A1 noradrenergic neurons tonically inhibit sympathoexcitatory neurons of C1 area in rat brainstem

Granata, Antonio; Numao, Yoshinobu; Kumada, Mamoru; Reis, Donald J.

doi:10.1016/0006-8993(86)91198-4

Cited by 138 publications

(37 citation statements)

References 42 publications

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“…More likely, the physiological responses could result from influences of the pressor region on relay nuclei such as the caudal ventrolateral medulla or the rostral ventrolateral GLYCINE AND THE DORSAL VAGAL NVCLEUS/Talman 667 medulla. The latter may be a tonic vasomotor center, 12 while the former is a depressor zone that may effect cardiovascular changes through both sympathetic 13 and humoral mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Glycine microinjected in the rat dorsal vagal nucleus increases arterial pressure.

Talman

1988

Hypertension

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SUMMARY Microinjections (25 nl) of glycine into the dorsal motor nucleus of the vagus in 21 rats elicited dose-dependent increases of arterial pressure and heart rate that were not seen with injections adjacent to the dorsal motor nucleus of the vagus. The responses to glycine were neurally mediated and could be blocked either by local pretreatment with strychnine or by combined vagotomy and ganglionic blockade. The data suggest that glycine receptors on, or in the region of, neurons of the dorsal motor nucleus of the vagus may have a role in the regulation of arterial pressure and heart rate. glycinergic mechanisms in the dorsal vagal complex has received little attention. We have previously shown 1 that glycine microinjected into the cardiovascular portion of the nucleus tractus solitarii (NTS) elicited hypotension and bradycardia. Microinjections ventral to that nucleus produced pressor responses and tachycardia. Others 2 have demonstrated pressor and tachycardic responses when glycine was injected into the dorsal vagal complex. In this study we sought to determine the cardiovascular effects of the microinjection of glycine into the dorsal motor nucleus of the vagus (DMV) and ventral-most portions of the NTS. Materials and MethodsTwenty-one adult male Sprague-Dawley rats (Biolabs, St. Paul, MN, USA) were anesthetized with halothane (1.5%) delivered in 100% oxygen through a nasal mask. The animals were instrumented with femoral venous and arterial cannulas for intravenous delivery of drugs and for recording of intra-arterial pressure, respectively. Arterial pressure (AP), mean arterial pressure (MAP), and heart rate (HR), calculated by a tachygraph from the arterial pulse wave, were displayed on channels of a polygraph (Model 7, Grass,

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Section: Discussionmentioning

confidence: 99%

Glycine microinjected in the rat dorsal vagal nucleus increases arterial pressure.

Talman

1988

Hypertension

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Section: Caudal Ventrolateral Medullamentioning

confidence: 99%

“…32,34 Cardiovascular responses to lesion or stimulation of the CVLM are mediated through RVLM neurons. 35 Both anatomical and functional data suggest that CVLM neurons inhibit sympathoexcitatory neurons in the RVLM.Retrograde tracing studies indicate that the CVLM contains cells that project to the RVLM. 36 These neurons form symmetric (inhibitory) synapses with adrenergic and nonadrenergic neurons in the RVLM.…”

