Central catecholaminergic neurons are involved in expression of the 10-Hz rhythm in SND

1996 ◽  
Vol 270 (2) ◽  
pp. R333-R341 ◽  
Author(s):  
H. S. Orer ◽  
S. Zhong ◽  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Intravenous Administration ◽  
Sympathetic Nerve ◽  
Ventrolateral Medulla ◽  
Imidazoline Receptors ◽  
Catecholaminergic Neurons ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Nerve Discharge ◽  
Lower Frequencies

We studied the effects of adrenoceptor agonists and antagonists on sympathetic nerve discharge (SND) of urethan-anesthetized, baroreceptor-denervated cats. In cats in which a 10-Hz rhythm coexisted with irregular 2- to 6-Hz oscillations in SND, intravenous clonidine, an alpha 2-adrenoceptor agonist, blocked the 10-Hz rhythm without affecting power at lower frequencies. In contrast, power at frequencies < or = 6 Hz was depressed by clonidine in cats in which the 10-Hz rhythm was absent. These effects were reversed by intravenous administration of alpha 2-adrenoceptor antagonists, idazoxan and rauwolscine. Rauwolscine is devoid of affinity for imidazoline receptors. Furthermore, in cats untreated with clonidine, idazoxan and rauwolscine enhanced or induced the 10-Hz rhythm without affecting power at lower frequencies. Prazosin, an alpha 1-adrenoceptor antagonist, selectively blocked the 10-Hz rhythm in SND. Finally, the 10-Hz rhythm in SND was blocked by microinjection of clonidine into the rostral or caudal ventrolateral medulla. The results support the view that central catecholaminergic neurons play a role in expression of the 10-Hz rhythm in SND.

The Effect of Imidazoline Receptors and α2-adrenoceptors on the Anesthetic Requirement (MAC) for Halothane in Rats 

1997 ◽  
Vol 87 (4) ◽  
pp. 963-967 ◽  
Author(s):  
Kiyokazu Kagawa ◽  
Tadanori Mammoto ◽  
Yukio Hayashi ◽  
Takahiko Kamibayashi ◽  
Takashi Mashimo ◽  
...  
Keyword(s):  
Minimum Alveolar Concentration ◽  
Inhibitory Effect ◽  
Imidazoline Receptors ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
The Central Nervous System ◽  
Anesthetic Requirement ◽  
Alpha2 Adrenoceptor ◽  
Pharmacologic Actions

Background Recent evidences have documented that several pharmacologic actions of alpha2-adrenoceptor agonists are mediated via activation of not only alpha2-adrenoceptors, but also by imidazoline receptors, which are nonadrenergic receptors in the central nervous system. However, the effect of imidazoline receptors on the anesthesia is not well known, and it is important to clarify the effects of both receptors on anesthesia. Methods Seventy-two rats were anesthetized with halothane, and the anesthetic requirement for halothane was evaluated as minimum alveolar concentration (MAC). The MAC for halothane was determined in the presence of dexmedetomidine (0, 10, 20, and 30 microg/kg, intraperitoneally [IP]), a selective alpha2-adrenoceptor agonist with weak affinity for imidazoline receptors. Then, the authors evaluated the inhibitory effect of rauwolscine (20 mg/kg, IP), an alpha2-adrenoceptor antagonist with little affinity for imidazoline receptors, on the MAC-reducing action of dexmedetomidine (30 microg/kg). Further, the effect of rilmenidine (20, 50, 100, 1000 microg/kg, IP), a selective imidazoline receptor agonist, on the MAC for halothane was also investigated. Results Dexmedetomidine decreased the MAC for halothane dose-dependently, and this MAC-reducing action of dexmedetomidine was completely blocked by rauwolscine. Rilmenidine alone did not change the MAC for halothane. Conclusions The present data indicate that the anesthetic sparing action of dexmedetomidine is most likely mediated through alpha2- adrenoceptors, and the stimulation of imidazoline receptors exerts little effect on the anesthetic requirement for halothane.

