Reflex pressor response to arterial phenylbiguanide: role of abdominal sympathetic visceral afferents

1998 ◽  
Vol 275 (6) ◽  
pp. H2025-H2035 ◽  
Author(s):  
Liang-Wu Fu ◽  
John C. Longhurst
Keyword(s):  
Serotonin Receptor ◽  
Pressor Response ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Visceral Afferents ◽  
Reflex Response ◽  
Selective Agonist ◽  
Cervical Vagotomy ◽  
Increased Activity

Phenylbiguanide (PBG), a 5-HT3 (serotonin) receptor agonist, has been used in many studies as a “selective” agonist to elicit reflex bradycardia and hypotension through activation of cardiac and pulmonary vagal afferents. Because we have shown that endogenous 5-HT stimulates ischemically sensitive abdominal sympathetic afferents through 5-HT3 receptors, we investigated the possibility that left ventricular (LV) and intra-arterial administration of PBG may evoke a competing reflex response by increasing the activity of sympathetic visceral afferents in anesthetized cats. Mean arterial pressure (MAP) and heart rate (HR) were monitored. When both vagal and sympathetic afferents were intact, PBG (40 μg/kg, injected into the LV) significantly decreased MAP and HR in 8 of 10 cats but increased MAP in the remaining 2 cats. After bilateral cervical vagotomy, LV PBG significantly increased MAP. PBG (40 μg/kg ia) significantly increased MAP and HR, whereas intravenous PBG significantly decreased MAP and HR ( n = 10 cats). Furthermore, the pressor response to PBG (40 μg /kg ia) was reduced by 68% ( P < 0.05; n = 4 cats) by celiac and mesenteric ganglionectomies. In studies of single-unit abdominal sympathetic afferents, intra-arterial but not intravenous PBG (40 μg/kg) significantly increased activity of 10 ischemically sensitive afferents but not ischemically insensitive afferents. Blockade of 5-HT3 receptors with tropisetron (200 μg/kg iv) eliminated the response of the afferents and the pressor response to PBG. These data indicate that PBG administered into the LV usually, but not always, evokes a depressor response that is converted to a pressor response following cervical vagotomy. Also, intra-arterial PBG induces a pressor response by stimulating 5-HT3receptors largely associated with ischemically sensitive abdominal sympathetic afferents.

Intravenous morphine-induced activation of vagal afferents: peripheral, spinal, and CNS substrates mediating inhibition of spinal nociception and cardiovascular responses

1992 ◽  
Vol 68 (4) ◽  
pp. 1027-1045 ◽  
Author(s):  
A. Randich ◽  
C. L. Thurston ◽  
P. S. Ludwig ◽  
J. D. Robertson ◽  
C. Rasmussen
Keyword(s):  
Intravenous Administration ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ibotenic Acid ◽  
Vagal Afferents ◽  
Spinothalamic Tract ◽  
Depressor Response ◽  
Arterial Blood ◽  
Intravenous Morphine ◽  
Cervical Vagotomy

1. Intravenous administration of 1.0 mg/kg of morphine produces inhibition of the nociceptive tail-flick (TF) reflex, hypotension, and bradycardia in the pentobarbital-anesthetized rat. The present experiments examined peripheral, spinal, and supraspinal relays for inhibition of the TF reflex and cardiovascular responses produced by morphine (1.0 mg/kg iv) in the pentobarbital-anesthetized rat using 1) bilateral cervical vagotomy, 2) spinal cold block or mechanical lesions of the dorsolateral funiculi (DLFs), or 3) nonselective local anesthesia or soma-selective lesions of specific CNS regions. Intravenous morphine-induced inhibition of responses of unidentified, ascending, and spinothalamic tract (STT) lumbosacral spinal dorsal horn neurons to noxious heating of the hindpaw were also examined in intact and bilateral cervical vagotomized rats. 2. Bilateral cervical vagotomy significantly attenuated inhibition of the TF reflex and bradycardia produced by intravenous administration of morphine. Bilateral cervical vagogtomy changed the normal depressor response produced by morphine into a sustained pressor response. Inhibition of the TF reflex in intact rats was not due to changes in tail temperature. 3. Spinal cold block significantly attenuated inhibition of the TF reflex, the depressor response, and the bradycardia produced by intravenous administration of morphine. However, bilateral mechanical transections of the DLFs failed to significantly affect either inhibition of the TF reflex or cardiovascular responses produced by this dose of intravenous morphine. 4. Microinjection of either lidocaine or ibotenic acid into the nuclei tracti solitarii (NTS), rostromedial medulla (RMM), or ventrolateral pontine tegmentum (VLPT) attenuated morphine-induced inhibition of the TF reflex. Similar microinjections into either the periaqueductal gray (PAG) or the dorsolateral pons (DLP) failed to affect morphine-induced inhibition of the TF reflex. 5. Microinjection of either lidocaine or ibotenic acid into the NTS, RMM, VLPT, DLP, or rostral ventrolateral medulla (RVLM) attenuated the depressor response produced by morphine, although baseline arterial blood pressure (ABP) was affected by ibotenic acid microinjections in the DLP. In all these cases, the microinjections failed to reveal a sustained pressor response as was observed with bilateral cervical vagotomy. Similar microinjections into the PAG failed to affect the depressor response produced by morphine. 6. The lidocaine and ibotenic acid microinjection treatments also showed that the bradycardic response produced by morphine depends on the integrity of the NTS, RMM, RVLM, and possibly the DLP, but not the PAG or VLPT.(ABSTRACT TRUNCATED AT 400 WORDS)

