Glycine microinjected into nucleus tractus solitarii of rat acts through cholinergic mechanisms

1991 ◽  
Vol 260 (4) ◽  
pp. H1326-H1331 ◽  
Author(s):  
W. T. Talman ◽  
J. M. Colling ◽  
S. C. Robertson
Keyword(s):  
Heart Rate ◽  
Nmda Receptor ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Cardiovascular Regulation ◽  
Nucleus Tractus Solitarii ◽  
Receptor Blockade ◽  
Receptor Complex ◽  
Cholinergic Mechanisms ◽  
Nmda Receptor Complex

Previous studies have demonstrated the release of glycine from neurotransmitter pools in the region of the nucleus tractus solitarii (NTS) where cardiovascular afferents terminate. Microinjection of glycine into NTS elicits decreases in arterial pressure and heart rate; these effects are also produced by glutamate or acetylcholine. As glycine may act both at the N-methyl-D-aspartate (NMDA)-receptor complex and centrally to release acetylcholine, we have sought to determine whether the cardiovascular responses to exogenous glycine are mediated through glutamatergic or cholinergic mechanisms. Responses to glycine microinjected into the NTS of anesthetized rats were not affected by blockade of the NMDA receptor complex but, like acetylcholine, were blocked by muscarinic receptor blockade. Physostigmine prolonged responses to glycine. Subthreshold doses of glycine, which augmented responses to acetylcholine microinjected into NTS, either decreased or had no effect on glutamate or NMDA. This study supports a role for glycine in cardiovascular regulation by the NTS and suggests that the actions of glycine may be effected, at least in part, through cholinergic mechanisms.

Histamine receptor H1 in the nucleus tractus solitarii regulates arterial pressure and heart rate in rats

2011 ◽  
Vol 301 (2) ◽  
pp. H523-H529 ◽  
Author(s):  
Mohammad E. Bhuiyan ◽  
Hidefumi Waki ◽  
Sabine S. Gouraud ◽  
Miwa Takagishi ◽  
Akira Kohsaka ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Histamine Receptor ◽  
Cardiovascular Regulation ◽  
Nucleus Tractus Solitarii ◽  
Central Brain ◽  
Specific Antagonist ◽  
Dose Dependent ◽  
The Brain

Axons of histamine (HA)-containing neurons are known to project from the posterior hypothalamus to many areas of the brain, including the nucleus tractus solitarii (NTS), a central brain structure that plays an important role in regulating arterial pressure. However, the functional significance of NTS HA is still not fully established. In this study, we microinjected HA or 2-pyridylethylamine, a HA-receptor H1-specific agonist, into the NTS of urethane-anesthetized Wister rats to identify the potential functions of NTS HA on cardiovascular regulation. When HA or H1-receptor-specific agonist was bilaterally microinjected into the NTS, mean arterial pressure (MAP) and heart rate (HR) were significantly increased, whereas pretreatment with the H1-receptor-specific antagonist cetirizine into the NTS significantly inhibited the cardiovascular responses. The maximal responses of MAP and HR changes induced by HA or H1-receptor-specific agonist were dose dependent. We also confirmed gene expression of HA receptors in the NTS and that the expression level of H1 mRNA was higher than that of the other subtypes. In addition, we found that H1 receptors are mainly expressed in neurons of the NTS. These findings suggested that HA within the NTS may play a role in regulating cardiovascular homeostasis via activation of H1 receptors expressed in the NTS neurons.

Use of sinoaortic denervation to study the role of baroreceptors in cardiovascular regulation

1994 ◽  
Vol 266 (5) ◽  
pp. R1705-R1710 ◽  
Author(s):  
A. M. Schreihofer ◽  
A. F. Sved
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Neural Activity ◽  
Nucleus Tractus Solitarius ◽  
Cardiovascular Responses ◽  
Cardiovascular Regulation ◽  
Small Degree ◽  
Baroreceptor Reflex ◽  
Arterial Baroreceptors

To assess the role of arterial baroreceptors in cardiovascular regulation, many studies have used rats in which baroreceptor afferents have been surgically destroyed. However, interpretation of studies using sinoaortic-denervated (SAD) rats is complicated by variability in the extent of baroreceptor denervation. We have compared cardiovascular regulation in rats with total sinoaortic cardiovascular regulation in rats with total sinoaortic denervation, as assessed by the abolition of reflex changes in heart rate (HR) to increases and decreases in arterial pressure (AP), with rats that underwent the same denervation procedure but still had residual (although markedly blunted) reflex changes in HR to changes in AP. In totally SAD rats, the lability of AP was greatly exaggerated compared with sham-denervated rats, although the average AP was equivalent. In contrast, partially SAD rats had elevated AP, and although AP was more labile than in sham-denervated rats, it was less labile than in totally SAD rats. In addition, cardiovascular responses elicited by elimination of neural activity in the nucleus tractus solitarius (NTS) were qualitatively different between the two groups of rats; destruction of the NTS increased AP similarly in partially SAD rats and sham-denervated rats, whereas this treatment did not alter AP in totally SAD rats. Thus there are marked differences in SAD rats with no residual arterial baroreceptor reflex function compared with SAD rats with even a small degree of residual baroreceptor reflex function. These studies highlight the importance of carefully characterizing SAD rats used in studying the role of the baroreceptor reflex in cardiovascular regulation.

Cardiovascular responses to head-stand posture

1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
High Pressure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Skin Temperature ◽  
Cardiovascular Responses ◽  
Posterior Tibial Artery ◽  
Nervous Control ◽  
Posterior Tibial

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963

Glibenclamide attenuates adenosine-induced bradycardia and coronary vasodilatation

1991 ◽  
Vol 261 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
F. L. Belloni ◽  
T. H. Hintze
Keyword(s):  
Heart Rate ◽  
Cardiovascular Responses ◽  
K Channel ◽  
Receptor Blockade ◽  
Beta Adrenergic ◽  
Coronary Vasodilatation ◽  
Cervical Vagotomy ◽  
Adenosine Antagonism ◽  
Anesthetized Dogs ◽  
Control State

The effects of the ATP-sensitive K(+)-channel blocker glibenclamide on the cardiovascular responses to adenosine in dogs were determined. Adenosine (0.01-20 mumol/kg iv) caused coronary vasodilatation, arterial hypotension, and bradycardia in dogs with either combined beta-adrenergic and muscarinic receptor blockade or with bilateral cervical vagotomy plus beta-adrenergic receptor blockade. The 50% effective dose for adenosine-induced coronary dilatation was increased from 0.13 +/- 0.04 mumol/kg in the control state to 1.1 +/- 0.5 mumol/kg after 2 mg/kg of glibenclamide (P less than 0.001). Adenosine at 5 mumol/kg reduced heart rate by 19 +/- 5% from a baseline of 158 +/- 6 beats/min in five anesthetized dogs. After glibenclamide (10 mg/kg), this dose of adenosine failed to cause a significant change in heart rate. The arterial hypotensive effects of adenosine were also attenuated by glibenclamide. Thus glibenclamide inhibited adenosine-induced bradycardia, hypotension, and coronary dilatation. On the other hand, glibenclamide did not affect the reductions in heart rate caused by vagus nerve stimulation. The mechanism of this adenosine antagonism is not known but, in the case of bradycardia, it does not appear to involve any of the steps shared in common by both adenosine-induced and vagal responses of the sinoatrial node.

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