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confidence: 99%

Role of the Medulla Oblongata in Hypertension

et al. 2001

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Abstract-Brain pathways controlling arterial pressure are distributed throughout the neuraxis and are organized in topographically selective networks. In this brief review, we will focus on the medulla oblongata. The nucleus tractus solitarius (NTS) is the primary site of cardiorespiratory reflex integration. It is well accepted that lesions or other perturbations in the NTS can result in elevations of arterial pressure (AP), with many of the associated features so commonly found in humans. However, recent studies have shown 2 distinct subpopulations of neurons within the NTS that can influence AP in opposite ways. Commissural NTS neurons located on the midline may contribute to maintenance of hypertension in spontaneously hypertensive rats (SHR), because small lesions in this area result in a very significant reduction in AP. Also involved in this blood pressure regulation network are 2 distinct regions of the ventrolateral medulla: caudal (CVLM) and rostral (RVLM). Neurons in CVLM are thought to receive baroreceptor input and to relay rostrally to control the activity of the RVLM. Projections from CVLM to RVLM are inhibitory, and a lack of their activity may contribute to development of hypertension. The RVLM is critical to the tonic and reflexive regulation of AP. In different experimental models of hypertension, RVLM neurons receive significantly more excitatory inputs. This results in enhanced sympathetic neuronal activity, which is essential for the development and maintenance of the hypertension. Key Words: brain Ⅲ chemoreceptors Ⅲ homeostasis Ⅲ hypertension, experimental Ⅲ sympathetic nervous system Ⅲ nitric oxide Ⅲ angiotensin Ⅲ sympathectomy E ssential hypertension is one of the most common disorders affecting human health. That the sympathetic nervous system participates in control of arterial pressure is indisputable; the controversy regards its role in the pathogenesis of human hypertension. Over the past decade, there has been an increasing awareness that the central nervous system (CNS) has a critical role in the development and maintenance of elevated arterial pressure. Presently, it seems clear that in both clinical and experimental hypertension, an increased vascular resistance to flow is an essential ingredient of the disorder. We could say, narrowing down the problem, that the disagreement rests on the answer to a simple question: which comes first, the neural or the humoral factor? Certainly this controversy is not going to finish here, but our purpose is to show how recent experimental data have put a re-emphasis on the neural factor and, by consequence, on the sympathetic nervous system, in particular the medulla oblongata.Re-emphasis is indeed the correct word, because in the 1930s the treatment for serious hypertension was mainly surgical, not clinical, and the approach was interruption of the splanchnic nerves. By the beginning of the 1940s, 2 approaches had been developed to remove the sympathetic chain, one by Keith Grimson 1 and another, less radical, by Reginald Smithwick. 2 These s...

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“…Transection of the cervical spinal cord in the cat causes a profound fall in blood pressure that can be attributed to a reduction in the basal level of activity in sympathetic nerves (Alexander, 1946;Ardell, Barman & Gebber, 1982). Similarly, destruction of neurones in the RVLM or inhibition of their activity produces large decreases in blood pressure, heart rate and sympathetic nerve discharge (Pilowsky, West & Chalmers, 1985;Dean & Coote, 1986; Granata, Numao, Kumada & Reis, 1986;Willette, Punnen-Grandy, Krieger & Sapru, 1987). However, MS 8255 the contribution of this area to cardiovascular control is not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Selective control of sympathetic pathways to the kidney, spleen and intestine by the ventrolateral medulla in rats.

Hayes

Weaver

1990

The Journal of Physiology

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SUMMARY1. Electrical activity of multifibre renal, splenic, mesenteric and greater splanchnic nerves and 13th thoracic white rami was recorded in artificially respired, urethaneanaesthetized rats. Discharge of neurones in the rostral ventrolateral medulla was blocked by unilateral microinjections of the inhibitory amino acid glycine and effects on the electrical activity of these sympathetic nerves were compared.2. Blockade of the rostral ventrolateral medulla caused greater decreases in discharge of renal than splenic nerves and had no consistent effect on mesenteric nerves. This blockade also decreased the discharge of the preganglionic white rami more than that of the preganglionic splanchnic nerves.3. Postganglionic responses to rostral ventrolateral medulla blockade were always greater than preganglionic responses.4. The arterial pressure and renal nerve responses to rostral ventrolateral medulla blockade in urethane-anaesthetized rats were not different from those in rats anaesthetized with a-chloralose.5. These findings demonstrate that pre-and postganglionic sympathetic pathways to the kidney are more dependent upon excitatory drive from the rostral ventrolateral medulla than pathways directed to the spleen and intestine.

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A1 noradrenergic neurons tonically inhibit sympathoexcitatory neurons of C1 area in rat brainstem

Cited by 138 publications

References 42 publications

Glycine microinjected in the rat dorsal vagal nucleus increases arterial pressure.

Glycine microinjected in the rat dorsal vagal nucleus increases arterial pressure.

Role of the Medulla Oblongata in Hypertension

Selective control of sympathetic pathways to the kidney, spleen and intestine by the ventrolateral medulla in rats.

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