Studies of reflexogenic effects of capsaicin and neuropeptides on neural afferents in the dog parietal pericardium

Staszewska-Woolley, Janina; Nolan, P.N.; Luk, Denise E.

doi:10.1016/0143-4179(91)90131-2

Cited by 7 publications

(7 citation statements)

References 31 publications

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“…In fact when the chemoceptive reflex was triggered by capsaicin, indomethacin was ineffective, as previously observed for other kinds of capsaicin-induced reflexes (Staszewska-Woolley et al, 1991). These results also indicate that the excitatory effect of BK and that of capsaicin are produced on the same population of bladder afferents through different mechanisms as established for the activation of intracellular effectors by these agents on sensory neurones in culture (Dray et al, 1988a).…”

Section: Discussionsupporting

confidence: 63%

Pharmacological analysis of the local and reflex responses to bradykinin on rat urinary bladder motility in vivo

Lecci

Giuliani

Meini

et al. 1995

British J Pharmacology

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1 The topical application of bradykinin (BK) (0.05-5000 pmol/rat) onto the serosal surface of the urinary bladder in urethane-anaesthetized rats, evoked low amplitude tonic contractions (not exceeding 25 mmHg) or high amplitude (about 50 mmHg), phasic reflex contractions (chemoceptive micturition reflex) which were abolished by bilateral ablation of the pelvic ganglia. In ganglionectomized rats, BK induced only a local, tonic-type contraction.2 Systemic capsaicin pretreatment (164 jmol kg-', 4 days before) reduced the incidence of chemoceptive reflex induced by BK (500 pmol/rat) but had no effect on the magnitude of the tonic-type contraction elicited by BK in ganglionectomized rats. Indomethacin (1 I mol kg-', 20 min before) reduced the incidence but not the amplitude of the reflex contractions induced by topical application of BK (500 pmol/rat). In ganglionectomized rats, indomethacin (1 IlAmol kg-', 20 min before) decreased the amplitude of the tonic contraction evoked by BK. Indomethacin did not affect the chemoceptive reflex induced by topical application of capsaicin (15 nmol/rat) onto the bladder. 3 Intrathecal administration of the tachykinin NK, receptor antagonists, RP 67,580 (10 nmol/rat) or SR 140,333 (10 nmol/rat), abolished the chemoceptive reflex induced by BK without modifying the magnitude of the tonic contraction. SR 140,333 (10 nmol/rat) also abolished the occurrence of the chemoceptive reflex induced by capsaicin. 4 Intravenous administration of the B2 receptor antagonist, Hoe 140 (35 nmol kg-', 10 min before) abolished the reflex and local effects induced by BK on bladder motility but failed to modify the chemoceptive reflex induced by topical application of capsaicin (15 nmol/rat). 5 Intrathecal administration of Hoe 140 (10 nmol/rat) reduced the incidence of the chemoceptive reflex induced by BK but had no effect on the amplitude of the local motor response. Likewise, Hoe 140 (10 nmol/rat, i.t.) reduced the incidence of reflex bladder contractions induced by topical application of capsaicin (15 nmol/rat) without affecting the magnitude of the tonic-type contraction. 6 These findings indicate that BK stimulates motility through B2 receptors in the rat urinary bladder. BK activates the reflex response by stimulating capsaicin-sensitive afferent nerves with a contribution from prostanoids. At the spinal cord level, tachykinin NK, and BK B2 receptors could also be involved in the chemoceptive reflex induced by BK or capsaicin.

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Section: Discussionsupporting

confidence: 63%

Pharmacological analysis of the local and reflex responses to bradykinin on rat urinary bladder motility in vivo

Lecci

Giuliani

Meini

et al. 1995

British J Pharmacology

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“…Our previous [28] and present studies all found that the expression of CGRP in the hearts of diabetic mice was significantly lower than that in the non-diabetic hearts, which is in agreement with previous reports showing that rat sensory dorsal root ganglia (DRG) neurons respond to STZ-induced diabetes with decreased expression of the precursor of CGRP [29]. Moreover, a reduction in the CGRP mRNA has been reported in the DRG of diabetic rats along with reduced levels of sciatic nerve CGRP-like immunoreactivity [30]. It is noteworthy that, aside from the effect on CGRP, the degeneration of sensory nerves induced by DM is a quite nonspecific change that involves decreased expression of TRPV1 and other neuropeptides in the heart [18].…”

Section: Discussionsupporting

confidence: 83%

Up-regulation of calcitonin gene-related peptide protects streptozotocin-induced diabetic hearts from ischemia/reperfusion injury

