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.

Effects of spinal cord transection on sympathetic discharge in decerebrate-unanesthetized cats

1989 ◽  
Vol 257 (6) ◽  
pp. R1506-R1511 ◽  
Author(s):  
L. C. Weaver ◽  
R. D. Stein
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Spectral Analysis ◽  
Spinal Cord Transection ◽  
Renal Nerves ◽  
Frequency Range ◽  
Renal Nerve ◽  
Sympathetic Discharge ◽  
Nerve Discharge

Previous experiments in our laboratory have shown that discharge of splenic, mesenteric, and splanchnic nerves is well maintained after spinal cord transection in chloralose-anesthetized cats (8, 9, 11). The primary purpose of this investigation was to determine if maintained sympathetic discharge could be observed after spinal transection in the absence of chloralose anesthesia. In cats anesthetized with alphaxalone-alphadolone, changes in splanchnic discharge, blood pressure, and heart rate caused by decerebration and removal of the forebrain were observed. This procedure decreased blood pressure, increased heart rate, and had no immediate effect on sympathetic discharge or its rhythm (assessed by power density spectral analysis). One hour after decerebration and termination of anesthesia, splanchnic discharge had increased by approximately 36%. Next, effects of spinal cord transection on discharge of splanchnic, mesenteric, and renal nerves were observed in the decerebrate-unanesthetized cats. Splanchnic discharge decreased by 50%, mesenteric nerve discharge was unchanged, and renal nerve discharge decreased by 97%. Therefore, splanchnic nerve discharge was not as well maintained in decerebrate-unanesthetized cats as it had been in chloralose-anesthetized animals, and the remaining splanchnic discharge appeared to affect mesenteric nerves preferentially. Finally, spectral analysis of the splanchnic discharge demonstrated that before cord transection, most of the signal was in the 0- to 6-Hz frequency range, whereas after transection the proportion of signal in this frequency range was significantly reduced and the proportion in higher frequencies (7-25 Hz) was significantly increased. This loss of low-frequency rhythmicity is consistent with findings in our previous studies in chloralose-anesthetized cats.

scholarly journals On the effects of joining the cervical sympathetic nerve with the chorda tympani.

1904 ◽  
Vol 73 (488-496) ◽  
pp. 99-99
Author(s):  
John Newport Langley ◽  
Hugh Kerr Anderson
Keyword(s):  
Peripheral Nerve ◽  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Sympathetic Nerve ◽  
Nerve Cells ◽  
The Other ◽  
Chorda Tympani ◽  
Cervical Ganglion ◽  
Cervical Sympathetic ◽  
Cervical Sympathetic Nerve

It is well known that the cervical sympathetic nerve and the chorda tympani have opposite actions upon the blood-vessels of the sub-maxillary gland, the former causing contraction of the vessels, and the latter, dilatation. Evidence has been given by one of us that the chorda tympani if united with the cervical sympathetic, can in time make connection with the nerve cells of the superior cervical ganglion and become in part vaso-constrictor fibres. Our experiments have been directed to determine whether the cervical sympathetic if allowed an opportunity of becoming connected with the peripheral nerve cells in the course of the chorda tympani will in part change their function from vaso-constrictor to vaso-dilator. Two experiments were made on anæsthetised cats, both give similar results, but one was much more conclusive on the point at issue than the other, and here we shall speak of that only. The superior cervical ganglion was excised and the central end of the cervical sympathetic nerve was joined to the peripheral end of the lingual, which contains the chorda tympani fibres. After allowing time for union and regeneration of the nerves, the cervical sympathetic was stimulated; it caused prompt flushing of the sub-maxillary glands, and the effect was repeatedly obtained.