Effects of α-adrenoceptor agonists and antagonists on thyroid hormone secretion

1985 ◽  
Vol 108 (2) ◽  
pp. 184-191 ◽  
Author(s):  
Bo Ahrén
Keyword(s):  
Thyroid Hormone ◽  
Dose Level ◽  
Hormone Secretion ◽  
High Dose ◽  
Inhibitory Effects ◽  
High Dose Level ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists

Abstract. The effects of various α-adrenoceptor agonists and antagonists on blood radioiodine levels were studied in mice pre-treated with 125I and thyroxine. The non-selective α-adrenoceptor agonist noradrenaline and the selective α1-adrenoceptor agonist phenylephrine both enhanced blood radioiodine levels. Noradrenaline was more potent than phenylephrine. Contrary, the selective α2-adrenoceptor agonist clonidine depressed basal levels of blood radioiodine. The non-selective α-adrenoceptor antagonist phentolamine and the selective α1-adrenoceptor antagonist prazosin both inhibited the noradrenaline-induced elevation of radioiodine levels, whereas the α2-adrenoceptor antagonist yohimbine had no such effect, except at a high dose level. All three α-adrenoceptor agonists, noradrenaline, phenylephrine and clonidine, inhibited the radioiodine response to TSH. In addition, TSH-induced increase in radioiodine levels was inhibited by prazosin, whereas yohimbine had no effect. Phentolamine inhibited the radioiodine response to TSH when given 2 h prior to TSH, whereas when given 15 min prior to TSH the response to TSH was potentiated by Phentolamine. It is concluded, that under in vivo conditions in the mouse, α1-adrenoceptor activation stimulates basal thyroid hormone secretion and inhibits TSH-induced thyroid hormone secretion. Further, α2-adrenoceptor activation inhibits basal thyroid hormone secretion. In addition, TSH-induced thyroid hormone secretion is inhibited by α1-adrenoceptor antagonism. Thus, α-adrenoceptors induce both stimulatory and inhibitory effects of thyroid function.

Role of the brain stem in generating the 2- to 6-Hz oscillation in sympathetic nerve discharge

1993 ◽  
Vol 265 (5) ◽  
pp. R1026-R1035 ◽  
Author(s):  
S. Zhong ◽  
Z. S. Huang ◽  
G. L. Gebber ◽  
S. M. Barman
Keyword(s):  
Brain Stem ◽  
Sympathetic Nerve ◽  
Cervical Spinal Cord ◽  
Ventrolateral Medulla ◽  
Population Activity ◽  
A Value ◽  
Decerebrate Cats ◽  
The Brain ◽  
Nerve Discharge

We tested the hypothesis that brain stem circuits normally generate a 2- to 6-Hz oscillation in sympathetic nerve discharge (SND). Experiments were performed on baroreceptor-denervated decerebrate cats and urethan-anesthetized rats in which renal or splanchnic SND was recorded along with field potentials (population activity) from sites in the rostral ventrolateral medulla, medullary raphe, or medullary lateral tegmental field. Our major findings were as follows. 1) Population activity recorded from the three medullary regions contained a 2- to 6-Hz oscillation. 2) The 2- to 6-Hz oscillation in population activity recorded from some medullary sites was correlated to that in SND. Peak coherence in the 2- to 6-Hz band approached a value of 1 in some cases. 3) Whereas cervical spinal cord transection abolished or markedly reduced SND, the 2- to 6-Hz oscillation in medullary activity was essentially unchanged. These results support the view that the 2- to 6-Hz oscillation in SND can be generated in the brain stem of cats and rats.

scholarly journals Catecholamines modulate podocyte function.

