Effects of baroreceptor reflex on efferent pulmonary sympathetic nerve activity in anesthetized cat

We analyzed the baroceptor reflex effect on efferent pulmonary sympathetic nerve activity (PSNA) in anesthetized cats. PSNA was recorded from the central end of the cut nerve bundle, which was isolated from the lobar artery supplying the diaphragmatic lobe. Renal sympathetic nerve activity (RSNA) and aortic blood pressure (AP) were also simultaneously measured. There were grouped discharges synchronous with cardiac cycle and its respiratory modulation in PSNA. In a given cardiac cycle, the discharge patterns differed between the pulmonary and renal nerves. Average sympathetic nerve activity and AP obtained from 100 consecutive cardiac cycles showed that the baroreceptor reflex delay time on the pulmonary nerve (266 ms) was longer than that on the renal nerve (195 ms). The data indicate nonuniformity in the cardiac-related PSNA and RSNA. The grouped PSNA disappeared with hexamethonium bromide, indicating that PSNA originates from postganglionic efferent fibers. To examine the baroreflex response of PSNA, AP was increased by 70 mmHg with phenylephrine and decreased by 70 mmHg with nitroprusside. PSNA changed inversely to the changes in mean aortic pressure (MAP). In the delta MAP-delta PSNA curve, delta PSNA reached the maximum level (74%) and the noise level at -56 +/- 4 and 58 +/- 4 mmHg, respectively. The mean slope of the curve was 1.5 +/- 0.1%/mmHg. RSNA also responded inversely to the MAP change.(ABSTRACT TRUNCATED AT 250 WORDS)

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Dynamic arterial baroreflex in rabbits with heart failure induced by rapid pacing

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.1.h92 ◽

1994 ◽

Vol 267 (1) ◽

pp. H92-H99 ◽

Cited By ~ 3

Author(s):

H. Masaki ◽

T. Imaizumi ◽

Y. Harasawa ◽

A. Takeshita

Keyword(s):

Heart Failure ◽

Transfer Function ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Aortic Pressure ◽

Arterial Baroreflex ◽

Nerve Activity ◽

Renal Nerve ◽

Renal Nerve Activity ◽

Rapid Pacing

Excessive sympathetic nerve activity in heart failure could be attributable to impaired arterial baroreflex function. Employing transfer function analysis, we evaluated the arterial baroreflex in control rabbits (n = 8) and in rabbits with rapid pacing-induced heart failure (n = 10) in a dynamic manner. Rabbits in the heart-failure group showed elevated filling pressures, depressed first derivative of left ventricular pressure, pulmonary congestion, and an increased level of plasma norepinephrine. Varying aortic pressure pseudorandomly and recording responses in renal nerve activity, we calculated the transfer function from aortic pressure to renal nerve activity. The gain of the transfer function was similar between control and heart-failure rabbits over 0.04–0.4 Hz as well as the phase and the coherence, indicating that the dynamic arterial baroreflex was preserved in our rabbit heart-failure model. Vagotomy increased the gain of the arterial baroreflex over 0.04–0.4 Hz in control (P < 0.05) but not in heart-failure rabbits, indicating that vagal afferents, which normally inhibit the dynamic arterial baroreflex, no more did so in heart failure. We conclude that excessive sympathetic nerve activity in heart failure may not be due to impaired dynamic arterial baroreflex, but that this apparently preserved arterial baroreflex in heart failure may be due to impaired cardiopulmonary baroreflex.

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Area postrema excites and inhibits sympathetic-related neurons in rostral ventrolateral medulla in rabbit

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.3.h1075 ◽

1994 ◽

Vol 266 (3) ◽

pp. H1075-H1086 ◽

Cited By ~ 3

Author(s):

C. G. Wilson ◽

A. C. Bonham

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Cardiac Cycle ◽

Area Postrema ◽

Rostral Ventrolateral Medulla ◽

Ventrolateral Medulla ◽

Nerve Activity ◽

Spike Triggered Averaging ◽

Discharge Patterns ◽

Alpha Chloralose

This study investigated the effects of area postrema stimulation on the activity of cardiovascular-related neurons in the rostral ventrolateral medulla and determined whether the effects were mediated by cell bodies. Results are based on recordings of extracellular spikes from 113 neurons in 37 alpha-chloralose- or pentobarbital sodium-anesthetized rabbits. Single sequential stimuli evoked an excitation (onset, 22 +/- 8 ms; duration, 20 +/- 14 ms) followed by an inhibition (onset, 53 +/- 21 ms; duration, 127 +/- 82 ms) in 1) 58 neurons with discharge patterns that were correlated with sympathetic nerve activity (determined by spike-triggered averaging) and with the cardiac cycle (determined by post-R wave-triggered histograms) and that were inhibited by increasing arterial pressure and 2) 27 neurons that exhibited a cardiac rhythm but not a sympathetic rhythm. Area postrema-evoked excitation and inhibition were markedly attenuated by kainic acid injections in area postrema, suggesting that both inputs were derived from cell bodies. The results suggest that area postrema neurons may modulate the activity of medullary neurons in the baroreflex-sympathetic arc as well as neurons in other networks that share baroreceptor input but may not be related to sympathetic nerve activity.