Late Discharges in Dog's Sympathetic Ganglia

1972 ◽  
Vol 50 (3) ◽  
pp. 263-269 ◽  
Author(s):  
S. S. Chen
Keyword(s):  
Superior Cervical Ganglion ◽  
Stimulus Frequency ◽  
Sympathetic Ganglia ◽  
Late Response ◽  
Before And After ◽  
Cervical Ganglion ◽  
High Stimulus ◽  
Time Courses ◽  
Preganglionic Stimulation ◽  
Muscarinic And Nicotinic Receptors

In the dog a preganglionic stimulation at a high stimulus frequency for 10–15 s elicited a two-wave response, early and late responses in the perfused ear (vasoconstriction), as well as early and late contractions in the nictitating membrane. Both the late contraction and the late response could be aborted by cooling the superior cervical ganglion, and restored by rewarming the ganglion. Both were resistant to atropine and hexamethonium combined. Their magnitude depended upon the duration of stimulation and upon the stimulus frequency used. Their time courses were similar both before and after hexamethonium or chilling. Therefore, it is concluded that they are manifestations of late discharges in the superior cervical ganglion, which are independent of both muscarinic and nicotinic receptors in the ganglion. A similar but less prominent phenomenon was demonstrated in the lumbosacral sympathetic ganglion of the dog by studying the responses of the retractor penis muscle and the perfused hind limb to preganglionic stimulation.

Diencephalic regions contributing to sympathetic nerve discharge in anesthetized cats

1988 ◽  
Vol 254 (2) ◽  
pp. R249-R256 ◽  
Author(s):  
Z. S. Huang ◽  
K. J. Varner ◽  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Medial Forebrain Bundle ◽  
Significant Component ◽  
Medial Thalamus ◽  
Dependent Component ◽  
Medial Hypothalamus ◽  
Alpha Chloralose ◽  
Frequency Current ◽  
Nerve Discharge

We reported that the forebrain is responsible for a significant component (38%) of inferior cardiac postganglionic sympathetic nerve discharge (SND) in baroreceptor-denervated cats anesthetized with alpha-chloralose [Huang et al., Am. J. Physiol. 252 (Regulatory Integrative Comp. Physiol. 21): R645-R652, 1987]. The current study was initiated to assess the contribution of various diencephalic regions to the forebrain-dependent component of SND in this preparation. For this purpose, the reductions in inferior cardiac SND and blood pressure produced acutely by midbrain transection at stereotaxic plane A3 in nonlesioned control cats were compared with those in cats in which diencephalic lesions were made with radio-frequency current. Lesions of the anterior medial hypothalamus including the paraventricular nucleus failed to attenuate the decreases in SND and blood pressure produced by midbrain transection. In contrast, the effects of midbrain transection were significantly attenuated by lesions of the lateral hypothalamus (including medial forebrain bundle), posterior medial hypothalamus, or the medial thalamus. We conclude that both the hypothalamus and medial thalamus contribute to SND in anesthetized cats.

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.

scholarly journals VII. On the progressive paralysis of the different classes of nerve cells in the superior cervical ganglion

1890 ◽  
Vol 47 (286-291) ◽  
pp. 379-390 ◽  
Keyword(s):  
Superior Cervical Ganglion ◽  
Sympathetic Nerve ◽  
Nerve Cells ◽  
Optic Axis ◽  
Nictitating Membrane ◽  
Cervical Ganglion

It is well known that by stimulating the sympathetic nerve in the neck the following effects can be produced :—(1) Retraction of the nictitating membrane; (2) protrusion of the eyeball and opening of the eye; (3) turning the eye, if previous to stimulation the optic axis is directed nasally, so that the optic axis is directed straight forwards, or it may be forwards and a little outwards

Central respiratory modulation of medullary sympathoexcitatory neurons in rat

1989 ◽  
Vol 256 (3) ◽  
pp. R739-R750 ◽  
Author(s):  
J. R. Haselton ◽  
P. G. Guyenet
Keyword(s):  
Sympathetic Nerve ◽  
Vasomotor Tone ◽  
Unit Recording ◽  
Large Peak ◽  
Respiratory Modulation ◽  
Comparison Of The Results ◽  
Sympathetic Vasomotor Tone ◽  
Sympathetic Discharge ◽  
Respiratory Generator ◽  
Nerve Discharge