1998 ◽  
Vol 9 (3) ◽  
pp. 335-345 ◽  
Author(s):  
T B Huber ◽  
J Gloy ◽  
A Henger ◽  
P Schollmeyer ◽  
R Greger ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Patch Clamp Technique ◽  
Extracellular Solution ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Beta 2 ◽  
Cl Conductance ◽  
Stimulation Of ◽  
Ion Conductances

The aim of this study was to investigate the influence of adrenoceptor agonists on the intracellular calcium activity ([Ca2+]i), membrane voltage (Vm), and ion conductances (Gm) in differentiated mouse podocytes. [Ca2+]i was measured by the Fura-2 fluorescence method in single podocytes. Noradrenaline and the alpha 1-adrenoceptor agonist phenylephrine induced a reversible and concentration-dependent biphasic increase of [Ca2+]i in podocytes (EC50 approximately 0.1 microM for peak and plateau), whereas the alpha 2-adrenoceptor agonist UK 14.304 did not influence [Ca2+]i. The [Ca2+]i response induced by noradrenaline was completely inhibited by the alpha 1-adrenoceptor antagonist prazosin (10 nM). In a solution with a high extracellular K+ (72.5 mM), [Ca2+]i was unchanged and the [Ca2+]i increase induced by noradrenaline was not inhibited by the L-type Ca2+ channel blocker nicardipine (1 microM). Vm and Gm were examined with the patch-clamp technique in the slow whole-cell configuration. Isoproterenol, phenylephrine, and noradrenaline depolarized podocytes and increased Gm. The order of potency for the adrenoceptor agonists was isoproterenol (EC50 approximately 1 nM) > noradrenaline (EC50 approximately 0.3 microM) > phenylephrine (EC50 approximately 0.5 microM). The beta 2-adrenoceptor antagonist ICI 118.551 (5 to 100 nM) inhibited the effect of isoproterenol on Vm. Stimulation of adenylate cyclase by forskolin mimicked the effect of isoproterenol on Vm and Gm (EC50 approximately 40 nM). Isoproterenol induced a time- and concentration-dependent increase of cAMP in podocytes. The effect of isoproterenol was unchanged in the absence of Na+ or in an extracellular solution with a reduced Ca2+ concentration, whereas it was significantly increased in an extracellular solution with a reduced Cl- concentration (from 145 to 32 mM). The data indicate that adrenoceptor agonists regulate podocyte function: They increase [Ca2+]i via an alpha 1-adrenoceptor and induce a depolarization via a beta 2-adrenoceptor. The depolarization is probably due to an opening of a cAMP-dependent Cl- conductance.

Lateral tegmental field neurons of cat medulla: a potential source of basal sympathetic nerve discharge

1985 ◽  
Vol 54 (6) ◽  
pp. 1498-1512 ◽  
Author(s):  
G. L. Gebber ◽  
S. M. Barman
Keyword(s):  
Slow Wave ◽  
Sympathetic Nerve ◽  
Baroreceptor Reflex ◽  
Raphe Nuclei ◽  
Ventrolateral Medulla ◽  
Related Activity ◽  
Medullary Raphe ◽  
Reflex Activation ◽  
Raphé Nuclei ◽  
Nerve Discharge

A study was made of 170 neurons of the lateral tegmental field (LTF) of the cat medulla with spontaneous activity temporally related to the 2- to 6-Hz slow wave in inferior cardiac postganglionic sympathetic nerve discharge (as demonstrated with spike-triggered averaging). LTF neurons were excited by the iontophoresis of L-glutamate, and an inflection on the rising phase of their action potentials was observed. Thus, the site of extracellular unit recording presumably was in the region of the cell body. The lag between LTF unit spike occurrence and the peak of the 2- to 6-Hz slow wave in sympathetic nerve discharge (SND) was unchanged when blood pressure and, thus, baroreceptor nerve activity were lowered to a level at which the phase relationship between the slow wave and the cardiac cycle was disrupted. Thus, the discharges of LTF neurons apparently were more closely associated with those of elements of "efferent" brain stem networks controlling SND than with those of interneurons in the afferent limb of the baroreceptor reflex arc. LTF neurons with sympathetic nerve- and cardiac-related activity were classified into three types depending on their responses to elevated carotid sinus pressure (i.e., baroreceptor reflex activation). Of the 82 neurons tested, 33 were inhibited, 16 were excited, and 33 were unaffected by baroreceptor reflex activation. Using data collected in this and previous studies from our laboratory, we compared the firing times of neurons in the LTF, rostral ventrolateral medulla, and medullary raphe nuclei relative to the peak of the sympathetic nerve slow wave. LTF neurons that were inhibited by baroreceptor reflex activation are presumed to subserve a sympathoexcitatory function. These neurons fired significantly earlier during the sympathetic nerve slow wave than their counterparts in the rostral ventrolateral medulla and medullary raphe nuclei. LTF neurons classified as sympathoinhibitory (i.e., excited by baroreceptor reflex activation) fired significantly earlier than their counterparts in the medullary raphe nuclei. These data raise the possibility that LTF neurons are closer (at least in a temporal sense) to the region of origin of the 2- to 6-Hz component of SND than are ventrolateral medullary and raphe neurons. The firing times of sympathoexcitatory and sympathoinhibitory LTF neurons were not significantly different. These data are discussed relative to potential mechanisms involved in generating SND. Microstimulation of the second thoracic spinal segment was used to determine whether the axons of LTF neurons with sympathetic nerve-related activity projected to this level.(ABSTRACT TRUNCATED AT 400 WORDS)