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Reflex effects of thermal stimulation on sympathetic nerve activity to skin and kidney

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.2.271 ◽

1976 ◽

Vol 230 (2) ◽

pp. 271-278 ◽

Cited By ~ 27

Author(s):

I Ninomiya ◽

S Fujita

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Cardiac Cycle ◽

Maximum Level ◽

Bath Temperature ◽

Thermal Stimulation ◽

Nerve Activity ◽

Whole Brain ◽

Continuous Cooling ◽

Small Change

Effects of peripheral and central thermoreceptor reflexes on sympathetic nerve activity to the skin (SkNA) and kidney (RNA) were compared in anesthetized cats. Sudden warming of the skin produced a rapid increase of RNA, wheras sudden cooling produced a rapid increase of SkNA. When the bath temperature (TB) was 17.6, 29.7, and 41.9 degrees C, the normalized SkNA was 100, 82, and 48%, while the normalized RNA was 81, 90, and 100%, respectively. Similarly, under open baroceptor loop conditions, SkNA changed inversely with TB, while RNA changed proportionally to TB. Changes in the temperature of the whole brain including hypothalamus (Thy) modified the amplitude of grouped RNA and SkNA synchronously with the cardiac cycle. At TB of 32.4 degrees C, when Thy was altered in a range of 30-42 degrees C, SkNA reached a maximum level at a Thy of 38.4 degrees C, whereas RNA reached a maximum above 42 degrees C. In a Thy range of 38-42 degrees C, the slopes of the Thy-SkNA curve and Thy-RNA curve were 30 and +4%/degrees C, respectively. At Thy below 38 degrees C, SkNA and RNA changed in parallel with Thy. Continuous cooling of the skin modified the slope of the TB-SkNA curve, but a small change of Thy caused a shift of the TB-SkNA curve.

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Increased renal nerve activity in cardiac failure: arterial vs. cardiac baroreflex impairment

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.268.1.r112 ◽

1995 ◽

Vol 268 (1) ◽

pp. R112-R116 ◽

Cited By ~ 6

Author(s):

G. F. DiBona ◽

L. L. Sawin

Keyword(s):

Normal Control ◽

Cardiac Failure ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Baroreceptor Reflex ◽

Nerve Activity ◽

Renal Nerve ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Renal Sympathetic

Cardiac failure is characterized by increased renal sympathetic nerve activity that is associated with an impairment of both arterial and cardiac baroreceptor reflex function. These reflex dysfunctions are in the afferent limb at the level of the peripheral baroreceptors. This study sought to define the relative quantitative magnitude of the defects in arterial and cardiac baroreceptor function in cardiac failure. Renal sympathetic nerve activity was measured in anesthetized normal control rats and rats with cardiac failure (left coronary ligation) during sequential random order sinoaortic denervation and vagotomy to interrupt afferent input from the arterial and cardiac baroreceptors, respectively. Increases in renal sympathetic nerve activity after individual or combined sinoaortic denervation and vagotomy were less (P < 0.05 for both) in cardiac failure than in normal control rats in both order sequences (42 +/- 5 vs. 87 +/- 8%; 44 +/- 5 vs. 108 +/- 7%). In cardiac failure rats, vagotomy produced lesser increases (P < 0.05 for both) in renal sympathetic nerve activity than sinoaortic denervation in both order sequences (10 +/- 4 vs. 32 +/- 5%; 13 +/- 2 vs. 30 +/- 5%). The relative magnitude of impaired cardiac baroreceptor reflex function that is associated with the increased renal sympathetic nerve activity of cardiac failure is greater than that of impaired arterial baroreceptor reflex function.

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Opioid Modulation of Cardiac Sympathetic Nerve Activity of Baroreceptor Reflex in Rats

New Aspects in the Treatment of Failing Heart ◽

10.1007/978-4-431-68219-6_26 ◽

1992 ◽

pp. 148-150

Author(s):

Mitsuhiro Yoshioka ◽

Masahiro Tochihara ◽

Hiroko Togashi ◽

Hideya Saito

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Baroreceptor Reflex ◽

Cardiac Sympathetic Nerve ◽

Nerve Activity ◽

Cardiac Sympathetic Nerve Activity

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Role of nitric oxide in regulation of renal sympathetic nerve activity during hemorrhage in conscious rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.277.1.h8 ◽

1999 ◽

Vol 277 (1) ◽

pp. H8-H14 ◽

Cited By ~ 8

Author(s):

Yoshihide Fujisawa ◽

Naoko Mori ◽

Kouichi Yube ◽

Hiroshi Miyanaka ◽

Akira Miyatake ◽

...

