Effects of bradykinin and capsaicin on endings of afferent fibers from abdominal visceral organs

1984 ◽  
Vol 247 (3) ◽  
pp. R552-R559 ◽  
Author(s):  
J. C. Longhurst ◽  
M. P. Kaufman ◽  
G. A. Ordway ◽  
T. I. Musch
Keyword(s):  
Afferent Fiber ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Fiber Types ◽  
Afferent Pathways ◽  
Visceral Organs ◽  
C Fibers ◽  
C Fiber ◽  
The Right ◽  
Stimulation Of

Stimulation of sensory endings in abdominal visceral organs with capsaicin or bradykinin reflexly increases heart rate, blood pressure, and myocardial contractility through afferent pathways in splanchnic nerves. To determine the afferent fiber types stimulated, we recorded impulses in the right splanchnic nerve in 12 anesthetized cats after either injecting capsaicin (50-200 micrograms) or bradykinin (6.5-20 micrograms) into the descending thoracic aorta or applying pledgets soaked with these chemicals to a visceral organ. We studied 26 A- and 23 C-fibers, each with one receptive field in the mesentery, stomach, duodenum, jejunum, ileum, pancreas, liver, gallbladder, or porta hepatis. Endings of C-fibers generally were mechanically insensitive, whereas endings of A-fibers were mechanically sensitive. After a latency of 10.7 +/- 3.3 s, capsaicin increased the activity of 10 of 26 A-fibers from 2.0 +/- 0.9 to 9.9 +/- 2.6 impulses/s and 23 of 23 C-fibers from 0.2 +/- 0.1 to 13.0 +/- 1.6 impulses/s after a latency of 3.3 +/- 0.9 s. Bradykinin increased the activity of 15 of 26 A-fibers from 2.6 +/- 0.9 to 7.4 +/- 1.5 impulses/s after a latency of 17.0 +/- 1.7 s and 16 of 22 C-fibers from 0.4 +/- 0.2 to 4.7 +/- 1.2 impulses/s after a latency of 19.0 +/- 1.9 s. Capsaicin stimulated significantly more C- than A-fibers (P less than 0.001) and a significantly greater fraction of C-fibers than did bradykinin (P less than 0.007). We conclude that stimulation of splanchnic C-fiber afferents by capsaicin and both A- and C-fiber afferents by bradykinin is primarily responsible for the reflex cardiovascular responses caused by these chemicals.

Hypoxia, bradykinin, and prostaglandins stimulate ischemically sensitive visceral afferents

1987 ◽  
Vol 253 (3) ◽  
pp. H556-H567 ◽  
Author(s):  
J. C. Longhurst ◽  
L. E. Dittman
Keyword(s):  
Pressor Response ◽  
Splanchnic Nerve ◽  
Visceral Afferents ◽  
Visceral Organs ◽  
C Fibers ◽  
Systemic Hypoxia ◽  
C Fiber ◽  
Chemical Stimuli ◽  
Pg E2 ◽  
The Right

Ischemia of abdominal visceral organs is known to reflexly stimulate the cardiovascular system. The purpose of this study was to determine which of several potential chemical stimuli present during ischemia either directly stimulate or sensitize these afferents to respond to ischemia. Impulse activity was recorded in the right splanchnic nerve of anesthetized cats. First, we determined whether the afferents were ischemically sensitive by subjecting them to 2-6 min of regional ischemia through occlusion of the descending thoracic aorta. We then examined the afferents' response to systemic hypoxia by decreasing the inspired O2 and arterial injection of bradykinin or the prostaglandins (PG) E2, PGF2 alpha, or prostacyclin (PGI2). Sixty-one percent of the rapidly adapting A fibers and 47% of the C fibers were stimulated by ischemia, and of these, 78% of the A fibers and 44% of the C fibers tested were stimulated by hypoxia. The latency of response to hypoxia (60 +/- 12 s) was significantly longer than the chemoreceptor-induced pressor response (45 +/- 11 s). Each afferent stimulated by ischemia and/or hypoxia innervated a receptive field in the pylorus, intestine, porta hepatis, gallbladder or biliary tract, pancreas, or mesentery. Ninety percent of the ischemically sensitive A fibers and 80% of the ischemically sensitive C fibers responded to bradykinin, whereas 40% of the A fibers and 62% of the C fibers responded to PGE2, PGF2 alpha, or PGI2. Several endings responded to ischemia or hypoxia only after bradykinin or PGI2 had been injected. Thus approximately 50% of slowly adapting A and C fiber endings in abdominal visceral organs respond, or can be sensitized by bradykinin or PGI2 to respond, to ischemia and/or hypoxia. However, they are not as sensitive to hypoxia as carotid and aortic body chemoreceptors, since they respond well after the chemoreceptor-induced pressor response.

