scholarly journals Medullary GABAergic mechanisms contribute to electroacupuncture modulation of cardiovascular depressor responses during gastric distention in rats

2013 ◽  
Vol 304 (5) ◽  
pp. R321-R332 ◽  
Author(s):  
Stephanie C. Tjen-A-Looi ◽  
Zhi-Ling Guo ◽  
Min Li ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Kynurenic Acid ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Sympathetic Outflow ◽  
Gastric Distention ◽  
Fos Protein ◽  
Hypotensive Response

Electroacupuncture (EA) at P5–P6 acupoints overlying the median nerves typically reduces sympathoexcitatory blood pressure (BP) reflex responses in eucapnic rats. Gastric distention in hypercapnic acidotic rats, by activating both vagal and sympathetic afferents, decreases heart rate (HR) and BP through actions in the rostral ventrolateral medulla (rVLM) and nucleus ambiguus (NAmb), leading to sympathetic withdrawal and parasympathetic activation, respectively. A GABAA mechanism in the rVLM mediates the decreased sympathetic outflow. The present study investigated the hypothesis that EA modulates gastric distention-induced hemodynamic depressor and bradycardia responses through nuclei that process parasympathetic and sympathetic outflow. Anesthetized hypercapnic acidotic rats manifested repeatable decreases in BP and HR with gastric distention every 10 min. Bilateral EA at P5–P6 for 30 min reversed the hypotensive response from −26 ± 3 to −6 ± 1 mmHg and the bradycardia from −35 ± 11 to −10 ± 3 beats/min for a period that lasted more than 70 min. Immunohistochemistry and in situ hybridization to detect c-Fos protein and GAD 67 mRNA expression showed that GABAergic caudal ventral lateral medulla (cVLM) neurons were activated by EA. Glutamatergic antagonism of cVLM neurons with kynurenic acid reversed the actions of EA. Gabazine used to block GABAA receptors microinjected into the rVLM or cVLM reversed EA's action on both the reflex depressor and bradycardia responses. EA modulation of the decreased HR was inhibited by microinjection of gabazine into the NAmb. Thus, EA through GABAA receptor mechanisms in the rVLM, cVLM, and NAmb modulates gastric distention-induced reflex sympathoinhibition and vagal excitation.

Gastric distension attenuates the hypotensive effect of intraduodenal glucose in healthy older subjects

2008 ◽  
Vol 295 (2) ◽  
pp. R472-R477 ◽  
Author(s):  
Diana Gentilcore ◽  
James H. Meyer ◽  
Christopher K. Rayner ◽  
Michael Horowitz ◽  
Karen L. Jones
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Gastric Emptying ◽  
Healthy Subjects ◽  
Hypotensive Effect ◽  
Gastric Distension ◽  
Two Dimensional ◽  
Current Management ◽  
Older Subjects ◽  
Hypotensive Response

Postprandial hypotension occurs frequently, and current management is suboptimal. Recent studies suggest that the magnitude of the fall in postprandial blood pressure (BP) may be attenuated by gastric distension. The aim of this study was to determine the effect of gastric distension on the hypotensive response to intraduodenal (ID) glucose. Eight healthy subjects (5 males, 3 females, aged 65–76 years) received an ID infusion of either 1) 50 g glucose in 300 ml saline (ID glucose) over 60 min ( t = 0–60 min), 2) 50 g glucose in 300 ml saline over 60 min and intragastric ( 4 ) infusion of 500 ml water between t = 7–10 min (IG water and ID glucose), or 3) ID saline (0.9%) infusion over 60 min and IG infusion of 500 ml water (IG water and ID saline) all followed by ID saline infusion for another 60 min ( t = 60–120 min) on three separate days. BP and heart rate (HR) were measured. Gastric emptying (GE) of the IG water was quantified by two-dimensional ultrasonography. Between t = 0–60 min, systolic and diastolic BP was greater ( P < 0.05 for both) with IG water and ID saline compared with IG water and ID glucose, and less ( P < 0.05 for both) with ID glucose compared with IG water and ID glucose. These effects were evident at relatively low IG volumes (∼300 ml). GE was faster with IG water and ID saline when compared with IG water and ID glucose. We conclude that, in healthy older subjects, IG administration of water markedly attenuates the hypotensive response to ID glucose, presumably as a result of gastric distension.