Keyword(s):

Nitric Oxide ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Saline Group ◽

Baroreceptor Reflex ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Conscious Rats ◽

Renal Sympathetic Nerve ◽

Renal Sympathetic

The effect of inhibition of nitric oxide (NO) synthesis on the responses of blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) during hemorrhaging was examined with the use of an NO synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), in conscious rats. In the 0.9% saline group, hemorrhage (10 ml/kg body wt) did not alter BP but significantly increased HR and RSNA by 88 ± 12 beats/min and 67 ± 12%, respectively. Intravenous infusion of l-NAME (50 μg ⋅ kg−1⋅ min−1) significantly attenuated these tachycardic and sympathoexcitatory responses to hemorrhage (14 ± 7 beats/min and 26 ± 12%, respectively). Pretreatment ofl-arginine (87 mg/kg) recovered the attenuation of HR and RSNA responses induced byl-NAME (92 ± 6 beats/min and 64 ± 10%, respectively).l-NAME by itself did not alter the baroreceptor reflex control of HR and RSNA. Hemorrhage increased the plasma vasopressin concentration, and its increment in thel-NAME-treated group was significantly higher than that in the 0.9% saline group. Pretreatment with the vascular arginine vasopressin V1-receptor antagonist OPC-21268 (5 mg/kg) recovered the attenuation of RSNA response induced byl-NAME (54 ± 7%). These results indicate that NO modulated HR and RSNA responses to hemorrhage but did not directly affect the baroreceptor reflex arch. It can be assumed that NO modulated the baroreflex function by altering the secretion of vasopressin induced by hemorrhage.

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Neural control of renal function in edema-forming states

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1988.254.6.r1017 ◽

1988 ◽

Vol 254 (6) ◽

pp. R1017-R1024 ◽

Cited By ~ 16

Author(s):

G. F. DiBona ◽

P. J. Herman ◽

L. L. Sawin

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Isotonic Saline ◽

Experimental Models ◽

Renal Nerves ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Duct Ligation ◽

Renal Sympathetic

To define the role of the renal nerves in renal sodium-retaining edema-forming states, experiments were conducted in conscious chronically instrumented rats with congestive heart failure (myocardial infarction), nephrotic syndrome (adriamycin injection), and hepatic cirrhosis (common bile duct ligation). In each experimental model, renal excretion, as water or sodium, of an acutely administered oral or intravenous isotonic saline load was significantly less than that in control rats. Bilateral renal denervation of the experimental rats restored their renal excretory response to that of the control rats. In addition, in response to the acute administration of a standard intravenous isotonic saline load, the decrease in efferent renal sympathetic nerve activity was significantly less in all three experimental models compared with that of control rats. These results suggest that the impaired ability to excrete an acute isotonic saline load in these experimental models is partially dependent on an increase in basal efferent renal sympathetic nerve activity that fails to suppress normally in response to the isotonic saline load.

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Effects of NO on baroreflex control of heart rate and renal nerve activity in conscious rabbits

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.270.6.r1361 ◽

1996 ◽

Vol 270 (6) ◽

pp. R1361-R1370 ◽

Cited By ~ 21

Author(s):

J. L. Liu ◽

H. Murakami ◽

I. H. Zucker

Keyword(s):

Heart Rate ◽

Sympathetic Nerve ◽

Baroreflex Sensitivity ◽

Sympathetic Nerve Activity ◽

Control Level ◽

Relative Role ◽

Nerve Activity ◽

Renal Nerve ◽

Baroreflex Control ◽

Synthase Inhibitor

Recent data suggest that nitric oxide (NO) plays a role in the modulation of sympathetic nerve activity and baroreflex sensitivity. Most of these studies have been carried out in anesthetized preparations, and little if any comparison has been made on the relative role of NO on the baroreflex control of heart rate and sympathetic nerve activity. In the present studies, the effect of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) on the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in conscious, instrumented rabbits. Intravenous bolus injections of 13 mg/kg of L-NNA decreased baseline HR (from 205.0 +/- 6.0 to 145.5 +/- 8.2 beats/min; P < 0.05) without significant changes in mean arterial pressure (MAP) and RSNA. L-NNA significantly reduced the lower plateau of the HR-MAP curves and increased the sensitivities of baroreflex control of HR and RSNA. L-Arginine (600 mg/kg i.v.) but not D-arginine reversed the above effects. The effects of L-NNA on baseline HR were not completely blocked by metoprolol (2 mg/kg) or by atropine (0.2 mg/kg). After pretreatment with metoprolol, baroreflex sensitivity was reduced and L-NNA increased baroreflex sensitivity back to the control level. After pretreatment with atropine, L-NNA still reduced the lower plateau but did not significantly affect baroreflex sensitivity. L-NNA increased the HR responses but not the RSNA response to electrical stimulation of the aortic nerve in chloralose-anesthetized, sinoaortic-denervated (SAD) rabbits. L-NNA had no effect on the HR response to right vagal stimulation. In both conscious intact and SAD rabbits, L-NNA did not increase baseline RSNA. These results suggest that endogenous NO decreases baroreflex control of HR and RSNA. Both sympathetic and parasympathetic components play a role in the effects of NO on the baroreflex control of HR. The effects of NO in the central nervous system play a more important role in the baroreflex control of HR than of RSNA.

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