Endogenous BK stimulates ischemically sensitive abdominal visceral C fiber afferents through kinin B2 receptors

1994 ◽  
Vol 267 (6) ◽  
pp. H2398-H2406 ◽  
Author(s):  
H. L. Pan ◽  
G. L. Stahl ◽  
S. V. Rendig ◽  
O. A. Carretero ◽  
J. C. Longhurst
Keyword(s):  
Receptor Antagonist ◽  
Impulse Activity ◽  
Discharge Rate ◽  
Visceral Afferents ◽  
C Fibers ◽  
C Fiber ◽  
Hoe 140 ◽  
B2 Receptors ◽  
The Right ◽  
Stimulation Of

Abdominal ischemia and reperfusion reflexly activate the cardiovascular system. In the present study, we evaluated the role of endogenously produced bradykinin (BK) in the stimulation of ischemically sensitive visceral afferents. Single-unit activity of abdominal visceral C fiber afferents was recorded from the right thoracic sympathetic chain of anesthetized cats during 5 min of abdominal ischemia. Abdominal ischemia increased the portal venous plasma BK level from 49 +/- 10 to 188 +/- 66 pg/ml (P < 0.05). Injection of BK (1 microgram/kg ia) into the descending aorta significantly increased impulse activity (0.88 +/- 0.16 impulses/s) of 10 C fibers, whereas a kinin B1-receptor agonist, des-Arg9-BK (1 microgram/kg), did not alter the discharge rate. Inhibition of kininase II activity with captopril (4 mg/kg i.v.) potentiated impulse activity of 14 ischemically sensitive C fibers (0.44 +/- 0.09 vs. precaptopril, 0.33 +/- 0.08 impulses/s; P < 0.05). In addition, a kinin B2-receptor antagonist (NPC-17731; 40 micrograms/kg i.v.) attenuated activity of afferents during ischemia (0.39 +/- 0.08 vs. pre-NPC-17731, 0.72 +/- 0.13 impulses/s; P < 0.05) and eliminated the response of 10 C fibers to BK. Another kinin B2-receptor antagonist, Hoe-140 (30 micrograms/kg iv), had similar inhibitory effects on six other ischemically sensitive C fibers. In 15 separate cats treated with aspirin (50 mg/kg i.v.), Hoe-140 (30 micrograms/kg i.v.) attenuated impulse activity of only 3 of 16 ischemically sensitive C fibers. These data suggest that BK produced during abdominal ischemia contributes to the stimulation of ischemically sensitive visceral C fiber afferents through kinin B2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary C-fibers reflexly increase secretion by tracheal submucosal glands in dogs

1985 ◽  
Vol 58 (3) ◽  
pp. 907-910 ◽  
Author(s):  
H. D. Schultz ◽  
A. M. Roberts ◽  
C. Bratcher ◽  
H. M. Coleridge ◽  
J. C. Coleridge ◽  
...  
Keyword(s):  
Gland Secretion ◽  
Right Atrial ◽  
Vagus Nerves ◽  
C Fibers ◽  
Airway Secretion ◽  
Submucosal Glands ◽  
C Fiber ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10–20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.

Differential responses of regional sympathetic activity and blood flow to visceral afferent stimulation

2001 ◽  
Vol 280 (6) ◽  
pp. R1781-R1789 ◽  
Author(s):  
Hui-Lin Pan ◽  
Dwight D. Deal ◽  
Zemin Xu ◽  
Shao-Rui Chen
Keyword(s):  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Visceral Afferents ◽  
Cardiovascular Reflexes ◽  
Efferent Activity ◽  
Blood Flows ◽  
The Right ◽  
Sympathetic Efferent Activity ◽  
Stimulation Of

