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.

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.

Dynamic changes in venous outflow by baroreflex and left ventricular distension

1988 ◽  
Vol 254 (2) ◽  
pp. R212-R221 ◽  
Author(s):  
S. Hoka ◽  
Z. J. Bosnjak ◽  
D. Siker ◽  
R. J. Luo ◽  
J. P. Kampine
Keyword(s):  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Nerve Activity ◽  
Venous Outflow ◽  
Dynamic Changes ◽  
Venous Capacitance ◽  
Additional Group ◽  
Vascular Beds

We examined the dynamic changes in venous outflow from the splanchnic and extrasplanchnic vascular beds in response to carotid sinus (CS) baroreflex and left ventricular (LV) distension in 12 dogs anesthetized with pentobarbital sodium. Splenic sympathetic nerve activity was measured in an additional group of six dogs. A heart-lung bypass was used with constant cardiac output and constant venous pressure. LV distension was produced by inflating a balloon in the LV. LV distension and an increase in CS pressure from 50 to 200 mmHg decreased blood pressure by 26 +/- 5 and 30 +/- 6 mmHg and increased vascular capacitance by 5.5 +/- 0.9 and 4.5 +/- 1.2 ml/kg, respectively. Splanchnic venous outflow exhibited a transient decrease, whereas extrasplanchnic venous outflow showed a transient increase, in response to LV distension and increasing CS pressure, accompanied by a sustained decrease in splenic nerve activity. The results indicate important differences between splanchnic and extrasplanchnic components of the total venous system in terms of the regulation of venous capacitance. It is suggested that changes in venous capacitance produced by LV distension and CS baroreflex are primarily due to active changes in splanchnic venous tone.

scholarly journals Responses of cardiac sympathetic nerve activity to changes in circulating volume differ in normal and heart failure sheep

2008 ◽  
Vol 295 (3) ◽  
pp. R719-R726 ◽  
Author(s):  
Rohit Ramchandra ◽  
Sally G. Hood ◽  
Anna M. D. Watson ◽  
Clive N. May
Keyword(s):  
Heart Failure ◽  
Normal State ◽  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Cardiac Sympathetic Nerve ◽  
Volume Depletion ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity

Factors controlling cardiac sympathetic nerve activity (CSNA) in the normal state and those causing the large increase in activity in heart failure (HF) remain unclear. We hypothesized from previous clinical findings that activation of cardiac mechanoreceptors by the increased blood volume in HF may stimulate sympathetic nerve activity (SNA), particularly to the heart via cardiocardiac reflexes. To investigate the effect of volume expansion and depletion on CSNA we have made multiunit recordings of CSNA in conscious normal sheep and sheep paced into HF. In HF sheep ( n = 9) compared with normal sheep ( n = 9), resting levels of CSNA were significantly higher (34 ± 5 vs. 93 ± 2 bursts/100 heart beats, P < 0.05), mean arterial pressure was lower (76 ± 3 vs. 87 ± 2 mmHg; P < 0.05), and central venous pressure (CVP) was greater (3.0 ± 1.0 vs. 0.0 ± 1.0 mmHg; P < 0.05). In normal sheep ( n = 6), hemorrhage (400 ml over 30 min) was associated with a significant increase in CSNA (179 ± 16%) with a decrease in CVP (2.7 ± 0.7 mmHg). Volume expansion (400 ml Gelofusine over 30 min) significantly decreased CSNA (35 ± 12%) and increased CVP (4.7 ± 1.0 mmHg). In HF sheep ( n = 6) the responses of CSNA to both volume expansion and hemorrhage were severely blunted with no significant changes in CSNA or heart rate with either stimulus. In summary, these studies in a large conscious mammal demonstrate that in the normal state directly recorded CSNA increased with volume depletion and decreased with volume loading. In contrast, both of these responses were severely blunted in HF with no significant changes in CSNA during either hemorrhage or volume expansion.

Direct measurement of cardiac sympathetic efferent nerve activity during dynamic exercise

2002 ◽  
Vol 283 (5) ◽  
pp. H1896-H1906 ◽  
Author(s):  
Hirotsugu Tsuchimochi ◽  
Kanji Matsukawa ◽  
Hidehiko Komine ◽  
Jun Murata
Keyword(s):  
Sympathetic Nerve Activity ◽  
Cardiac Pacemaker ◽  
Dynamic Exercise ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Parasympathetic Nerve ◽  
Cardiac Sympathetic Nerve Activity ◽  
Exercise Onset ◽  
Time Courses ◽  
S Period

The assumption that tachycardia during light to moderate exercise was predominantly controlled by withdrawal of cardiac parasympathetic nerve activity but not by augmentation of cardiac sympathetic nerve activity (CSNA) was challenged by measuring CSNA during treadmill exercise (speed, 10–60 m/min) for 1 min in five conscious cats. As soon as exercise started, CSNA and heart rate (HR) increased and mean arterial pressure (MAP) decreased; their time courses at the initial 12-s period of exercise were irrespective of the running speed. CSNA increased 168–297% at 7.1 ± 0.4 s from the exercise onset, and MAP decreased 8–13 mmHg at 6.0 ± 0.3 s, preceding the increase of 40–53 beats/min in HR at 10.5 ± 0.4 s. CSNA remained elevated during the later period of exercise, whereas HR and MAP gradually increased until the end of exercise. After the cessation of exercise, CSNA returned quickly to the control, whereas HR was slowly restored. In conclusion, cardiac sympathetic outflow augments at the onset of and during dynamic exercise even though the exercise intensity is low to moderate, which may contribute to acceleration of cardiac pacemaker rhythm.

