Cardiac receptors

2012 ◽  
pp. 39-47
Author(s):  
Todd Kiefer ◽  
Mihai V. Podgoreanu
Keyword(s):  
Cardiac Receptors

Responses of neurons in rostral ventrolateral medulla to activation of cardiac receptors in rats

2000 ◽  
Vol 279 (5) ◽  
pp. H2549-H2557 ◽  
Author(s):  
De-Pei Li ◽  
Hui-Lin Pan
Keyword(s):  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Single Unit Activity ◽  
Afferent Pathways ◽  
Sympathetic Control ◽  
Stellate Ganglia ◽  
Cervical Vagotomy ◽  
The Mean ◽  
Cardiac Receptors ◽  
Stimulation Of

Ischemic stimulation of cardiac receptors reflexly excites the cardiovascular system. However, the supraspinal mechanisms involved in this reflex are not well defined. This study examined the responses of barosensitive neurons in the rostral ventrolateral medulla (RVLM) to stimulation of cardiac receptors and the afferent pathways involved in these responses. Single-unit activity of RVLM neurons was recorded in α-chloralose-anesthetized rats. Cardiac receptors were stimulated by epicardial application of 10 μg/ml of bradykinin (BK). Barosensitive neurons were silenced by stimulation of baroreceptors. Application of BK increased the mean arterial pressure from 65.2 ± 1.9 to 89.3 ± 2.9 mmHg and excited RVLM barosensitive neurons from 6.2 ± 0.7 to 10.7 ± 0.9 impulses/s ( P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive neurons. Blockade of stellate ganglia abolished the response of barosensitive neurons to BK. Cervical vagotomy significantly increased the baseline discharges of RVLM barosensitive neurons but had no effect on their responses to BK. Thus this study indicates that stimulation of cardiac receptors selectively activates RVLM barosensitive neurons through sympathetic afferent pathways. This information suggests that the RVLM barosensitive neurons are likely involved in the sympathetic control of circulation during myocardial ischemia.

Hypoxia-induced differential modulation of adenosinergic and muscarinic receptors in rat heart

1993 ◽  
Vol 75 (3) ◽  
pp. 1123-1128 ◽  
Author(s):  
R. Kacimi ◽  
J. P. Richalet ◽  
B. Crozatier
Keyword(s):  
Chronic Hypoxia ◽  
Dissociation Constants ◽  
Receptor Density ◽  
Differential Modulation ◽  
Chronotropic Response ◽  
Constant Displacement ◽  
A1 Receptor ◽  
Muscarinic M2 Receptors ◽  
Cardiac Receptors ◽  
Quinuclidinyl Benzilate

To better understand the decreased chronotropic response to catecholamines in chronic hypoxia, we compared the inhibitory pathways regulating adenylate cyclase in rats exposed for 30 days to hypobaric hypoxia (380 Torr; HX) with those in control rats (CT) by the analysis of adenosinergic A1-receptors (8-cyclopentyl-1,3-[3H]dipropylxanthine) and muscarinic M2-receptors ([3H]quinuclidinyl benzilate). A1-receptor density was decreased by 46% in sarcolemmal preparations without a change in the affinity for agonist [(R)-phenylisopropyladenosine]. M2-receptor density was increased (HX: 280 +/- 16 fmol/mg, CT: 188 +/- 15 fmol/mg; n = 7; P < 0.001) without a change in dissociation constant. Displacement of [3H]quinuclidinyl benzilate by carbachol indicated significant decreases in the dissociation constants of both superhigh- (HX: 73 +/- 19 nM, CT: 182 +/- 42 nM; P < 0.001) and high-affinity binding sites (HX: 4 +/- 1 microM, CT: 12 +/- 3 microM; P < 0.001). Our data show that chronic hypoxia leads to differential modulation of cardiac receptors with a downregulation of adenosine receptors and increases in muscarinic receptor affinity and density, which may contribute to the blunted responsiveness of the heart to catecholamines.