The sympathetic nervous system is essential for the cardiovascular responses to stimulation of visceral afferents. It remains unclear how the reflex-evoked sympathetic output is distributed to different vascular beds to initiate the hemodynamic changes. In the present study, we examined changes in regional sympathetic nerve activity and blood flows in anesthetized cats. Cardiovascular reflexes were induced by either electrical stimulation of the right splanchnic nerve or application of 10 μg/ml of bradykinin to the gallbladder. Blood flows were measured using colored microspheres or the Transonic flow meter system. Sympathetic efferent activity was recorded from the left splanchnic, inferior cardiac, and tibial nerves. Stimulation of visceral afferents decreased significantly blood flows in the celiac (from 49 ± 4 to 25 ± 3 ml/min) and superior mesenteric (from 35 ± 4 to 23 ± 2 ml/min) arteries, and the vascular resistance in the splanchnic bed was profoundly increased. Consistently, stimulation of visceral afferents decreased tissue blood flows in the splanchnic organs. By contrast, activation of visceral afferents increased significantly blood flows in the coronary artery and portal vein but did not alter the vascular resistance of the femoral artery. Furthermore, stimulation of visceral afferents increased significantly sympathetic efferent activity in the splanchnic (182 ± 44%) but not in the inferior cardiac and tibial nerves. Therefore, this study provides substantial new evidence that stimulation of abdominal visceral afferents differentially induces sympathetic outflow to the splanchnic vascular bed.

Role of summation of afferent input in cardiovascular reflexes from splanchnic nerve stimulation

1996 ◽  
Vol 270 (3) ◽  
pp. H849-H856 ◽  
Author(s):  
H. L. Pan ◽  
Z. B. Zeisse ◽  
J. C. Longhurst
Keyword(s):  
Electrical Stimulation ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Afferent Input ◽  
Sympathetic Chain ◽  
Cardiovascular Reflexes ◽  
C Fibers ◽  
Greater Splanchnic Nerve ◽  
The Right

Stimulation of abdominal sympathetic visceral afferents reflexly excites the cardiovascular system. The present study examined the role of summation of afferent input in this reflex. Single-unit activity of A delta- and C-fiber afferents was recorded from the right thoracic sympathetic chain in anesthetized cats to determine the relationship between intensities of electrical stimulation and the types of nerve fibers within the right greater splanchnic nerve. The differential effect of cooling on A delta- and C-fiber axons in the sympathetic chain also was examined by recording single-unit afferent activity. Reflex cardiovascular responses were induced by electrical stimulation of the central cut end of the right greater splanchnic nerve. We observed that the numbers of A delta and C fibers activated by electrical stimulation were proportional to the intensity of stimulation. However, neither local cooling nor intensity of stimulation provided a means to separate A delta and C fibers contained in the sympathetic chain. The results demonstrate that the magnitude of excitatory cardiovascular reflexes is frequency dependent and is related directly to intensity of electrical stimulation, suggesting that both adequate discharge frequency of the afferent and sufficient numbers of afferents recruited are crucial factors for full expression of reflex cardiovascular responses.

Signal transduction in activation of ischemically sensitive abdominal visceral afferents: role of PKC

1998 ◽  
Vol 275 (3) ◽  
pp. H1024-H1031 ◽  
Author(s):  
Zhi-Ling Guo ◽  
Liang-Wu Fu ◽  
J. David Symons ◽  
John C. Longhurst
Keyword(s):  
Signal Transduction ◽  
Impulse Activity ◽  
Visceral Afferents ◽  
C Fibers ◽  
Kinase C ◽  
C Fiber ◽  
Afferent Nerve Endings ◽  
The Right ◽  
Stimulation Of

Abdominal ischemia reflexly activates the cardiovascular system by stimulating abdominal visceral afferent nerve endings. Whereas many ischemic metabolites responsible for activating these nerves have been identified (e.g., bradykinin), their precise mechanism of action is unclear. Protein kinase C (PKC) is an important part of the signal transduction process underlying the action of metabolites such as bradykinin and is a regulator of neuronal activity. Therefore, we hypothesized that PKC contributes to stimulation of ischemically sensitive abdominal visceral afferents. Single-unit activity was recorded from the right thoracic sympathetic chain of anesthetized cats. Exogenous activation of PKC using phorbol 12,13-dibutyrate (PDBu, 5 μg/kg ia) increased the impulse activity of ischemically sensitve C-fiber afferents from 0.04 ± 0.01 to 0.67 ± 0.23 impulses/s ( n = 11; P < 0.05). The influence of endogenous activation of PKC also was evaluated during 10 min of mesenteric ischemia. Inhibition of PKC using PKC-(19—36) (20 μg/kg iv) reduced ischemia-induced increases in afferent activity from 0.46 ± 0.11 to 0.19 ± 0.08 impulses/s ( n = 7, P < 0.05). Moreover, PKC-(19—36) (20 μg/kg iv) reduced the response of ischemically sensitive C fibers to bradykinin (0.5–1.0 μg/kg ia) from 1.18 ± 0.20 to 0.66 ± 0.14 impulses/s ( n = 13, P < 0.05). These results indicate that PKC contributes to activation of abdominal visceral afferents during ischemia and specifically to part of the bradykinin-induced activation of these afferents.