Neurogenic-nitric oxide interactions affecting brachial artery mechanics in humans: roles of vessel distensibility vs. diameter

2008 ◽  
Vol 295 (4) ◽  
pp. R1181-R1187 ◽  
Author(s):  
Deborah A. Salzer ◽  
Philip J. Medeiros ◽  
Rosemary Craen ◽  
J. Kevin Shoemaker
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Brachial Artery ◽  
Lower Body Negative Pressure ◽  
Cold Pressor ◽  
Sympathetic Outflow ◽  
Sympathetic Activation ◽  
Baseline Diameter ◽  
Conduit Vessel

The purpose of this investigation was to assess the interactive influence of sympathetic activation and supplemental nitric oxide (NO) on brachial artery distensibility vs. its diameter. It was hypothesized that 1) sympathetic activation and NO competitively impact muscular conduit artery (brachial artery) mechanics, and 2) neurogenic constrictor input affects conduit vessel stiffness independently of outright changes in conduit vessel diastolic diameter. Lower body negative pressure (LBNP) and a cold pressor stress (CPT) were used to study the changes in conduit vessel mechanics when the increased sympathetic outflow occurred with and without changes in heart rate (LBNP −40 vs. −15 mmHg) and blood pressure (CPT vs. LBNP). These maneuvers were performed in the absence and presence of nitroglycerin. Neither LBNP nor CPT altered brachial artery diastolic diameter; however, distensibility was reduced by 25 to 54% in each reflex (all P < 0.05). This impact of sympathetic activation on brachial artery distensibility was not altered by nitroglycerin supplementation (21–54%; P < 0.05), although baseline diameter was increased by the exogenous NO ( P < 0.05). The results indicate that sympathetic excitation can reduce the distensibility of the brachial artery independently of concurrent changes in diastolic diameter, heart rate, and blood pressure. However, exogenous NO did not minimize or reverse brachial stiffening during sympathetic activation. Therefore, sympathetic outflow appears to impact the stiffness of this conduit vessel rather than its diastolic diameter or, by inference, its local resistance to flow.

scholarly journals Modulation of cardiopulmonary depressor reflex in nucleus ambiguus by electroacupuncture: roles of opioids and γ-aminobutyric acid

2012 ◽  
Vol 302 (7) ◽  
pp. R833-R844 ◽  
Author(s):  
Stephanie C. Tjen-A-Looi ◽  
Peng Li ◽  
Min Li ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Low Frequency ◽  
Vagal Afferents ◽  
Nucleus Ambiguus ◽  
Aminobutyric Acid ◽  
Vagal Activity ◽  
Induced Hypotension ◽  
Cardiopulmonary Receptors ◽  
Depressor Reflex