Role of vagal and spinal sensory pathways on eupneic diaphragmatic activity

1986 ◽  
Vol 60 (2) ◽  
pp. 479-485 ◽  
Author(s):  
Y. Jammes ◽  
M. J. Mathiot ◽  
S. Delpierre ◽  
C. Grimaud
Keyword(s):  
Spinal Reflexes ◽  
Vagal Afferents ◽  
Tracheal Occlusion ◽  
Sensory Pathways ◽  
Cervical Vagotomy ◽  
Experimental Protocols ◽  
Spinal Section ◽  
Spinal Afferents ◽  
Alpha Chloralose

The interactions between vagal and spinal afferents in the control of eupneic diaphragmatic activity were studied in two groups of cats anesthetized either with pentobarbital sodium (SPB) or with ethyl carbamate-alpha-chloralose (ECC), which enhanced spinal reflexes. Under both conditions of anesthesia two experimental protocols were performed: 1) bilateral cervical vagotomy followed by spinal section at C8 level or 2) spinal section followed by vagotomy. Changes in integrated diaphragmatic activity (Edi) were studied during eupneic ventilation and tracheal occlusion at end expiration. Vagotomy always significantly increased the amplitude of Edi during eupnea (SPB + 30%; ECC + 15%) and prolonged its duration (Tdi) (SPB + 110%; ECC + 75%) but did not modify the overall shape of the Edi vs. time relationship. Spinal section induced reverse changes in the amplitude of Edi, whether vagal afferents were present or suppressed and modified the shape of the Edi wave, but did not significantly modify Tdi. These results indicate that both vagal and spinal afferents may participate in the control of eupneic inspiration but exert different and interdependent influences on the recruitment and firing time of phrenic motoneurons. In addition, Tdi measured during tracheal occlusion (Todi) was markedly prolonged under ECC anesthesia. In this situation spinal section reduced Todi, which became close to the values obtained in intact or spinal cats under SPB anesthesia. Thus the response to tracheal occlusion at end expiration cannot be interpreted as resulting from the sole suppression of volume related vagal information.

Cardiorespiratory responses to chemical activation of right ventricular receptors

1987 ◽  
Vol 63 (2) ◽  
pp. 733-739 ◽  
Author(s):  
T. G. Waldrop ◽  
D. C. Mullins
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Chemical Activation ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Cardiorespiratory Function ◽  
Cervical Vagotomy ◽  
The Right

Previous reports have shown that activation of left ventricular receptors with sympathetic afferents elicits increases in respiratory output and arterial pressure. The purpose of the present study was to determine whether similar responses are produced by chemical activation of epicardial receptors in the right ventricle. Receptors were stimulated by applying either capsaicin (10 micrograms) or bradykinin (500 ng) to the epicardial surface of the right ventricle in anesthetized cats. Application of either chemical evoked an increase in respiratory output (phrenic nerve activity), a decrease in heart rate, and a nonsignificant increase in arterial pressure in intact cats. However, capsaicin and bradykinin produced significant increases in arterial pressure, heart rate, and respiratory output after bilateral cervical vagotomy. In contrast, a fall in both heart rate and arterial pressure with only small increases in respiratory output were evoked after bilateral removal of the stellate ganglia in cats with intact vagi. Only small responses to the chemical stimulation of right ventricular receptors persisted after combined vagotomy and stellate ganglionectomy. These findings suggest that 1) activation of epicardial receptors with sympathetic afferents originating in the right ventricle causes an increase in cardiorespiratory function, and 2) activation of right ventricular receptors with vagal afferents produces decreases in heart rate and arterial pressure.