Fractal Noises and Motions in Time Series of Presympathetic and Sympathetic Neural Activities

2006 ◽  
Vol 95 (2) ◽  
pp. 1176-1184 ◽  
Author(s):  
Gerard L. Gebber ◽  
Hakan S. Orer ◽  
Susan M. Barman
Keyword(s):  
Time Series ◽  
Sympathetic Nerve ◽  
Point Processes ◽  
Sympathetic Neurons ◽  
Spike Trains ◽  
Ventrolateral Medulla ◽  
Scaling Exponent ◽  
Long Range Correlations ◽  
Allan Factor ◽  
Nerve Discharge

We used Allan factor analysis to classify time series of the discharges of single presympathetic neurons in the cat medullary lateral tegmental field (LTF) and rostral ventrolateral medulla (RVLM) and of the postganglionic vertebral sympathetic nerve. These time series fell into two classes of fractal-based point processes characterized by statistically self-similar behavior reflecting long-range correlations among data points. Classification of a time series as either a fractional Gaussian noise (fGn)–or fractional Brownian motion (fBm)–based point process depended on the scaling exponent, α, of the power law in the Allan factor curve. fGn is defined as 0 < α < 1 and fBm as 1 < α < 3. The process responsible for the fractal spike trains of 11 of 12 classifiable LTF neurons with sympathetic nerve-related activity was fGn. In contrast, the process responsible for the fractal spike trains of eight of nine classifiable RVLM presympathetic neurons was fBm. The time series of simultaneously recorded vertebral sympathetic nerve discharge and the arterial pulse also were fBm-based signals. Because a fBm signal is the cumulative sum of the elements comprising the corresponding fGn signal, these results show smoothing of fractal time series in a feedforward direction from medullary presympathetic neurons to postganglionic sympathetic neurons. This may involve integration by RVLM neurons of their LTF inputs or independent fractal processes acting at different levels of the network controlling sympathetic nerve discharge. Whether feedforward smoothing of fractal signals is a feature in other neural systems is open to investigation.

A comparative study of the acute effects of cetamolol (AI-27,303), atenolol, propranolol, and dexpropranolol on blood pressure, sympathetic nerve and ganglion activity of cats

1983 ◽  
Vol 61 (7) ◽  
pp. 693-698 ◽  
Author(s):  
J. Jaramillo
Keyword(s):  
Blood Pressure ◽  
Comparative Study ◽  
Intravenous Administration ◽  
Superior Cervical Ganglion ◽  
Sympathetic Nerve ◽  
Sympathetic Ganglia ◽  
Acute Effects ◽  
Cervical Ganglion ◽  
Sympathetic Discharge ◽  
Nerve Discharge

The effects of cetamolol (AI-27,303, Betacor®), atenolol, propranolol, and dexpropranolol were evaluated in 36 chloralose–urethane anesthetized cats. Blood pressure, sympathetic nerve discharge, and ganglionic activity (from the superior cervical ganglion) were recorded after the intravenous administration of 2.5, 5.0, and 10 mg/kg doses of the compounds. The results indicate that cetamolol and atenolol decreased blood pressure and discharge in the postganglionic sympathetic nerve and impaired transmission at the level of sympathetic ganglia. Propranolol and dexpropranolol given at the same doses produced a larger decrease in blood pressure, but increased the sympathetic discharge and had no effect on ganglionic spike amplitude.