Zheng

Han

Yao

et al. 2012

International Journal of Cardiology

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“…Bilateral vagotomy and systemic administration of atropine do not attenuate pressor responses and tachycardia when BK is applied to the heart (31). In a study conducted in dogs, bilateral sectioning of the upper thoracic (T1-T4) white rami communicantes and stellectomy, but not vagotomy, eliminates the dose-related pressor effects and tachycardia to local application of CAP to the parietal pericardium (36). These results suggest that the excitatory afferent effects on thoracic neurons of epicardial BK and CAP are likely to result from the stimulation of cardiac sympathetic, CAP-sensitive, primary afferents.…”

Section: Discussionmentioning

confidence: 94%

“…Intrapericardial injections of RTX desensitized cardiac sympathetic afferent fibers but not the somatic afferent fibers that converged onto the same spinal neurons. Investigators in previous studies administered large systemic doses of CAP or RTX to neonatal rats (15,33) or adult rats (24,36) to permanently deplete TRPV1-expressing afferent neurons and fibers. This protocol destroys both somatic and visceral CAP-sensitive afferent fibers.…”

Section: Discussionmentioning

confidence: 99%

Responses of thoracic spinal neurons to activation and desensitization of cardiac TRPV1-containing afferents in rats

Qin¹,

Farber²,

Miller³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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-The purpose of this study was to examine how upper thoracic spinal neurons responded to activation and desensitization of cardiac transient receptor potential vanilloid-1 (TRPV1)-containing afferent fibers. Extracellular potentials of single T3 spinal neurons were recorded in pentobarbital-anesthetized, paralyzed, and ventilated male rats. To activate cardiac nociceptive receptors, a catheter was placed in the pericardial sac to administer various chemicals: bradykinin (BK; 10 g/ml, 0.2 ml), capsaicin (CAP, 10 g/ml, 0.2 ml), or a mixture of algesic chemicals (AC; 0.2 ml) containing adenosine 10 Ϫ3 M, BK, serotonin, histamine, and PGE2, 10 Ϫ5 M for each. Spinal neurons that responded to intrapericardial BK and/or CAP were used in this study. Results showed that 81% (35/43) of the neurons had excitatory responses to both intrapericardial BK and CAP, and the remainder responded to either BK or CAP. Intrapericardial resiniferatoxin (RTX) (0.2 g/ml, 0.2 ml, 1 min), which desensitizes TRPV1-containing nerve endings, abolished excitatory responses to both BK (n ϭ 8) and CAP (n ϭ 7), and to AC (n ϭ 5) but not to somatic stimuli. Intrapericardial capsazepine (1 mg/ml, 0.2 ml, 3 min), a specific antagonist of TRPV1, sharply attenuated excitatory responses to CAP in 5/5 neurons, but responses to BK in 5/5 neurons was maintained. Additionally, intrapericardial capsazepine had no significant effect on excitatory responses to AC in 3/3 neurons. These data indicated that intrapericardial BK-initiated spinal neuronal responses were linked to cardiac TRPV1-containing afferent fibers, but were not dependent on TRPV1. Intraspinal signaling for cardiac nociception was mediated through CAP-sensitive afferent fibers innervating the heart. bradykinin; capsaicin; resiniferatoxin; sympathetic afferent; vagal afferent MYOCARDIAL ISCHEMIA RELEASES several metabolites, including bradykinin (BK) and protons, which activate cardiac chemosensitive and mechanoreceptive receptors and elicit angina pectoris and cardiovascular responses (8 -14, 39). Physiological and pharmacological studies show that BK activates cardiac nociceptors and sympathoexcitatory responses via kinin B2 receptors located in thinly myelinated A␦ and unmyelinated C-fiber afferent endings in the heart (1,23,39,40). The afferent fibers transmitting the action potentials enter the upper thoracic spinal cord where spinal neurons, spinothalamic tract cells, spinoreticular tract, and other ascending pathway neurons process this information (2-6, 27). However, the signaling mechanisms involved in detection of myocardial ischemia and activation of cardiac sympathetic or spinal afferent nerve endings are not fully known.Recently, it has been suggested that the transient receptor potential vanilloid-1 (TRPV1), an important nonspecific cation channel activated by capsaicin (CAP), noxious heat, and protons, also is involved in the production of angina pectoris associated with myocardial ischemia (25). TRPV1-expressing afferent nerves are widely distributed on the epicardial surface of...

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Studies of reflexogenic effects of capsaicin and neuropeptides on neural afferents in the dog parietal pericardium

Cited by 7 publications

References 31 publications

Pharmacological analysis of the local and reflex responses to bradykinin on rat urinary bladder motility in vivo

Pharmacological analysis of the local and reflex responses to bradykinin on rat urinary bladder motility in vivo

Up-regulation of calcitonin gene-related peptide protects streptozotocin-induced diabetic hearts from ischemia/reperfusion injury

Responses of thoracic spinal neurons to activation and desensitization of cardiac TRPV1-containing afferents in rats

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