Characterization of an esophagocardiovascular reflex in the rat

1997 ◽  
Vol 272 (6) ◽  
pp. R1783-R1791 ◽  
Author(s):  
C. W. Loomis ◽  
D. Yao ◽  
D. Bieger
Keyword(s):  
Pressor Response ◽  
Topical Administration ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
Thoracic Spinal Cord ◽  
Arterial Blood ◽  
Thoracic Spinal ◽  
Cervical Vagotomy ◽  
Spinal Afferents ◽  
Sites Of Action

A cardiovascular reflex evoked by esophageal distension (ECR) in urethan-anesthetized male Sprague-Dawley rats was studied to 1) determine whether the relevant sensory input from the esophagus is conveyed by vagal and/or spinal afferents and 2) evaluate the effects and sites of action of antinociceptive agents. Esophageal distension evoked a rise in arterial blood pressure and heart rate that increased linearly with the log of inflation pressure (25-150 mmHg). Distension (100 mmHg for 20 s) of the lower esophagus was a more effective stimulus than distension of the upper esophagus. The ECR was attenuated by unilateral and abolished by bilateral cervical vagotomy and dose dependently inhibited by morphine (1.0-4.0 mg/kg iv) or by intrathecal (T4-T5) administration of dexmedetomidine (DX, 0.05-0.5 microgram), but not by intrathecal (T4-T5) morphine (4-16 micrograms) or intrathecal (L1-L2) or intravenous DX (0.05-0.5 microgram). The ECR was also inhibited by capsaicin and by the topical administration of DX or morphine to the solitary complex. The pressor response persisted after intravenous pancuronium, scopolamine, and methscopolamine. The ECR circuit appears to consist of vagal afferents, efferent sympathetic preganglionic pathways originating in the thoracic spinal cord, and bulbospinal neurons yet to be identified. This reflex fulfills some criteria of a nociceptive event, but this interpretation requires further investigation.

Role of cardiac sympathetics in the tonic circulatory restraint by vagal afferents

1979 ◽  
Vol 237 (4) ◽  
pp. H528-H534
Author(s):  
T. Shimizu ◽  
D. F. Peterson ◽  
V. S. Bishop
Keyword(s):  
Arterial Pressure ◽  
Cardiac Contractility ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Pressure Response ◽  
Vagal Afferents ◽  
Inhibitory Effects ◽  
Vagal Blockade ◽  
Afferent Vagal

In anesthetized cats with aortic nerves sectioned and carotid arteries occluded, we determined the role of cardiac sympathetic nerves on the tonic inhibitory restraint by cardiac vagal afferents on the cardiovascular system. The effect of afferent vagal blockade on mean arterial pressure and cardiac contractility was determined when sympathetic tone to the heart was altered. Bilateral cardiac sympathectomy produced a significant decrease in left ventricular dP/dt and attenuated the arterial pressure response to afferent vagal cold block to less than 40% of the control. The increase in dP/dt normally observed with vagal blockade was also reduced significantly. Increasing dP/dt by efferent stimulation of cardiac sympathetic nerves restored the arterial pressure response to vagal blockade to near control levels. While the vagal inhibitory activity appeared to be dependent on the resting dP/dt, left ventricular peak pressure did not seem to be contributing to the reflex. Thus, the inhibitory effects of vagally mediated reflexes from the heart which contribute to arterial pressure regulation appear to be influenced by changes in cardiac contractility induced by cardiac sympathetic nerve stimulation.

Reflex Effects of Pulmonary Venous Congestion: Role of Vagal Afferents

Physiology ◽  
1990 ◽  
Vol 5 (3) ◽  
pp. 95-99
Author(s):  
K Ravi ◽  
CT Kappagoda
Keyword(s):  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Venous Congestion ◽  
Vagal Afferents ◽  
Fluid Flux ◽  
Natural Stimulus ◽  
Extravascular Fluid ◽  
Large Airways

The rapidly adapting receptors of the lung are stimulated by changes in extravascular fluid space of the large airways. The natural stimulus to these receptors appears to be a fluid flux from the vasculature. These receptors are probably involved in certain reflexes associated with left ventricular dysfunction.

