scholarly journals Cardiovascular responses elicited by a new endogenous angiotensin in the nucleus tractus solitarius of the rat

2011 ◽  
Vol 300 (1) ◽  
pp. H230-H240 ◽  
Author(s):  
Vineet C. Chitravanshi ◽  
Hreday N. Sapru
Keyword(s):  
Nucleus Tractus Solitarius ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Vagus Nerves ◽  
Medial Nucleus ◽  
Male Wistar Rats ◽  
Bilateral Vagotomy ◽  
Prior Application ◽  
Greater Splanchnic Nerve

Cardiovascular effects of angiotensin-(1–12) [ANG-(1–12)] were studied in the medial nucleus of the tractus solitarius (mNTS) in anesthetized, artificially ventilated, adult male Wistar rats. Microinjections (100 nl) of ANG-(1–12) (0.06 mM) into the mNTS elicited maximum decreases in mean arterial pressure (MAP; 34 ± 5.8 mmHg) and heart rate (HR; 39 ± 3.7 beats/min). Bilateral vagotomy abolished ANG-(1–12)-induced bradycardia. Efferent greater splanchnic nerve activity was decreased by microinjections of ANG-(1–12) into the mNTS. Blockade of ANG type 1 receptors (AT1Rs; using ZD-7155 or L-158,809), but not ANG type 2 receptors (AT2Rs; using PD-123319), significantly attenuated ANG-(1–12)-induced cardiovascular responses. Simultaneous inhibition of both angiotensin-converting enzyme (ACE; using captopril) and chymase (using chymostatin) completely blocked the effects of ANG-(1–12). Microinjections of A-779 [ANG-(1–7) antagonist] did not attenuate ANG-(1–12)-induced responses. Pressure ejection of ANG-(1–12) (0.06 mM, 2 nl) caused excitation of barosensitive mNTS neurons, which was blocked by prior application of the AT1R antagonist. ANG-(1–12)-induced excitation of mNTS neurons was also blocked by prior sequential applications of captopril and chymostatin. These results indicate that 1) microinjections of ANG-(1–12) into the mNTS elicited depressor and bradycardic responses by exciting barosensitive mNTS neurons; 2) the decreases in MAP and HR were mediated via sympathetic and vagus nerves, respectively; 3) AT1Rs, but not AT2Rs, mediated these actions of ANG-(1–12); 4) the responses were mediated via the conversion of ANG-(1–12) to ANG II and both ACE and chymase were involved in this conversion; and 5) ANG-(1–7) was not one of the metabolites of ANG-(1–12) in the mNTS.

scholarly journals The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1–12) and angiotensin II

2011 ◽  
Vol 300 (3) ◽  
pp. H951-H960 ◽  
Author(s):  
Hideki Arakawa ◽  
Vineet C. Chitravanshi ◽  
Hreday N. Sapru
Keyword(s):  
Arcuate Nucleus ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Induced Responses ◽  
Ang Ii ◽  
Vagus Nerves ◽  
Hypothalamic Arcuate Nucleus ◽  
Male Wistar Rats ◽  
Bilateral Vagotomy ◽  
Greater Splanchnic Nerve

