Cardiac Sympathetic Nerves in Rats: Anatomical and Functional Features

Yasunaga, K; Nosaka, Shoichiro

doi:10.2170/jjphysiol.29.691

Cited by 18 publications

(7 citation statements)

References 29 publications

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“…It is noteworthy that the time course of heart rate response to IOR/R stimulation was longer than that of cardiac sympathetic nerve activity. This finding was supported by the report of Yasunaga and Nosaka (1979) [9] that an electrical stimulation of the cardiac sympathetic nerve produced a tachycardiac response that continued long after stimulation.…”

Section: Discussionsupporting

confidence: 64%

“…Furthermore, heart rate response was also much larger when the stimulus was delivered to the right elbow joint, as opposed to left, in spinalized rats. A laterality of the heart rate response to noxious cutaneous stimulation in spinalized rats has previously been reported by Kimura et al (1995) [5], and this phenomenon was suggested to be a reflection of the influence of cardiac sympathetic nerves on the right side of the heart, particularly those that innervate the sinus node [7][8][9][10] (Fig. 9).…”

Section: Discussionsupporting

confidence: 54%

“…Nerve dissection and recording of cardiac sympathetic nerve activity. Since the influence of the right cardiac sympathetic nerve on sinus rhythm is greater than that of the left cardiac sympathetic nerve [7][8][9][10], we made our recordings from the right nerve (N = 4). With the rats in a prone position, the cardiac sympathetic nerves were visualized after the removal of the right second costal bone.…”

Section: Experiments Were Performed On 3-5 Month Old Malementioning

confidence: 99%

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The Articulo-Cardiac Sympathetic Reflex in Spinalized, Anesthetized Rats

Nakayama¹,

Suzuki²,

Ito³

2006

J. Physiol. Sci

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Somatic afferent regulation of heart rate by noxious knee joint stimulation has been proven in anesthetized cats to be a reflex response whose reflex center is in the brain and whose efferent arc is a cardiac sympathetic nerve. In the present study we examined whether articular stimulation could influence heart rate by this efferent sympathetic pathway in spinalized rats. In central nervous system (CNS)-intact rats, noxious articular movement of either the knee or elbow joint resulted in an increase in cardiac sympathetic nerve activity and heart rate. However, although in acutely spinalized rats a noxious movement of the elbow joint resulted in a significant increase in cardiac sympathetic nerve activity and heart rate, a noxious movement of the knee joint had no such effect and resulted in only a marginal increase in heart rate. Because this marginal increase was abolished by adrenalectomy suggests that it was due to the release of adrenal catecholamines. In conclusion, the spinal cord appears to be capable of mediating, by way of cardiac sympathetic nerves, the propriospinally induced reflex increase in heart rate that follows noxious stimulation of the elbow joint, but not the knee joint.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionsupporting

confidence: 54%

Section: Experiments Were Performed On 3-5 Month Old Malementioning

confidence: 99%

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The Articulo-Cardiac Sympathetic Reflex in Spinalized, Anesthetized Rats

Nakayama¹,

Suzuki²,

Ito³

2006

J. Physiol. Sci

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“…Electrical stimulation of the cardiac sympathetic nerve is shown here in the mouse to increase HR, as shown previously in the other species (Liddell & Sherrington, 1929; Yasunaga & Nosaka, 1979). Following a period of sympathetic stimulation in the mouse, there is a prolonged attenuation of subsequent cardiac vagal activity.…”

Section: Discussionsupporting

confidence: 87%

Galanin and neuropeptide Y reduce cholinergic transmission in the heart of the anaesthetised mouse

Smith-White

Iismaa

Potter

2003

British J Pharmacology

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1 This study investigated the effects of galanin (GAL) on inhibition of cholinergic (vagal) activity in the mouse heart using control galanin knockout (GAL-KO) and GAL-1R receptor knockout (GAL-1R-KO) mice. 2 In pentobarbitone anaesthetised mice, supramaximal stimulation every 30 s of the vagus nerve innervating the heart, increased pulse interval (PI) by approximately 50 ms or decreased heart rate by approximately 100 beats min À1. This response was attenuated by intravenous administration of GAL (dose ranged from 0.8 to 13 nmol kg À1 ) in a dose-dependent manner. 3 In GAL-KO mice, the magnitude of inhibition of the increase in PI (DPI) following a bolus dose of GAL was not different from the DPI in control mice, and neuropeptide Y (NPY), previously shown to attenuate vagal inhibitory activity in mice, evoked a comparative inhibition of DPI in GAL-KO mice. 4 In GAL-1R-KO mice, an intravenous, bolus injection of GAL had no inhibitory effect on vagal activity. 5 In control mice, stimulation of the sympathetic nerve at 25 V, 10 Hz for 2 min in the presence of propranolol evoked a long-lasting attenuation of DPI. The inhibitory effect on DPI was reduced in the presence of the NPY Y 2 antagonist, BIIE0246. 6 In GAL-1R-KO mice, stimulation of the sympathetic nerve in the presence of propranolol evoked an attenuation of DPI not significantly different from the response in control mice in the presence of BIIE0246. Following administration of BIIE0246 in GAL-1R-KO mice, the inhibition of DPI that followed stimulation of the sympathetic nerve was abolished. 7 These findings support the view that the nerve terminals of parasympathetic neurons in the mouse heart possess both GAL-1R and NPY Y 2 receptors which, when activated, reduce acetylcholine release.