Splenic afferents and some of their reflex responses

1982 ◽  
Vol 242 (3) ◽  
pp. R247-R254 ◽  
Author(s):  
N. L. Herman ◽  
D. R. Kostreva ◽  
J. P. Kampine
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Venous Pressure ◽  
Systemic Blood Pressure ◽  
Contractile Force ◽  
Afferent Nerve ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
C Fibers ◽  
Stimulation Period

Afferent nerve activity was recorded from the distal ends of cut splenic nerves in pentobarbital- (35 mg/kg) anesthetized mongrel dogs (15-20 kg). Increases in splenic venous pressure (SVP) produced either by manual compression of discrete portions of the spleen or splenic contraction produced by injection of epinephrine (100 micrograms) into the splenic artery or vein of an occluded spleen produced significant increases in SVP and splenic afferent nerve activity. Increases in splenic afferent nerve activity were linearly related to increases in SVP. Histological sections of nerves from which afferent recordings were obtained demonstrated that all afferents were unmyelinated C-fibers. Electrical stimulation of the cut central end of splenic nerves resulted in marked reflex increases in both renal and cardiopulmonary sympathetic efferent nerve activity that remained elevated throughout the stimulation period. Reflex increase in cardiopulmonary sympathetic efferent nerve activity was associated with increases in right (22-45%) and left (11-19%) ventricular contractile force measured with Brodie-Walton strain gauge transducers, in heart rate (5-15 beats/min), and in blood pressure (5-10 mmHg). This study is the first to demonstrate both the existence of low-pressure baroreceptors in the spleen and that these splenic afferents can reflexly alter cardiopulmonary and renal sympathetic efferent nerve activity, heart rate, ventricular contractile force, and systemic blood pressure.

Atrial receptor modulation of renal nerve activity in the nonhuman primate

1982 ◽  
Vol 242 (6) ◽  
pp. F592-F598 ◽  
Author(s):  
J. P. Gilmore ◽  
S. Echtenkamp ◽  
C. R. Wesley ◽  
I. H. Zucker
Keyword(s):  
Significant Influence ◽  
Nonhuman Primate ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Balloon Inflation ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Receptor Modulation ◽  
Renal Nerve Activity ◽  
Cervical Vagotomy

Experiments were done in the nonhuman primate Macaca fascicularis to determine the extent to which low-pressure receptors modulate renal nerve activity (RNA). Left atrial pressure (LAP) was increased either by inflating a balloon in the left atrium or by intravascular volume expansion. Arterial pressure (AP) was increased by the administration of epinephrine. Balloon inflation produced variable changes in RNA when all reflexes were intact. In the bilateral vagotomized animal, balloon inflation significantly increased RNA. Compared with the intact state, neither carotid sinus denervation nor sinoaortic denervation had a significant influence on RNA during balloon inflation. The response of both baroreceptor-denervated groups, however, was significantly less than that of the vagotomized group. Vagotomy plus sinoaortic denervation essentially prevented any effect of balloon inflation on RNA. Volume expansion produced a greater inhibition of RNA per increase in AP than did epinephrine. However, this difference was abolished after bilateral cervical vagotomy. These experiments demonstrate a significant influence and interplay of low- and high-pressure receptors on RNA in the nonhuman primate.

scholarly journals Both central command and exercise pressor reflex activate cardiac sympathetic nerve activity in decerebrate cats

2009 ◽  
Vol 296 (4) ◽  
pp. H1157-H1163 ◽  
Author(s):  
Hirotsugu Tsuchimochi ◽  
Shawn G. Hayes ◽  
Jennifer L. McCord ◽  
Marc P. Kaufman
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventral Root ◽  
Central Command ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Exercise Pressor Reflex ◽  
Cardiac Sympathetic Nerve Activity ◽  
Pressor Reflex ◽  
Decerebrate Cats

Both static and dynamic exercise are known to increase cardiac pump function as well as arterial blood pressure. Feedforward control by central command and feedback control by the exercise pressor reflex are thought to be the neural mechanisms causing these effects during exercise. It remains unknown as to how each mechanism activates cardiac sympathetic nerve activity (CSNA) during exercise, especially at its onset. Thus we examined the response of CSNA to stimulation of the mesencephalic locomotor region (MLR, i.e., central command) and to static muscle contraction of the triceps surae muscles or stretch of the calcaneal tendon in decerebrate cats. We found that MLR stimulation immediately increased CSNA, which was followed by a gradual increase in heart rate, mean arterial pressure, and ventral root activity in a stimulus intensity-dependent manner. The latency of the increase in CSNA from the onset of MLR stimulation ranged from 67 to 387 ms. Both static contraction and tendon stretch also rapidly increased CSNA. Their latency from the development of tension in response to ventral root stimulation ranged from 78 to 670 ms. These findings suggest that both central command and the muscle mechanoreflex play a role in controlling cardiac sympathetic outflow at the onset of exercise.

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