The hypothalamic arcuate nucleus (ARCN) has been reported to play a significant role in cardiovascular regulation. It has been hypothesized that the ARCN may be one of the sites of cardiovascular actions of angiotensins (ANGs). Experiments were carried out in urethane-anesthetized, artificially ventilated, adult male Wistar rats. The ARCN was identified by microinjections of N-methyl-d-aspartic acid (NMDA; 10 mM). Microinjections (50 nl) of ANG-(1–12) (1 mM) into the ARCN elicited increases in mean arterial pressure (MAP), heart rate (HR), and greater splanchnic nerve activity (GSNA). The tachycardic responses to ANG-(1–12) were attenuated by bilateral vagotomy. The cardiovascular responses elicited by ANG-(1–12) were attenuated by microinjections of ANG II type 1 receptor (AT1R) antagonists but not ANG type 2 receptor (AT2R) antagonist. Combined inhibition of ANG-converting enzyme (ACE) and chymase in the ARCN abolished ANG-(1–12)-induced responses. Microinjections of ANG II (1 mM) into the ARCN also increased MAP and HR. Inhibition of ARCN by microinjections of muscimol (1 mM) attenuated the pressor and tachycardic responses to intravenously administered ANG-(1–12) and ANG II (300 pmol/kg each). These results indicated that 1) microinjections of ANG-(1–12) into the ARCN elicited increases in MAP, HR, and GSNA; 2) HR responses were mediated via both sympathetic and vagus nerves; 3) AT1Rs, but not AT2Rs, in the ARCN mediated ANG-(1–12)-induced responses; 4) both ACE and chymase were needed to convert ANG-(1–12) to ANG II in the ARCN; and 5) ARCN plays a role in mediating the cardiovascular responses to circulating ANGs.

scholarly journals Cardiovascular responses to microinjections of urocortin 3 into the nucleus tractus solitarius of the rat

2009 ◽  
Vol 296 (2) ◽  
pp. H325-H332 ◽  
Author(s):  
Takeshi Nakamura ◽  
Kazumi Kawabe ◽  
Hreday N. Sapru
Keyword(s):  
Nucleus Tractus Solitarius ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Artificial Cerebrospinal Fluid ◽  
Peptide Family ◽  
Male Wistar Rats ◽  
Bilateral Vagotomy ◽  
Urocortin 3 ◽  
Greater Splanchnic Nerve

Urocortin 3 (Ucn3) is a new member of the corticotropin-releasing factor (CRF) peptide family and is considered to be a specific and endogenous ligand for CRF type 2 receptors (CRF2Rs). The presence of CRF2Rs has been reported in the nucleus tractus solitarius (NTS) of the rat. It was hypothesized that the activation of CRF2Rs in the medial NTS (mNTS) may play a role in cardiovascular regulation. This hypothesis was tested in urethane-anesthetized, artificially ventilated, adult male Wistar rats. Microinjections (100 nl) of Ucn3 (0.03, 0.06, 0.12, and 0.25 mM) into the mNTS of anesthetized rats elicited decreases in mean arterial pressure (MAP: 5.0 ± 1.0, 21.6 ± 2.6, 20.0 ± 2.8, and 12.7 ± 3.4 mmHg, respectively) and heart rate (HR: 7.8 ± 2.6, 46.2 ± 9.3, 34.5 ± 8.4, and 16.6 ± 4.9 beats/min, respectively). Microinjections of artificial cerebrospinal fluid (100 nl) into the mNTS did not elicit cardiovascular responses. Maximum decreases in MAP and HR were elicited by 0.06 mM concentration of Ucn3. Cardiovascular responses to Ucn3 were similar in unanesthetized midcollicular decerebrate rats. A bilateral vagotomy completely abolished Ucn3-induced bradycardia. The decreases in MAP and HR elicited by Ucn3 (0.06 mM) were completely blocked by astressin (1 mM; nonselective CRFR antagonist) and K41498 (5 mM; selective CRF2R antagonist). Microinjections of Ucn3 (0.06 mM) into the mNTS decreased the efferent greater splanchnic nerve activity. After the blockade of CRF2Rs in the mNTS, a Ucn3-induced decrease in the efferent sympathetic nerve discharge was abolished. These results indicate that Ucn3 microinjections into the mNTS exerted excitatory effects on the mNTS neurons via CRF2Rs, leading to depressor and bradycardic responses.

scholarly journals Cardiovascular responses to microinjections of urocortins into the NTS: role of inotropic glutamate receptors