Endogenous histamine stimulates ischemically sensitive abdominal visceral afferents through H1 receptors

1997 ◽  
Vol 273 (6) ◽  
pp. H2726-H2737 ◽  
Author(s):  
Liang-Wu Fu ◽  
Hui-Lin Pan ◽  
John C. Longhurst
Keyword(s):  
Receptor Agonist ◽  
Gastric Wall ◽  
Cardiovascular Responses ◽  
Visceral Afferents ◽  
Direct Stimulation ◽  
C Fibers ◽  
Endogenous Histamine ◽  
C Fiber ◽  
Increased Activity ◽  
Stimulation Of

Abdominal ischemia stimulates sympathetic visceral afferents to reflexly activate the cardiovascular system. We have shown previously that topical application of histamine (HA) to the gastric wall causes reflex cardiovascular responses and have documented increased histamine concentrations in intestinal lymph and portal venous plasma during brief abdominal ischemia. In the present study, we hypothesized that histamine produced during ischemia activates ischemically sensitive C-fiber afferents by stimulation of H1 receptors. Nerve activity of single-unit abdominal visceral C-fiber afferents was recorded from the right thoracic sympathetic chain of anesthetized cats. Injection of histamine (25 μg/kg ia) significantly increased activity of nine ischemically sensitive C fibers from 0.09 ± 0.06 to 1.11 ± 0.20 imp/s. An H1-receptor agonist, 2-(3-chlorophenyl)histamine (250 μg/kg ia), also increased activity of these afferents from 0.11 ± 0.04 to 0.64 ± 0.18 imp/s ( P < 0.05). Furthermore, an H1-receptor antagonist (pyrilamine, 0.2 mg/kg iv) significantly attenuated the increased activity in 11 other C fibers from 0.91 ± 0.16 to 0.35 ± 0.06 imp/s (ischemia vs. pyrilamine + ischemia) and eliminated the response of 9 separate ischemically sensitive afferents to histamine. Conversely, both the H2-receptor agonist dimaprit (500 μg/kg ia) and the H3-receptor agonist ( R)-α-methylhistamine (250 μg/kg ia) did not significantly alter the activity of these nine afferents. In nine separate cats treated with indomethacin (5 mg/kg iv), pyrilamine (0.2 mg/kg iv) further significantly attenuated the increased activity in seven of nine C fibers during ischemia, and indomethacin (5 mg/kg iv) attenuated the response of eight other afferents to histamine. These data suggest that during mesenteric ischemia endogenous histamine contributes to the activation of afferents through direct stimulation of histamine H1 receptors and that histamine’s stimulating effect on these afferents is dependent partially on production of prostaglandins.

scholarly journals Stimulation of vagal pulmonary C fibers by inhaled wood smoke in rats

1998 ◽  
Vol 84 (1) ◽  
pp. 30-36 ◽  
Author(s):  
C. J. Lai ◽  
Y. R. Kou
Keyword(s):  
Hydroxyl Radical ◽  
Combined Treatment ◽  
Wood Smoke ◽  
Radical Scavenger ◽  
C Fibers ◽  
Hydroxyl Radical Scavenger ◽  
C Fiber ◽  
Delayed Phase ◽  
Stimulation Of ◽  
Sustained Increase

Lai, C. J., and Y. R. Kou. Stimulation of vagal pulmonary C fibers by inhaled wood smoke in rats. J. Appl. Physiol. 84(1): 30–36, 1998.—This study investigated the stimulation of vagal pulmonary C fibers (PCs) by wood smoke. We recorded impulses from PCs in 58 anesthetized, open-chest, and artificially ventilated rats and delivered 6 ml of wood smoke into the lungs. Within 1 or 2 s after the smoke delivery, an intense and nonphasic burst of discharge [Δ = +7.4 ± 0.7 (SE) impulses/s, n = 68] was evoked in 60 of the 68 PCs studied and lasted for 4–8 s. This immediate stimulation was usually followed by a delayed and more sustained increase in C-fiber activity (Δ = +2.0 ± 0.4 impulses/s). The overall stimulation was not influenced by removal of smoke particulates ( n = 15) or by pretreatment with vehicle ( n = 8) for dimethylthiourea (DMTU; a hydroxyl radical scavenger) or indomethacin (Indo; a cyclooxygenase inhibitor). The immediate-phase stimulation was not affected by pretreatment with Indo ( n= 8) but was largely attenuated by pretreatment with DMTU ( n = 12) or by a combined treatment with DMTU and Indo (DMTU+Indo; n = 8). Conversely, the delayed-phase stimulation was partially suppressed either by DMTU or by Indo but was totally abolished by DMTU+Indo. These results suggest that 1) the stimulation of PCs is linked to the gas phase of wood smoke and 2) hydroxyl radical, but not cyclooxygenase products, is involved in the immediate-phase stimulation, whereas both metabolites are responsible for evoking the delayed-phase stimulation.