Function of lateral reticular nucleus in central cardiovascular regulation in the cat

1977 ◽  
Vol 232 (2) ◽  
pp. H157-H166
Author(s):  
M. R. Thomas ◽  
R. F. Ulrichsen ◽  
F. R. Calaresu
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Cardiovascular Regulation ◽  
Reticular Nucleus ◽  
Lateral Reticular Nucleus ◽  
Functional Connections ◽  
Cervical Vagotomy ◽  
The Right ◽  
Stimulation Of

The role of the lateral reticular nucleus (LRN) in central cardiovascular regulation was investigated in cats. In 15 cerebellectomized and nine intact chloralosed cats stimulation of 115 histologically verified sites in the LRN elicited increases in arterial pressure and heart rate; the latter was abolished by propranolol but not by bilateral cervical vagotomy. The pressor response was significantly greater in intact animals. Electrical activity was recorded from the right inferior cardiac nerve (ICN) during stimulation fo the LRN and of a vasomotor region in the posteromedial hypothalamus (PMH). Stimulation of sites in the LRN and in the PMH, on both sides, elicited a response in the right ICN that was consistently abolished during baroreceptor excitation. Medullary transection 3 mm rostral to the LRN did not abolish the ICN response to LRN stimulation. The conclusions are drawn that stimulation of the LRN elicits cardiovascular responses probably due to excitation of groups of neurons in this nucleus located in a descending sympathetic pathway originating in the PMH and that these responses can be inhibited by excitation of baroreceptors. In view of the known functional connections of the LRN with the somatomotor system it is suggested that this nucleus may play a major role in somatosympathetic reflexes.

The effect of afterload on the cardiodepressor reflex response to coronary artery occlusion in dogs

1985 ◽  
Vol 63 (12) ◽  
pp. 1560-1564 ◽  
Author(s):  
E. L. Fallen ◽  
W. S. Beattie ◽  
G. A. Tait
Keyword(s):  
Stroke Volume ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Reflex Response ◽  
Acute Ischemia ◽  
Myocardial Segment ◽  
Circumflex Artery ◽  
Cervical Vagotomy

The acute hemodynamic responses to anterior and posterior wall ischemia were examined at different afterloads in 30 open-chest anaesthetized dogs. Regional and global left ventricular responses to acute ischemia were also measured before and following bilateral cervical vagotomy in 18 dogs. As the preocclusion afterload (mean aortic pressure) was progressively raised with intravenous methoxamine, a significant decrease in stroke volume occurred following circumflex artery occlusion, whereas no change in stroke volume occurred following occlusion of the left anterior descending artery. Bilateral cervical vagotomy completely inhibited the decrease in stroke volume during circumflex occlusion at high afterload. Vagotomy had no effect on the hemodynamic response to acute anterior wall ischemia. Reversible cold vagal block in paced hearts at high afterload unmasked compensatory inotropy in the nonischemic anterior myocardial segment during circumflex occlusion. Restoring vagal tone by rewarming attenuated the fractional shortening of the nonischemic segment. The results indicate that a relationship exists between myocardial wall tension and reflex cardioinhibition during acute posterior wall but not anterior wall ischemia in dogs.

Role of hilar nerve afferents in hyperpnea of exercise

1985 ◽  
Vol 59 (3) ◽  
pp. 798-806 ◽  
Author(s):  
C. Flynn ◽  
H. V. Forster ◽  
L. G. Pan ◽  
G. E. Bisgard
Keyword(s):  
Minute Ventilation ◽  
Blood Gases ◽  
Vagal Afferents ◽  
Vagus Nerves ◽  
Inspiratory Time ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Cervical Vagotomy

The objective of this study was to determine the role of hilar nerve (lung vagal) afferents in the hyperpnea of exercise. Ten ponies were studied before and 2–4 wk and 3–12 mo after sectioning only the hilar branches of the vagus nerves (HND). After HND, lung volume feedback to the medullary centers was attenuated as indicated in the anesthetized state by 1) attenuation or absence of the Hering-Breuer inflation reflex (P less than 0.01) and 2) attenuation of the lengthened inspiratory time (TI) when the airway was occluded at end expiration (P less than 0.01). Moreover, after HND in the awake state, there was an increase in the ratio of TI to total cycle time (P less than 0.01). These changes verify a compromise in lung innervation comparable to cervical vagotomy. Resting arterial PCO2, PO2, and pH were not altered following HND (P greater than 0.10). Moreover, at three levels of mild and moderate treadmill exercise, no difference in either the temporal pattern or the absolute levels of arterial blood gases and arterial pH was found between pre- and post-HND studies (P greater than 0.10). In addition, minute ventilation (VE) at rest and during exercise was not altered by HND (P greater than 0.10). However, 2–4 wk after HND the increase in breathing frequency (f) during exercise was less, whereas the increase in tidal volume during exercise was greater than pre-HND (P less than 0.05). The reduced f was due to an increase in TI with no change in expiratory time. We conclude that lung afferents via the hilar nerves influence the pattern of breathing at rest and during exercise in ponies.

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