The role of cardiac receptors in clonidine-induced vagal bradycardia

1979 ◽  
Vol 54 (1-2) ◽  
pp. 109-118 ◽  
Author(s):  
Björn Lisander ◽  
Göran Wennergren
Keyword(s):  
Vagal Bradycardia ◽  
Cardiac Receptors

Effects of tonic vagal input on breathing pattern in newborn rabbits

1985 ◽  
Vol 59 (1) ◽  
pp. 223-228 ◽  
Author(s):  
T. Trippenbach ◽  
G. Kelly ◽  
D. Marlot
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Vagal Activity ◽  
Respiratory Effects ◽  
Tracheal Pressure ◽  
Negative Pressure Breathing ◽  
Lung Deflation ◽  
Reflex Stimulation ◽  
Cardiac Receptors ◽  
Respiratory Reflex

Respiratory effects of positive and negative pressure breathing were studied in 1- and 4-day-old rabbit pups anesthetized with ketamine (50 mg/kg, im) and acepromazine (3 mg/kg, im). We recorded tidal volume (VT), tracheal pressure (Ptr), and integrated diaphragmatic EMG (DiEMG). Inspiratory (TI) and expiratory time (TE) were measured from the records of DiEMG. During breathing with increased Ptr by 1 or 2 cmH2O, VT, minute ventilation (VE), and respiratory rate (f) decreased. Changes in f relied on a TE prolongation. Neither DiEMG nor its rate of rise (DiEMGt) were affected. Except for VT decrease during positive Ptr, all other effects disappeared after vagotomy. Our results indicate that an increase in tonic vagal activity interacts with the mechanisms controlling TE and has no effect on depth and duration of inspiration. When Ptr decreased by 1 and 2 cmH2O, VE increased due to an increase in f. Increase in f relied on shortening of both TI and TE; the TE effect being more pronounced. DiEMG and DiEMGt also increased. Adverse effects of lung deflation and vagotomy strongly suggest that the respiratory reflex stimulation due to decrease in Ptr does not rely on inhibition of the slowly adapting stretch receptor activity. Therefore other excitatory vagal inputs must be responsible for this response. We propose two vagally mediated inputs: the irritant and/or the cardiac receptors.

Metoclopramide blocks the phenyl diguanide and 5-hydroxytryptamine induced cardiorespiratory reflexes in cats and dogs

1988 ◽  
Vol 66 (6) ◽  
pp. 776-782 ◽  
Author(s):  
K. Ravi ◽  
N. B. Dev
Keyword(s):  
Left Atrial ◽  
Right Atrial ◽  
Excitatory Effect ◽  
Reflex Responses ◽  
Cardiorespiratory Responses ◽  
C Fiber ◽  
Spontaneously Breathing ◽  
Cardiac Receptors ◽  
Sensory Endings ◽  
Stimulation Of

The effects of metoclopramide on the reflex cardiorespiratory responses elicited by stimulation of pulmonary J receptors by right atrial injections of phenyl diguanide (PDG), 5-hydroxytryptamine (5-HT), and capsaicin were investigated in anesthetized spontaneously breathing cats. It was observed that while metoclopramide blocked the responses to PDG and 5-HT injections, it spared the responses to capsaicin injections. Similarly, metoclopramide was without effect on the reflex responses following activation of pulmonary C-fiber receptors (J receptors) by capsaicin in dogs. Reflex cardiorespiratory responses elicited by left atrial injections of PDG and 5-HT, owing to stimulation of cardiac receptors in cats, and reflex responses following right or left atrial injections of PDG and 5-HT, owing to stimulation of aortic chemoreceptors in dogs, were also found to be blocked by metoclopramide. Afferent impulse activity recorded from aortic chemoreceptors of dogs showed that while metoclopramide depressed the excitatory effect of PDG and 5-HT on them, it did not produce any effect on their spontaneous activity and their excitation by hypoxia. The results from the reflex studies show that metoclopramide is capable of antagonizing the reflex responses following the activation of the cardiopulmonary afferents by PDG and 5-HT. Based on the effects on aortic chemoreceptor afferents, it is suggested that PDG, 5-HT, and metoclopramide may be acting upon the regenerative region of the sensory endings.

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