Stimulation of cardiopulmonary receptors with phenylbiguanide (PBG) elicits depressor cardiovascular reflex responses, including decreases in blood pressure and heart rate mediated in part by the brain stem parasympathetic cardiac neurons in the nucleus ambiguus (NAmb). The present study examined NAmb neurotransmitter mechanisms underlying the influence of electroacupuncture (EA) on the PBG-induced hypotension and bradycardia. We hypothesized that somatic stimulation during EA modulates PBG responses through opioid and γ-aminobutyric acid (GABA) modulation in the NAmb. Anesthetized and ventilated cats were studied during repeated stimulation with PBG or cardiac vagal afferents while low-frequency EA (2 Hz) was applied at P5–6 acupoints overlying the median nerve for 30 min and NAmb neuronal activity, heart rate, and blood pressure were recorded. Microinjection of kainic acid into the NAmb attenuated the PBG-induced bradycardia from −60 ± 11 to −36 ± 11 beats/min. Likewise, EA reduced the PBG-induced depressor and bradycardia reflex by 52 and 61%, respectively. Cardiac vagal afferent evoked preganglionic cellular activity in the NAmb was reduced by EA for about 60 min. Blockade of opioid or GABAA receptors using naloxone and gabazine reversed the EA-related modulation of the evoked cardiac vagal activity by 73 and 53%, respectively. Similarly, naloxone and gabazine reversed EA modulation of the negative chronotropic responses from −11 ± 5 to −23 ± 6 and −13 ± 4 to −24 ± 3 beats/min, respectively. Thus EA at P5–6 decreases PBG evoked hypotension and bradycardia as well as the NAmb PBG-sensitive preganglionic cardiac vagal outflow through opioid and GABA neurotransmitter systems.

Lesions of A1 noradrenergic cells affect AVP release and heart rate during hemorrhage

1987 ◽  
Vol 253 (5) ◽  
pp. H1012-H1017 ◽  
Author(s):  
G. A. Head ◽  
A. W. Quail ◽  
R. L. Woods
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Volume ◽  
Ventrolateral Medulla ◽  
Sham Operation ◽  
Noradrenergic Neurons ◽  
Reflex Tachycardia ◽  
Conscious Rabbits ◽  
Plasma Arginine

The role of A1 noradrenergic cells of the ventrolateral medulla in the changes in mean arterial pressure (MAP), heart rate (HR), and plasma arginine vasopressin (AVP) after slow continuous hemorrhage (2% blood vol/min up to 35%) was examined by comparing responses in conscious rabbits before and 3 wk after a sham operation or A1 lesions. In the control experiments, MAP fell minimally up to the withdrawal of 20% of blood volume after which it fell abruptly to 20-30 mmHg below control by the 35% level. Plasma AVP increased nonlinearly during progressive hemorrhage with significant increases occurring only after 25% of blood volume was removed. In contrast, HR increased linearly after the onset of bleeding. After A1 lesions, which destroyed 84% (range 80-94%) of the noradrenergic cells, the amount of AVP released and the tachycardia during hemorrhage were reduced by 83 and 61%, respectively (P less than 0.005), but the fall in MAP was minimally affected. Basal values of MAP, HR, or plasma AVP were not affected by the lesions. These results suggest that during hemorrhage in conscious rabbits A1 noradrenergic neurons are important for the secretion of AVP and the reflex tachycardia but play little role in the maintenance of blood pressure.

scholarly journals The hypotensive response to oral fat is comparable but slower compared with carbohydrate in healthy elderly subjects

2006 ◽  
Vol 95 (2) ◽  
pp. 340-345 ◽  
Author(s):  
Renuka Visvanathan ◽  
Michael Horowitz ◽  
Ian Chapman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Area Under The Curve ◽  
Elderly Subjects ◽  
High Fat ◽  
Postprandial Hypotension ◽  
Healthy Elderly ◽  
Hypotensive Response ◽  
Healthy Elderly Subjects

The objective of the present study was to determine the comparative hypotensive responses to drinks containing predominantly fat and carbohydrate (CHO) in healthy elderly subjects. Using a randomised, cross-over study, the participants, twelve elderly subjects, six of them female (72·2 (sd 5·7) years), were investigated. On three separate days, blood pressure (BP) and heart rate were measured following ingestion of 300ml drinks containing: (1) CHO (75g glucose and 93g Polyjoule (CHO polymer) providing 2732kJ (653kcal)); (2) 88% fat (cream blended with milk providing 2732kJ (653kcal)); (3) water. Systolic BP decreased following the CHO drink (P<0·001) and the high-fat drink (P<0·001) but not water; there was no difference in the magnitude of the decrease between the CHO drink and the drink containing fat (13·4v. 15·6mmHg). However, the onset of the fall was slower after the fat-containing drink (13·0v. 26·5min (P=0·01); area under the curve for 0–30min for CHO drink −6·5v. fat-containing drink 125·4 mmHg×min (P=0·043)). We conclude that ingestion of a high-fat drink results in a comparable fall in BP to a CHO drink although the onset is relatively slower. These observations may have implications for the management of postprandial hypotension.