2009 ◽  
Vol 296 (6) ◽  
pp. H2022-H2029 ◽  
Author(s):  
Takeshi Nakamura ◽  
Hreday N. Sapru
Keyword(s):  
Glutamate Receptors ◽  
Nucleus Tractus Solitarius ◽  
Cardiovascular Responses ◽  
New Members ◽  
Corticotrophin Releasing Factor ◽  
Affinity Ligand ◽  
Medial Nucleus ◽  
Peptide Family ◽  
Male Wistar Rats ◽  
Afferent Terminals

Urocortin 1 (Ucn1) and urocortin 3 (Ucn3) are new members of the corticotrophin-releasing factor (CRF) peptide family. Ucn1 is a ligand for both the CRF type 1 receptors (CRF1Rs) and the CRF type 2 receptors (CRF2Rs), whereas Ucn3 is a high-affinity ligand for the CRF2Rs. Recently, we reported that Ucn3 microinjections into the medial nucleus tractus solitarius (mNTS) elicit decreases in mean arterial pressure (MAP) and heart rate (HR) (Nakamura T, Kawabe K, Sapru HN. Am J Physiol Heart Circ Physiol 296: H325–H332, 2009). The presence of CRF2Rs on afferent terminals has been reported in the mNTS of the rat. It was hypothesized that activation of CRF2Rs on afferent terminals in the mNTS may release glutamate, which, in turn, may elicit decreases in MAP and HR via activation of ionotropic glutamate receptors (iGLURs). This hypothesis was tested in urethane-anesthetized, artificially ventilated, adult male Wistar rats. Microinjections (100 nl) of Ucn1 (0.12 mM) into the mNTS elicited decreases in MAP and HR. The responses were partially blocked by microinjections of iGLUR antagonists into the mNTS. On the other hand, the decreases in MAP and HR elicited by microinjections of Ucn3 (0.06 mM) into the mNTS were completely blocked by microinjections of iGLUR antagonists into the mNTS. These results indicate that activation of CRF2Rs in the mNTS, by Ucn1 and Ucn3, releases glutamate, which, in turn, elicits decreases in MAP and HR via activation of iGLURs.

scholarly journals Cardiovascular effect of angiotensin-(1–12) in the caudal ventrolateral medullary depressor area of the rat

2014 ◽  
Vol 306 (3) ◽  
pp. H438-H449 ◽  
Author(s):  
Tetsuya Kawabe ◽  
Kazumi Kawabe ◽  
Hreday N. Sapru
Keyword(s):  
Gaba Receptors ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Ang Ii ◽  
Nerve Activity ◽  
Intravenous Injections ◽  
Male Wistar Rats ◽  
Greater Splanchnic Nerve

Angiotensin (ANG)-(1–12) excites neurons via ANG II type 1 receptors (AT1Rs), which are present in the caudal ventrolateral medullary depressor area (CVLM). We hypothesized that microinjections of ANG-(1–12) into the CVLM may elicit decreases in mean arterial pressure (MAP), heart rate (HR), and sympathetic nerve activity. This hypothesis was tested in urethane-anesthetized adult male Wistar rats. Microinjections of ANG-(1–12) into the CVLM elicited decreases in MAP, HR, and greater splanchnic nerve activity (GSNA). ANG-(1–12)-induced responses consisted of initial (first 1–8 min) and delayed (8–24 min) phases. Prior microinjections of losartan, A-779, and captopril into the CVLM blocked initial, delayed, and both phases of ANG-(1–12) responses, respectively. Blockade of GABA receptors in the rostral ventrolateral medullary pressor area (RVLM) attenuated cardiovascular responses elicited by microinjections of ANG-(1–12) into the ipsilateral CVLM. Microinjections of ANG-(1–12) into the CVLM potentiated the reflex decreases and attenuated the reflex increases in GSNA elicited by intravenous injections of phenylephrine and sodium nitroprusside, respectively. These results indicate that microinjections of ANG-(1–12) into the CVLM elicit decreases in MAP, HR, and GSNA. Initial and delayed phases of these responses are mediated via ANG II and ANG-(1–7), respectively; the effects of ANG II and ANG-(1–7) are mediated via AT1Rs and Mas receptors, respectively. Captopril blocked both phases of ANG-(1–12) responses, indicating that angiotensin-converting enzyme is important in mediating these responses. GABA receptors in the RVLM partly mediate the cardiovascular responses to microinjections of ANG-(1–12) into the CVLM. Microinjections of ANG-(1–12) into the CVLM modulate baroreflex responses.