Diaphragmatic responses to graded stimulation of pulmonary C-fibers with capsaicin

1985 ◽  
Vol 59 (5) ◽  
pp. 1487-1494 ◽  
Author(s):  
J. R. Coast ◽  
S. S. Cassidy
Keyword(s):  
Dose Response ◽  
Strain Gauge ◽  
Contraction Rate ◽  
C Fibers ◽  
C Fiber ◽  
Shallow Breathing ◽  
Fiber Stimulation ◽  
Rapid Shallow Breathing ◽  
Stimulation Of

It has been suggested that pulmonary C-fiber stimulation is responsible for the rapid shallow breathing that accompanies pulmonary edema. However, pulmonary C-fiber stimulation also causes apnea. To determine whether it was possible for both responses to occur from one stimulus, we infused varying concentrations of capsaicin (a compound that selectively stimulates C-fiber receptors in the dog) into an in situ vascularly isolated dog lung and measured rates and strengths of diaphragmatic contractions with a strain gauge sutured to the diaphragm and electromyogram electrodes implanted in the diaphragm. There was a dose response to capsaicin in that increased doses were related directly with the duration of cessation of diaphragmatic contractions (2–100 s) and inversely with the latency from the start of stimulation to the beginning of the cessation of diaphragmatic contractions (100–5 s). There was no evidence, however, of rapid shallow breathing in this set of experiments. Either a gradual return to normal rate from prolonged contraction intervals or no change in contraction rate was seen, depending on capsaicin concentration. We conclude that the primary diaphragmatic response to pulmonary C-fiber stimulation is a cessation of diaphragmatic contractions rather than rapid shallow contractions.

scholarly journals Reflex cardiorespiratory events from esophageal origin are heightened by preterm birth

2017 ◽  
Vol 123 (2) ◽  
pp. 489-497 ◽  
Author(s):  
Stéphanie Nault ◽  
Nathalie Samson ◽  
Charlène Nadeau ◽  
Djamal Djeddi ◽  
Jean-Paul Praud
Keyword(s):  
Preterm Birth ◽  
Arterial Pressure ◽  
Random Order ◽  
Neonatal Infection ◽  
Full Term ◽  
Simultaneous Stimulation ◽  
C Fibers ◽  
C Fiber ◽  
Cardiorespiratory Reflexes ◽  
Stimulation Of

The involvement of gastroesophageal refluxes in cardiorespiratory events of preterm infants remains controversial. While a few studies in full-term newborn animals have shown that stimulation of esophageal receptors leads to cardiorespiratory reflexes, the latter remain largely unknown, especially after premature birth. The present study aimed to 1) characterize the cardiorespiratory reflexes originating from esophageal receptors in newborn lambs and 2) test the hypotheses that preterm birth enhances reflex cardiorespiratory inhibition and that C-fibers are involved in these reflexes. Eight full-term lambs and 10 lambs born 14 days prematurely were studied. Following surgical instrumentation, a 6-h polysomnography was performed without sedation to record electrocardiogram, respiratory movements, arterial pressure, laryngeal constrictor muscle activity, state of alertness, and hemoglobin oxygen saturation. Five esophageal stimulations of the upper and/or lower esophagus, including rapid balloon inflation and/or HCl injection, were performed in random order. A second recording was performed in full-term lambs 24 h later, after C-fiber blockade by capsaicin. Results confirmed that esophageal stimulations induced inhibitory cardiorespiratory reflexes combined with protective mechanisms, including laryngeal closure, swallowing, coughing, increased arterial pressure, and arousal. Preterm birth heightened cardiorespiratory inhibition. The strongest cardiorespiratory inhibition was observed following simultaneous stimulation of the lower and upper esophagus. Finally, cardiorespiratory inhibition was decreased after C-fiber blockade. In conclusion, esophageal stimulation induces inhibitory cardiorespiratory reflexes, which are partly mediated by C-fibers and more pronounced in preterm lambs. Clinical relevance of these findings requires further studies, especially in conditions associated with increased cardiorespiratory events, e.g., neonatal infection. NEW & NOTEWORTHY Preterm birth heightens the cardiorespiratory events triggered by esophageal stimulation. The most extensive cardiorespiratory events are induced by simultaneous stimulation of the proximal and distal esophagus.

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