through CCKA receptors

2000 ◽  
Vol 129 (8) ◽  
pp. 1649-1654 ◽  
Author(s):  
Violeta Bucinskaite ◽  
Mieko Kurosawa ◽  
Thomas Lundeberg
Keyword(s):  
Nerve Activity ◽  
Efferent Nerve ◽  
Ccka Receptors ◽  
Vagal Efferent Nerve

Baroreflex control of sympathetic outflow in pregnant rats: effects of captopril

1990 ◽  
Vol 258 (6) ◽  
pp. R1417-R1423 ◽  
Author(s):  
M. E. Crandall ◽  
C. M. Heesch
Keyword(s):  
Base Line ◽  
Operating Pressure ◽  
Sympathetic Outflow ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Pregnant Rats ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Near Term ◽  
Renal Sympathetic

Arterial baroreflex control of renal sympathetic nerve activity (RSNA) was compared in nonpregnant (NP) and near-term pregnant (P) chloralose-anesthetized rats. Baroreflex curves were obtained by recording reflex changes in RSNA (expressed as a percent of base line) due to increases and decreases in mean arterial pressure (MAP) [intravenous phenylephrine and nitroprusside (NTP)]. The slope, midpoint (EP50), and threshold pressures of the baroreflex curves were compared. Base-line MAP was significantly lower in the pregnant animals (P = 96 +/- 3 vs. NP = 113 +/- 5 mmHg). The baroreflex curves of pregnant animals also had significantly lower threshold (P = 95 +/- 3 vs. NP = 110 +/- 5 mmHg) and midpoint values (P = 105 +/- 4 vs. NP = 119 +/- 5 mmHg). The response to unloading the baroreceptors was attenuated in the pregnant animals as indicated by a decrease in slope of the NTP portion of the baroreflex curve (P = 0.95 +/- 0.17 vs. NP = 1.61 +/- 0.29% nerve activity/mmHg). Responses to blockade of angiotensin-converting enzyme with captopril (2 mg/kg iv) were also examined. There were no differences in EP50 or slope among the control, captopril, and recovery baroreflex curves within either the nonpregnant or pregnant animals. However, after captopril, MAP decreased to a greater extent in the pregnant rats, yet RSNA increased to the same level for the two groups. Thus pregnancy results in a leftward shift of the baroreflex function curve toward a lower operating pressure range. In addition, pregnant rats demonstrated an impaired ability to increase sympathetic outflow above base-line values in response to a hypotensive challenge.

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