Responses of ferret lower esophageal sphincter to 5-hydroxytryptamine: pathways and receptor subtypes

1995 ◽  
Vol 268 (6) ◽  
pp. G1004-G1011 ◽  
Author(s):  
L. A. Blackshaw ◽  
V. Nisyrios ◽  
J. Dent
Keyword(s):  
Lower Esophageal Sphincter ◽  
Splanchnic Nerve ◽  
Lower Esophageal Sphincter Pressure ◽  
Receptor Subtypes ◽  
Sphincter Pressure ◽  
In Series ◽  
Bilateral Vagotomy ◽  
Excitatory Component ◽  
Esophageal Sphincter ◽  
Greater Splanchnic Nerve

In urethananesthetized ferrets, basal lower esophageal sphincter pressure (LESP) was unaffected by the 5-hydroxytryptamine3 (5-HT3) receptor antagonist granisetron (0.5 mg/kg) or by greater splanchnic nerve section (GSX), but increased after bilateral vagotomy. Peripheral vagal nerve stimulation caused LES relaxation, often followed by a brief contraction and a prolonged inhibition of LESP. Close intra-arterial injection of 5-HT (5-100 micrograms) had a biphasic effect on LESP, with a brief drop followed by a prolonged increase. Granisetron (0.5 mg/kg i.v.) abolished the initial relaxation and revealed an earlier peak of excitation. This was not influenced by subsequent vagotomy and GSX. In a series of eight additional experiments (series 2), granisetron was given after vagotomy and GSX. In series 2, 5-HT-induced relaxation was unaffected by vagotomy but was significantly reduced after GSX and was further reduced after granisetron, indicating that 5-HT3 receptor mechanisms may lie on a sympathetic neural pathway. Vagotomy had no effect on the excitatory component. GSX had no effect on the amplitude of excitation, but reduced its latency. Granisetron had no further effect on excitation in series 2. In a separate series of 13 experiments (series 3), the excitatory component of the LES response to 5-HT was abolished by ketanserin (2.5 mg/kg i.v.) , after which only relaxation occurred. Both 5-HT2 and 5-HT3 antagonists in combination abolished all effects of 5-HT on LESP. Atropine (400 micrograms/kg i.v., n = 7) had no effect on 5-HT-induced LES responses.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Cardiovascular regulation and expressions of NO synthase-tyrosine hydroxylase in nucleus tractus solitarius of ovine fetus

2003 ◽  
Vol 284 (4) ◽  
pp. H1057-H1063 ◽  
Author(s):  
Sheng-Xing Ma ◽  
Qun Fang ◽  
Brian Morgan ◽  
Michael G. Ross ◽  
Conrad R. Chao
Keyword(s):  
Blood Pressure ◽  
Tyrosine Hydroxylase ◽  
Arterial Blood Pressure ◽  
Nucleus Tractus Solitarius ◽  
Cardiovascular Responses ◽  
No Synthase ◽  
No Donor ◽  
Fetal Sheep ◽  
Medial Nucleus ◽  
Arterial Blood