The central respiratory generator exerts a modulatory influence on sympathetic nerve discharge. In cats the sympathoexcitatory neurons of the rostroventrolateral medulla (RVL) exhibit central respiratory modulation as well. Because RVL sympathoexcitatory neurons are largely responsible for the maintenance of sympathetic vasomotor tone, it is likely that the modulation of these neurons accounts for the central respiratory modulation of sympathetic discharge. In the present study experiments were performed to characterize the pattern of respiratory modulation of lumbar sympathetic nerve discharge (LSND) in the halothane-anesthetized rat. Phrenic-triggered averaging of LSND exhibited a small depression coincident with the onset of the phrenic burst followed by a large peak that was coincident with the cessation of the phrenic burst. Phrenic-triggered histograms of the activity of RVL sympathoexcitatory neurons exhibited three patterns of central respiratory modulation: inspiratory depression (I), inspiratory peak (II), and early inspiratory depression followed by a postinspiratory peak (III), a pattern that was very similar to that seen in LSND. Both nerve recording and single-unit recording experiments were performed in vagotomized rats with or without intact barosensory afferents. A comparison of the results suggested that, in the rat, the baroreflex does not modify or contribute to the central respiratory modulation of sympathetic output. Finally, a comparison was made between presumed nonadrenergic pacemaker-like neurons and putative C1 adrenergic neurons in the RVL. No differences were found in the patterns of central respiratory modulation.

Sites of action of ghrelin receptor ligands in cardiovascular control

2012 ◽  
Vol 303 (8) ◽  
pp. H1011-H1021 ◽  
Author(s):  
Brid Callaghan ◽  
Billie Hunne ◽  
Haruko Hirayama ◽  
Daniela M. Sartor ◽  
Trung V. Nguyen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Ganglia ◽  
Mesenteric Arteries ◽  
Rt Pcr ◽  
Growth Hormone Secretagogue Receptor ◽  
Nerve Activity ◽  
Growth Hormone Secretagogue

Circulating ghrelin reduces blood pressure, but the mechanism for this action is unknown. This study investigated whether ghrelin has direct vasodilator effects mediated through the growth hormone secretagogue receptor 1a (GHSR1a) and whether ghrelin reduces sympathetic nerve activity. Mice expressing enhanced green fluorescent protein under control of the promoter for growth hormone secretagogue receptor (GHSR) and RT-PCR were used to locate sites of receptor expression. Effects of ghrelin and the nonpeptide GHSR1a agonist capromorelin on rat arteries and on transmission in sympathetic ganglia were measured in vitro. In addition, rat blood pressure and sympathetic nerve activity responses to ghrelin were determined in vivo. In reporter mice, expression of GHSR was revealed at sites where it has been previously demonstrated (hypothalamic neurons, renal tubules, sympathetic preganglionic neurons) but not in any artery studied, including mesenteric, cerebral, and coronary arteries. In rat, RT-PCR detected GHSR1a mRNA expression in spinal cord and kidney but not in the aorta or in mesenteric arteries. Moreover, the aorta and mesenteric arteries from rats were not dilated by ghrelin or capromorelin at concentrations >100 times their EC50 determined in cells transfected with human or rat GHSR1a. These agonists did not affect transmission from preganglionic sympathetic neurons that express GHSR1a. Intravenous application of ghrelin lowered blood pressure and decreased splanchnic nerve activity. It is concluded that the blood pressure reduction to ghrelin occurs concomitantly with a decrease in sympathetic nerve activity and is not caused by direct actions on blood vessels or by inhibition of transmission in sympathetic ganglia.

Sign in / Sign up

Export Citation Format

Share Document