Hypertension alters GABA receptor-mediated inhibition of neurons in the nucleus of the solitary tract

Previous studies have demonstrated that microinjection of baclofen, a GABAB receptor agonist, into the nucleus of the solitary tract (NTS) results in an enhanced pressor response in hypertensive (HT) rats compared with normotensive (NT) rats, suggesting a possible alteration in the responses of neurons in this area to activation of GABAB receptors. The following studies were designed to determine whether HT alters the sensitivity of neurons in the NTS to GABA receptor agonists. Sham-operated NT and unilateral nephrectomized, renal-wrap HT Sprague-Dawley rats were anesthetized, and the responses of NTS neurons receiving aortic nerve (AN) afferent inputs to iontophoretic application of GABA, the GABAA receptor agonist muscimol, and the GABAB agonist baclofen were examined. The AN input was classified as monosynaptic (MSN) if the cell responded to each of two stimuli separated by 5 ms with an action potential. If the cell did not respond, the input was considered polysynaptic (PSN). In MSNs, inhibition of AN-evoked discharge by GABA was not altered in 1 wk of HT but was reduced in 4 wk of HT, whereas in PSNs, sensitivity to GABA was reduced at 1 and 4 wk of HT. In HT rats, inhibition of AN-evoked discharge by baclofen was enhanced in MSNs, but not in PSNs, after 1 and 4 wk of HT, whereas inhibition by muscimol was reduced in MSNs and PSNs at 1 and 4 wk of HT. Changes in sensitivity to muscimol and baclofen within MSNs were the same whether the MSN received a slowly or a rapidly conducted AN afferent input. The results demonstrate that early in HT the sensitivity of NTS neurons to inhibitory amino acids is altered and that these changes are maintained for ≥4 wk. The alterations are dependent on the subtype of GABA receptor being activated and whether the neuron receives a mono- or polysynaptic baroreceptor afferent input.

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Effect of electroacupuncture on pressor reflex during gastric distension

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00192.2002 ◽

2002 ◽

Vol 283 (6) ◽

pp. R1335-R1345 ◽

Cited By ~ 48

Author(s):

Peng Li ◽

Kasra Rowshan ◽

Melissa Crisostomo ◽

Stephanie C. Tjen-A-Looi ◽

John C. Longhurst

Keyword(s):

Peroneal Nerve ◽

Cardiovascular Response ◽

Pressor Response ◽

Gastric Wall ◽

Ventrolateral Medulla ◽

Gastric Distension ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Stomach Meridian ◽

Pressor Reflex

The effect of electroacupuncture (EA) on the reflex cardiovascular response induced by mechanical distension of the stomach was studied in ventilated male Sprague-Dawley rats anesthetized by ketamine and α-chloralose. Repeated balloon inflation of the stomach to produce 20 mmHg tension on the gastric wall induced a consistent rise in mean arterial pressure, while heart rate (372 ± 22 beats/min) was unchanged. This response was reversed by transection of the splanchnic nerves. Bilateral application of EA (1–2 mA, 2 Hz) at Neiguan-Jianshi acupoints (pericardial meridian, Pe 5–6) over the median nerve for 30 min significantly decreased the pressor response from 33 ± 6 to 18 ± 4 mmHg ( n = 7, P < 0.05). This effect began after 10 min of EA and continued for 40 min after termination of EA. EA at Zusanli-Shangquxu acupoints (stomach meridian, St 36–37) over the deep peroneal nerve similarly inhibited the pressor response. The effect lasted for 10 min after EA was stopped ( n = 6, P < 0.05), while EA at Guangming-Xuanzhong acupoints (gallbladder meridian, GB 37–39) over the superficial peroneal nerve did not inhibit the pressor response. Naloxone injected intravenously ( n = 6) immediately after termination of EA or administered by microinjection into the rostral ventrolateral medulla (rVLM) 25 min after initiation of EA ( n = 6) reversed the inhibition by EA, suggesting an opiate mechanism, including the rVLM, was involved.

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Baroreflex sensitivity is impaired in Sprague‐Dawley rats with spontaneous hydronephrosis independent of angiotensin II actions in the solitary tract nucleus

The FASEB Journal ◽

10.1096/fasebj.23.1_supplement.957.8 ◽

2009 ◽

Vol 23 (S1) ◽

Author(s):

Amy C Arnold ◽

Debra I Diz

Keyword(s):

Angiotensin Ii ◽

Baroreflex Sensitivity ◽

Solitary Tract Nucleus ◽

Solitary Tract ◽

Sprague Dawley ◽

Sprague Dawley Rats

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Regional effect of naltrexone in the nucleus of the solitary tract in blockade of NPY-induced feeding

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2000.278.2.r499 ◽

2000 ◽

Vol 278 (2) ◽

pp. R499-R503 ◽

Cited By ~ 29

Author(s):

C. M. Kotz ◽

M. J. Glass ◽

A. S. Levine ◽

C. J. Billington

Keyword(s):