The purpose of this study was to examine cardiovascular responses to fourth cerebral ventricle (4V) administration of nitroglycerin (NTG) or an inhibitor of nitric oxide (NO) synthase (NOS) in the near-term ovine and to determine whether, during birth, neuronal NOS (nNOS) is induced in noradrenergic A1 neurons in the medial nucleus tractus solitarius (mNTS). In chronically instrumented fetal sheep, 4V injection of NTG (1.2 nmol), an NO donor, produced an arterial blood depressor and a moderate decrease in heart rate. Arterial blood pressure is increased by 4V administration of N G-nitro-l-arginine methyl ester (10 nmnol), an inhibitor of NOS, in fetuses. Sections of the medulla from fetuses and newborn lambs were examined by using immunolabeling with tyrosine hydroxylase (TH) antibody combined with NADPH diaphorase (NADPHd) histochemistry, a marker of nNOS activity. The NADPHd-positive cells and TH-positive cells containing NADPHd reactivity were significantly increased in the mNTS of newborns compared with the fetuses. The results suggest that during birth, there is upregulation of NADPHd/nNOS in the noradrenergic neurons of mNTS resulting in a centrally mediated reduction of fetal arterial blood pressure.

Noradrenergic and neuropeptide Y mechanisms in guanethidine-sympathectomized rats

1990 ◽  
Vol 259 (2) ◽  
pp. R371-R375
Author(s):  
E. E. Benarroch ◽  
J. D. Schmelzer ◽  
K. K. Ward ◽  
D. K. Nelson ◽  
P. A. Low
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Vagus Nerves ◽  
Adult Rats ◽  
Peripheral Tissues ◽  
Cardiovascular Tissue ◽  
Potential Marker ◽  
Pressor Responses ◽  
Cervical Ganglion

The cardiovascular responses to sympathomimetic agents, the norepinephrine (NE) content in peripheral tissues, and the tissue content and cardiovascular effects of neuropeptide Y (NPY) were examined in anesthetized adult rats with guanethidine-induced sympathectomy (GuSx). We observed blunted pressor responses to tyramine, exaggerated pressor responses to phenylephrine, and markedly reduced NE contents in the atrium, femoral artery, superior cervical ganglion (SCG), and sciatic and vagus nerves. When tyramine responses were corrected for the NE content in the SCG, GuSx rats were similar to controls. A depletion of NPY levels in tissue resulted in an increased sensitivity to the pressor effects of intravenous NPY administration. GuSx, therefore, reproduces findings of postganglionic adrenergic failure in humans. Responses to the administration of sympathomimetic agents may reflect the degree of noradrenergic denervation. NPY may be a potential marker of chronic postganglionic sympathetic denervation in cardiovascular tissue.

Mechanism of cardiovascular effects of nociceptin microinjected into the nucleus tractus solitarius of the rat

2005 ◽  
Vol 288 (6) ◽  
pp. R1553-R1562 ◽  
Author(s):  
Vineet C. Chitravanshi ◽  
Hreday N. Sapru
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Nucleus Tractus Solitarius ◽  
Cardiovascular Effects ◽  
Gabaergic Neurons ◽  
Receptor Antagonists ◽  
Orl1 Receptor ◽  
Medial Nucleus