Medullary lateral tegmental field: an important source of basal sympathetic nerve discharge in the cat

2000 ◽  
Vol 278 (4) ◽  
pp. R995-R1004 ◽  
Author(s):  
Susan M. Barman ◽  
Gerard L. Gebber ◽  
Hakan S. Orer
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Sympathetic Nerve ◽  
Excitatory Amino Acid ◽  
Nmda Receptor Antagonist ◽  
Ventrolateral Medulla ◽  
Cardiac Sympathetic Nerve ◽  
Significant Component ◽  
Synaptic Drive ◽  
Nerve Discharge

We used blockade of excitatory amino acid (EAA) neurotransmission in the medullary lateral tegmental field (LTF) and rostral ventrolateral medulla (RVLM) to assess the roles of these regions in the control of inferior cardiac sympathetic nerve discharge (SND) and mean arterial pressure (MAP) in urethan-anesthetized, baroreceptor-denervated cats. Bilateral microinjection of a non- N-methyl-d-aspartate (NMDA)-receptor antagonist [1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]quinoxaline-7-sulfonamide (NBQX)] into the LTF significantly decreased SND to 46 ± 4% of control (as demonstrated with power-density spectral analysis) and MAP by 16 ± 6 mmHg. In contrast, bilateral microinjection of an NMDA-receptor antagonist [d(−)-2-amino-5-phosphonopentanoic acid (d-AP5)] into the LTF did not decrease SND or MAP. These results demonstrate that the LTF is an important synaptic relay in the pathway responsible for basal SND in the cat. Bilateral microinjection of NBQX or d-AP5 into the RVLM significantly decreased power in SND to 48 ± 5 or 61 ± 5% of control, respectively, and reduced MAP by 15 ± 2 or 8 ± 4 mmHg, respectively. These data indicate that EAA-mediated synaptic drive to RVLM-spinal sympathoexcitatory neurons accounts for a significant component of their basal activity.

scholarly journals Blockade of angiotensin AT1-receptors in the rostral ventrolateral medulla of spontaneously hypertensive rats reduces blood pressure and sympathetic nerve discharge

2001 ◽  
Vol 2 (1_suppl) ◽  
pp. S120-S124 ◽  
Author(s):  
Andrew M Allen
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Spontaneously Hypertensive Rat ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
At1 Receptors ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Nerve Discharge

Microinjections of angiotensin II (Ang II) into the rostral ventrolateral medulla (RVLM) induce a sympathetically-mediated increase in blood pressure (BP), through an interaction with AT1-receptors. Under basal conditions in anaesthetised animals, microinjections of AT 1-receptor antagonists into the RVLM have little, or no effect on BP, suggesting that the angiotensin input to this nucleus is not tonically active. In contrast, microinjections of AT1-receptor antagonists into the RVLM of sodium-deplete rats and TGR(mRen2)27 rats, induce a depressor response through sympatho-inhibition. This indicates that when the renin-angiotensin system is activated, angiotensin can act in the RVLM to support sympathetic nerve discharge and BP. This study examined whether angiotensin inputs to the RVLM are activated in the spontaneously hypertensive rat — a pathophysiological model which displays increases in both brain angiotensin levels and sympathetic nerve activity. Bilateral microinjections of the AT 1-receptor antagonist candesartan cilexetil, (1 nmol in 100 nl), into the RVLM of the spontaneously hypertensive rat induced a significant decrease in lumbar sympathetic nerve discharge (-18±2%) and BP (140±6 to 115±6 mmHg). In contrast, similar microinjections in the Wistar-Kyoto (WKY) rat had no effect on BP or sympathetic nerve discharge. These results are interpreted to suggest that Ang II inputs to the RVLM are activated in the spontaneously hypertensive rat to maintain an elevated level of sympathetic nerve discharge, even in the face of increased BP.

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