Cerebrospinal Fluid ◽

Food Intake ◽

Paraventricular Nucleus ◽

Opioid Receptors ◽

The Other ◽

Solitary Tract ◽

Sprague Dawley ◽

Regional Effect ◽

Sprague Dawley Rats ◽

Artificial Cerebrospinal Fluid

Naltrexone (NLTX) in the nucleus of the solitary tract (NTS) decreases feeding induced by neuropeptide Y (NPY) in the paraventricular nucleus (PVN). We sought to determine the NTS region most sensitive to NLTX blockade of PVN NPY-induced feeding. Male Sprague-Dawley rats were fitted with two cannulas; one in the PVN and one in a hindbrain region: caudal, medial, or rostral NTS or 1 mm outside the NTS. Animals received NLTX (0, 1, 3, 10, and 30 μg in 0.3 μl) into the hindbrain region just prior to PVN NPY (0.5 μg, 0.3 μl) or artificial cerebrospinal fluid (0.3 μl). Food intake was measured at 2 h following injection. PVN NPY stimulated feeding, and NLTX in the medial NTS significantly decreased NPY-induced feeding at 2 h, whereas administration of NLTX in the other hindbrain regions did not significantly influence PVN NPY induced feeding. These data suggest that opioid receptors in the medial NTS are most responsive to feeding signals originating in the PVN after NPY stimulation.

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Loss of hypoxic pulmonary vasoconstriction in chronic pneumonia is not mediated by nitric oxide

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.265.5.h1523 ◽

1993 ◽

Vol 265 (5) ◽

pp. H1523-H1528 ◽

Cited By ~ 4

Author(s):

D. G. McCormack ◽

N. A. Paterson

Keyword(s):

Nitric Oxide ◽

Pressor Response ◽

Hypoxic Pulmonary Vasoconstriction ◽

Sprague Dawley ◽

Absolute Increase ◽

Pulmonary Vasoconstriction ◽

Sprague Dawley Rats ◽

Before And After ◽

Inflammatory Processes ◽

The Difference

In pulmonary inflammatory processes such as pneumonia there is diminished hypoxic pulmonary vasoconstriction (HPV). We investigated whether the attenuated HPV in pneumonia is a due to excess nitric oxide (NO) release. Sprague-Dawley rats were anesthetized, and a slurry (0.06 ml) of infected agar beads (containing 6 x 10(5) Pseudomonas aeruginosa organisms) or control (sterile) beads was then injected into a distal bronchus through a tracheotomy. After the establishment of a chronic P. aeruginosa pneumonia (7-10 days later) animals were instrumented for hemodynamic monitoring, and the response to exposure to hypoxic gas (fraction of inspired O2 = 0.08) was recorded before and after the administration of NG-monomethyl-L-arginine (L-NMMA; 50 mg/kg), an inhibitor of NO synthesis. The hypoxic pressor response, as assessed by the absolute increase in pulmonary arterial pressure (PAP) and total pulmonary resistance (TPR), was reduced in infected animals compared with control animals. The change in PAP and TPR was 8.5 +/- 0.7 and 0.053 +/- 0.007, respectively, in control animals compared with 5.9 +/- 0.5 and 0.041 +/- 0.011 in infected animals. After L-NMMA the increase in PAP and TPR during hypoxia was greater in both control and infected animals. However, treatment with L-NMMA did not affect the difference between control and infected animals. We conclude that excess release of NO does not account for the attenuated hypoxic pressor response in pneumonia.

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Convulsant activity of a non-peptidic δ-opioid receptor agonist is not required for its antidepressant-like effects in Sprague-Dawley rats

Psychopharmacology ◽

10.1007/s00213-002-1179-y ◽

2002 ◽

Vol 164 (1) ◽

pp. 42-48 ◽

Cited By ~ 68

Author(s):

Daniel Broom ◽

Emily Jutkiewicz ◽

John Folk ◽

John Traynor ◽

Kenner Rice ◽

...

Keyword(s):

Opioid Receptor ◽

Receptor Agonist ◽

Sprague Dawley ◽

Opioid Receptor Agonist ◽

Sprague Dawley Rats ◽

Δ Opioid Receptor

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Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01149.2003 ◽

2005 ◽

Vol 288 (1) ◽

pp. H256-H262 ◽

Cited By ~ 40

Author(s):

Ana Carolina Rodrigues Dias ◽

Melissa Vitela ◽

Eduardo Colombari ◽

Steven W. Mifflin

Keyword(s):