scholarly journals Participation of 5-HT and AT1Receptors within the Rostral Ventrolateral Medulla in the Maintenance of Hypertension in the Goldblatt 1 Kidney-1 Clip Model

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Cássia T. Bergamaschi ◽  
Nyam F. Silva ◽  
Jose G. Pires ◽  
Ruy R. Campos ◽  
Henrique A. Futuro Neto
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
High Blood Pressure ◽  
Wistar Rats ◽  
Kynurenic Acid ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Receptor Blockade ◽  
Control Groups ◽  
Male Wistar Rats

The hypothesis that changes in neurotransmission within the rostral ventrolateral medulla (RVLM) are important to maintain the high blood pressure (BP) was tested in Goldblatt one kidney-one clip hypertension model (1K-1C). Male Wistar rats were anesthetized (urethane 1.2 g/kg, i.v.), and the effects of bilateral microinjections into the RVLM of the following drugs were measured in 1K-1C or control groups: glutamate (0.1 mol/L, 100 nL) and its antagonist kynurenic acid (0.02 mol/L, 100 nL), the angiotensin AT1receptor antagonist candesartan (0.01 mol/L, 100 nL), and the nonselective 5-HT receptor antagonist methiothepin (0.06 mol/L, 100 nL). Experiments in 1K-1C rats were performed 6 weeks after surgery. In anesthetized rats glutamate response was larger in hypertensive than in normotensive rats (H:Δ67±6.5; N:Δ43±3.54 mmHg). In contrast, kynurenic acid microinjection into the RVLM did not cause any change in BP in either group. The blockade of either AT1or 5-HT receptors within the RVLM decreased BP only in 1K-1C rats. A largest depressor response was caused by 5-HT receptor blockade. The data suggest that 5-HT and AT1receptors act tonically to drive RVLM in 1K-1C rats, and these actions within RVLM contribute to the pathogenesis of this model of hypertension.

Nitric oxide synthase inhibition does not affect regulation of muscle sympathetic nerve activity during head-up tilt

2003 ◽  
Vol 285 (5) ◽  
pp. H2105-H2110 ◽  
Author(s):  
Jian Cui ◽  
Rong Zhang ◽  
Thad E. Wilson ◽  
Sarah Witkowski ◽  
Craig G. Crandall ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
No Synthase ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Head Up Tilt

To test the hypothesis that systemic inhibition of nitric oxide (NO) synthase does not alter the regulation of sympathetic outflow during head-up tilt in humans, in eight healthy subjects NO synthase was blocked by intravenous infusion of NG-monomethyl-l-arginine (l-NMMA). Blood pressure, heart rate, cardiac output, total peripheral resistance (TPR), and muscle sympathetic nerve activity (MSNA) were recorded in the supine position and during 60° head-up tilt. In the supine position, infusion of l-NMMA increased blood pressure, via increased TPR, and inhibited MSNA. However, the increase in MSNA evoked by head-up tilt during l-NMMA infusion (change in burst rate: 24 ± 4 bursts/min; change in total activity: 209 ± 36 U/min) was similar to that during head-up tilt without l-NMMA (change in burst rate: 23 ± 4 bursts/min; change in total activity: 251 ± 52 U/min, n = 6, all P > 0.05). Moreover, changes in TPR and heart rate during head-up tilt were virtually identical between the two conditions. These results suggest that systemic inhibition of NO synthase with l-NMMA does not affect the regulation of sympathetic outflow and vascular resistance during head-up tilt in humans.

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