Microinjections (100 nl) of 0.15, 0.31, 0.62, and 1.25 mmol/l of nociceptin into the medial nucleus tractus solitarius (mNTS) elicited decreases in mean arterial pressure (11 ± 1.8, 20 ± 2.1, 21.5 ± 3.1, and 15.5 ± 1.9 mmHg, respectively) and heart rate (14 ± 2.7, 29 ± 5.5, 39 ± 5.2, and 17.5 ± 3.1 beats/min, respectively). Because maximal responses were elicited by microinjections of 0.62 mmol/l nociceptin, this concentration was used for other experiments. Repeated microinjections of nociceptin (0.62 mmol/l) into the mNTS, at 20-min intervals, did not elicit tachyphylaxis. Bradycardia induced by microinjections of nociceptin into the mNTS was abolished by bilateral vagotomy. The decreases in mean arterial pressure and heart rate elicited by nociceptin into the mNTS were blocked by prior microinjections of the specific ORL1-receptor antagonist [N-Phe1]-nociceptin-(1–13)-NH2 (9 mmol/l). Microinjections of the ORL1-receptor antagonist alone did not elicit a response. Prior combined microinjections of GABAA and GABAB receptor antagonists (2 mmol/l gabazine and 100 mmol/l 2-hydroxysaclofen, respectively) into the mNTS blocked the responses to microinjections of nociceptin at the same site. Prior microinjections of ionotropic glutamate receptor antagonists (2 mmol/l NBQX and 5 mmol/l d-AP7) also blocked responses to nociceptin microinjections into the mNTS. These results were confirmed by direct neuronal recordings. It was concluded that 1) nociceptin inhibits GABAergic neurons in the mNTS, 2) GABAergic neurons may normally inhibit the release of glutamate from the terminals of peripheral afferents in the mNTS, and 3) inhibition of GABAergic neurons by nociceptin results in an increase in the release of glutamate in the mNTS, which in turn elicits depressor and bradycardic responses via activation of ionotropic glutamate receptors on secondary mNTS neurons.

Greater splanchnic excitation of primate T1-T5 spinothalamic neurons

1984 ◽  
Vol 51 (3) ◽  
pp. 592-603 ◽  
Author(s):  
W. S. Ammons ◽  
R. W. Blair ◽  
R. D. Foreman
Keyword(s):  
Electrical Stimulation ◽  
Cell Activation ◽  
Receptive Fields ◽  
Splanchnic Nerve ◽  
Inhibitory Effect ◽  
Sympathetic Stimulation ◽  
Bilateral Vagotomy ◽  
Somatic Receptive Fields ◽  
Greater Splanchnic Nerve ◽  
Stimulation Of

Effects of electrical stimulation of the left greater splanchnic nerve (SPL) on T1-T5 spinothalamic (STT) neurons were determined. Eighty-five STT neurons were studied in 36 anesthetized monkeys (Macaca fascicularis). All neurons were excited by manipulation of their somatic receptive fields and by electrical stimulation of cardiopulmonary (CP) sympathetic afferent fibers. SPL stimulation excited 63 (74%) STT neurons. There was an increasing percentage of cells with SPL input at more caudal segments and in deeper laminae. Both SPL and CP sympathetic stimulation elicited early or both early and late responses. Latencies to cell activation were usually shorter for CP sympathetic stimulation than for SPL stimulation (5.4 +/- 0.8 versus 11.3 +/- 2.0 ms for early responses and 44.2 +/- 4.2 versus 111.0 +/- 6.6 ms for late responses). The maximum number of spikes per SPL or CP sympathetic stimulus was determined. In the T2 and T3 segments, early responses to CP sympathetic stimulation were significantly greater. However, at more caudal segments, responses to CP sympathetic input decreased while responses to SPL input increased until at T4 there was no difference in the two responses. In T5, responses to SPL input were greater. No differences in the magnitudes of late responses were observed in any of the segments. The response of six cells to SPL stimulation was inhibited by a train of conditioning stimuli applied to the left thoracic vagus nerve. Maximum inhibition occurred at a CT interval of 50 ms and test responses were significantly reduced at CT intervals as great as 200 ms. Bilateral vagotomy eliminated the inhibitory effect. Cutting the left sympathetic chain between the T5 and T6 rami communicantes eliminated 27% of the response to SPL stimulation. More caudal cuts reduced the response further until 71% of the response was abolished by a cut between T8 and T9. Lesions in the dorsolateral column of the spinal cord had little effect on the responses, while lesions of the lateral and ventrolateral columns reduced or abolished the responses. We conclude that SPL stimulation excites T1-T5 STT neurons by way of extraspinal and intraspinal pathways. SPL information is integrated with information from a variety of other visceral and somatic sources. SPL input to cells with somatic fields in the chest region may explain the clinical phenomenon of chest pain associated with abdominal disorders.

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