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

Reflex effects of hepatic baroreceptors on renal and cardiac sympathetic nerve activity

1980 ◽  
Vol 238 (5) ◽  
pp. R390-R394 ◽  
Author(s):  
D. R. Kostreva ◽  
A. Castaner ◽  
J. P. Kampine
Keyword(s):  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Vena Cava ◽  
Systemic Blood Pressure ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Cardiac Sympathetic Nerve Activity ◽  
Cervical Vagotomy ◽  
Hepatic Nerves

The reflex effects of hepatic low-pressure baroreceptors on renal and cardiopulmonary sympathetic efferent nerve activity were studied in mongrel dogs anesthetized with pentobarbital sodium. Systemic blood pressure, central venous pressure, hepatic, renal, and portal venous pressures were all measured during occlusion of the thoracic vena cava above the diaphragm, below the liver, and during occlusion of the portal vein. Renal and cardiopulmonary sympathetic efferent nerve activity was continuously recorded along with the hepatic efferent nerve activity during the caval occlusions. Hepatic baroreceptor excitation resulted in marked increases in hepatic afferent nerve activity and reflex increases in renal and cardiopulmonary sympathetic efferent nerve activity without a change in heart rate. Section of the anterior hepatic nerves eliminated the reflex increase in renal efferent nerve activity, but did not eliminate the increase in cardiopulmonary sympathetic efferent nerve activity. Carotid sinus denervation, bilateral cervical vagotomy, and phrenectomy did not alter the reflex responses to hepatic baroreceptor excitation. These hepatorenal and hepatocardiopulmonary reflexes may be important reflex mechanisms that are activated during congestive heart failure and cirrhosis of the liver.

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.

Excitation of cardiac sympathetic afferent nerves: effects on renal function

1981 ◽  
Vol 241 (5) ◽  
pp. R267-R270
Author(s):  
R. L. Meckler ◽  
L. J. Macklem ◽  
L. C. Weaver
Keyword(s):  
Renal Function ◽  
Chemical Stimulation ◽  
Afferent Neurons ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Afferent Nerves ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Stimulation Of

Cardiac sympathetic afferent nerves can reflexly alter renal efferent nerve activity during myocardial ischemia and in response to mechanical or chemical stimulation of cardiac receptors. They also may influence renal excretion of water and electrolytes; however, this potential influence on renal function has not been determined. Therefore, receptors of cardiac sympathetic afferent nerves were chemically stimulated by epicardial application of bradykinin to determine effects on renal function. Experiments were performed in anesthetized dogs in which cervical vagosympathetic trunks were severed and common carotid arteries were tied to diminish influences of arterial baroreceptors and vagal afferent nerves. Chemical stimulation of cardiac afferent neurons excited renal nerve activity and produced decreases in urine flow rate, glomerular filtration rate, and excretion of sodium and potassium. In contrast, no consistent changes in renal function were observed in control dogs, which did not undergo cardiac afferent stimulation. These data provide evidence that activation of cardiac sympathetic afferent neurons can lead to alterations in excretion of water and electrolytes as well as changes in renal nerve activity.

Vagal inhibition of respiratory-linked efferent activity in the carotid sinus nerve

1984 ◽  
Vol 247 (4) ◽  
pp. R681-R686
Author(s):  
D. R. Kostreva ◽  
G. L. Palotas ◽  
J. P. Kampine
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Respiratory Rhythm ◽  
Systemic Blood Pressure ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Efferent Activity ◽  
Central Origin ◽  
Spontaneously Breathing

The hypothesis tested in this study was that glossopharyngeal efferent nerve activity coursing through the carotid sinus nerve has a central origin. Efferent activity in the carotid sinus nerve exhibited a respiratory rhythm in spontaneously breathing, closed-chest, mongrel dogs anesthetized with pentobarbital sodium (30 mg/kg iv). Carotid sinus nerve activity was recorded from the intact or cut central end of the carotid sinus nerve. Diaphragm electromyogram (D-EMG), carotid sinus pressure, systemic blood pressure, and electrocardiogram were also recorded. Before vagotomy, small increases in carotid sinus efferent nerve activity (CSENA) synchronous with increases in the D-EMG were observed during spontaneous inspiration. Section of the contralateral cervical vagosympathetic trunk markedly potentiated the increases in CSENA. Bilateral superior cervical ganglionectomy or nodose ganglionectomy failed to alter the increases in CSENA. Section of the ipsilateral glossopharyngeal nerve near the skull abolished the CSENA. This study demonstrates that respiratory-modulated glossopharyngeal efferents course through the carotid sinus nerve to the carotid sinus or carotid body. These efferents may be part of a central respiratory regulatory mechanism that may rapidly alter the sensitivity of the carotid sinus baroreceptors and/or carotid body receptors on a breath-to-breath basis.

scholarly journals Effect of morphine on the adrenal efferent nerve activity in rats

1984 ◽  
Vol 36 ◽  
pp. 247
Author(s):  
Hiroko Togashi ◽  
Masaru Minami ◽  
Mieko Kurosawa ◽  
Iwao Saito ◽  
Akio Sato ◽  
...  
Keyword(s):  
Nerve Activity ◽  
Efferent Nerve
Sign in / Sign up

Export Citation Format

Share Document