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“…Since the influence of the right cardiac sympathetic nerve on sinus rhythm is greater than that of the left cardiac sympathetic nerve [10], recordings were made from the right nerve. With the rats in a prone position, the cardiac sympathetic nerves were dissected free following the removal of the second costal bone, as described previously [11,12], and their neuronal activity was amplified using a preamplifier (time constant 0.01 s; S-0476, Nihon Kohden, Tokyo) and sampled using an analog-to-digital converter (PowerLab/8, AD Instruments, Australia) at a rate of 2,000 samples/s that was rectified and integrated every 5 s. The signal recorded at the end of the experiment (after the rat had died) was set as the background noise.…”

Section: Methodsmentioning

confidence: 99%

Reflex Inhibition of Heart Rate and Efferent Cardiac Sympathetic Outflow Induced by Colorectal Distension in Anesthetized Rats

Suzuki²

2006

J. Physiol. Sci

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Colorectal distensions of 60 and 80 mmHg significantly reduced heart rate (HR) and cardiac sympathetic nerve activity in anesthetized rats. This bradycardiac response was not influenced by the intravenous administration of atropine, but was abolished by propranolol, suggesting that it was elicited by sympathetic but not vagal efferent nerves.Key words: colorectal distension, heart rate, cardiac sympathetic nerve activity.It has been reported that cardiovascular function is reflexively regulated by visceral noxious stimulation, such as distension of stomach [1], colorectum [2], biliary system [3], and uterus [4], in anesthetized animals. Our recent study demonstrated that a noxious range of colorectal distension (CRD) produced a reflexive decrease in blood pressure in anesthetized central nervous system (CNS)-intact rats via a reflexive inhibition of sympathetic vasoconstrictor nerve (renal sympathetic nerve) activity [5]. The decrease response of blood pressure induced by CRD in CNS-intact rats was reversed to increase response by spinalization at the 2nd cervical level (C2). Thus it was suggested that the reflex center of the CRD-induced inhibitory reflex modulation of blood pressure was at supraspinal levels in CNS-intact rats. There was also CRD-induced excitatory reflex modulation of blood pressure at the propriospinal levels, though the excitatory reflex was inhibited by the supraspinal structure in CNS-intact preparation [5].During these experiments on the blood pressure, we had observed that CRD produced bradycardia in association with a decrease in blood pressure in CNS-intact rats. It is well known that bradycardia is induced by visceral manipulation during surgery in human [6,7]. And these responses have been considered as a reflex response whose efferent is the cardiac vagus nerve. Using anesthetized rats, Grundy and Davison [8] suggested that the efferent path of bradycardia to a distension of the stomach was the cardiac vagus nerve. On the other hand, Robbins and Sato [4] reported that bradycardic responses to a distension of the uterus was not influenced by a bilateral vagotomy in anesthetized rats and suggested a contribution of the cardiac sympathetic nerve. It is interesting to learn the efferent paths and the reflex center of bradycardia induced by CRD.It has been reported that the cardiovascular response to CRD stimulation in anesthetized rats was unstable and fluctuated based on the depth of anesthesia [2]. Our previous study developed an anesthetized rat model of stable depressor response induced by CRD [5]. Using this rat model in the present study, we aimed to clarify the involvement of the cardiac sympathetic and parasympathetic nerves as efferent paths in the CRD-induced reflexive bradycardia. We also examined this reflex in spinalized rats to determine whether its reflex center was in the brain and/or the spinal cord. MethodsAdult male Wistar rats weighing 330-380 g (n = 16) were housed in a climate-controlled environment with food and water ad libitum. All animal experiments ...

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Cardiac Sympathetic Nerves in Rats: Anatomical and Functional Features

Cited by 18 publications

References 29 publications

The Articulo-Cardiac Sympathetic Reflex in Spinalized, Anesthetized Rats

The Articulo-Cardiac Sympathetic Reflex in Spinalized, Anesthetized Rats

Galanin and neuropeptide Y reduce cholinergic transmission in the heart of the anaesthetised mouse

Reflex Inhibition of Heart Rate and Efferent Cardiac Sympathetic Outflow Induced by Colorectal Distension in Anesthetized Rats

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