Nitric Oxide ◽

Solitary Tract ◽

Glutamatergic Transmission ◽

Sprague Dawley ◽

Renal Sympathetic Nerve Activity ◽

Sprague Dawley Rats ◽

Before And After ◽

Nos Inhibitor ◽

The Right ◽

Oxide Synthase

The neuromodulatory effect of NO on glutamatergic transmission has been studied in several brain areas. Our previous single-cell studies suggested that NO facilitates glutamatergic transmission in the nucleus of the solitary tract (NTS). In this study, we examined the effect of the nitric oxide synthase (NOS) inhibitor NG-nitro-l-arginine methyl ester (l-NAME) on glutamatergic and reflex transmission in the NTS. We measured mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) from Inactin-anesthetized Sprague-Dawley rats. Bilateral microinjections of l-NAME (10 nmol/100 nl) into the NTS did not cause significant changes in basal MAP, HR, or RSNA. Unilateral microinjection of ( RS)-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA, 1 pmol/100 nl) into the NTS decreased MAP and RSNA. Fifteen minutes after l-NAME microinjections, AMPA-evoked cardiovascular changes were significantly reduced. N-methyl-d-aspartate (NMDA, 0.5 pmol/100 nl) microinjection into the NTS decreased MAP, HR, and RSNA. NMDA-evoked falls in MAP, HR, and RSNA were significantly reduced 30 min after l-NAME. To examine baroreceptor and cardiopulmonary reflex function, l-NAME was microinjected at multiple sites within the rostro-caudal extent of the NTS. Baroreflex function was tested with phenylephrine (PE, 25 μg iv) before and after l-NAME. Five minutes after l-NAME the decrease in RSNA caused by PE was significantly reduced. To examine cardiopulmonary reflex function, phenylbiguanide (PBG, 8 μg/kg) was injected into the right atrium. PBG-evoked hypotension, bradycardia, and RSNA reduction were significantly attenuated 5 min after l-NAME. Our results indicate that inhibition of NOS within the NTS attenuates baro- and cardiopulmonary reflexes, suggesting that NO plays a physiologically significant neuromodulatory role in cardiovascular regulation.

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Central nervous system histamine regulates peripheral sympathetic activity

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.260.1.h218 ◽

1991 ◽

Vol 260 (1) ◽

pp. H218-H224 ◽

Cited By ~ 7

Author(s):

V. F. Akins ◽

S. L. Bealer

Keyword(s):

Hypertonic Saline ◽

Pressor Response ◽

Plasma Concentrations ◽

Central Administration ◽

Sprague Dawley ◽

Irreversible Inhibitor ◽

Brain Histamine ◽

Sprague Dawley Rats ◽

H1 Antagonist ◽

Peripheral Sympathetic Activity

Brain histamine (HA) was depleted in conscious Sprague-Dawley rats by central administration of alpha-fluoromethyl-histidine (alpha-FMH), an irreversible inhibitor of the HA synthesizing enzyme. Isotonic or hypertonic saline was infused intravenously at 10 microliters.100 g-1.min-1 for 30 min and mean arterial pressure (MAP) and heart rate (HR) were monitored. In addition, plasma vasopressin (AVP) and norepinephrine (NE) were measured pre- and postinfusion. Animals pretreated with alpha-FMH showed a delayed and attenuated pressor response and bradycardia during hypertonic saline (HTS) infusion and a significant reduction in plasma NE levels (-29 +/- 8% below control values). However, plasma concentrations of AVP were similar in both groups. Central pretreatment with the H1-antagonist pyrilamine (PYR) also delayed the onset and significantly attenuated the pressor response to HTS infusion, and caused dose-related decreases in plasma NE concentrations (-34 +/- 8, -47 +/- 5, and -52 +/- 7% after 60, 100, and 600 nmol PYR, respectively). These data indicate a role for central HA in peripheral sympathetic activation but not as a mediator of AVP release to a peripheral hyperosmotic stimulus.

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Responses of T2-4 spinal cord neurons to irritation of the lower airways in the rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.273.3.r1147 ◽

1997 ◽

Vol 273 (3) ◽

pp. R1147-R1157 ◽

Cited By ~ 7

Author(s):

T. Hummel ◽

J. N. Sengupta ◽

S. T. Meller ◽

G. F. Gebhart

Keyword(s):

Spinal Cord ◽

Afferent Input ◽

Sprague Dawley ◽

Spinal Neurons ◽

Thoracic Spinal Cord ◽

Spinal Cord Neurons ◽

Thoracic Spinal ◽

Balloon Distension ◽

Sprague Dawley Rats ◽

Lower Airways

The aim of the study was to investigate the information processing in the thoracic spinal cord (T2-4) after chemical irritation of the lower airways. Experiments were performed in pentobarbital sodium-anesthetized and pancuronium-paralyzed male Sprague-Dawley rats. Balloon distension of the esophagus was used as the search stimulus. Ammonia and smoke were applied by means of a tracheal cannula; they produced excitatory, inhibitory, and biphasic responses in a concentration-related manner (ammonia 39/39; smoke 23/ 39). Inhaled irritant-responsive neurons exhibited a number of similarities that have been described for neurons responding to stimulation of other thoracic viscera. These similarities relate to the distribution of neurons in the deeper laminae of the thoracic spinal cord, the relatively small number of neurons receiving input from the lower airways, the extensive convergent input from the skin and other thoracic viscera, and the pattern of responses. In addition, both stimulus-induced responses and spontaneous activity are subject to modulation from supraspinal sites. On the basis of responses to inhaled irritants after either spinal cord or vagus nerve block/transection, these T2-4 spinal neurons are likely to receive spinal afferent input that is modulated by vagal-brain stem input.

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