Inhibition of antidromic and substance P‐induced vasodilatation by a substance P antagonist

Rosell, Sune; Olgart, Leif; Gazelius, Bertil; Panopoulos, Panagiotis; Folkers, Karl; Hörig, Joachim

doi:10.1111/j.1748-1716.1981.tb06752.x

Cited by 142 publications

(23 citation statements)

References 8 publications

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“…Baccaglini-and Hogan in the rat saphenous nerve release one or more compounds that can produce local inflammatory changes in the surrounding tissue (42). Substance P is currently considered the most likely mediator of this neurogenic inflammation (43)(44)(45). However, it remains possible that some unmyelinated pain fibers contain and release other peptides, either alone or together with substance P.…”

Section: Neuronsmentioning

confidence: 99%

Some rat sensory neurons in culture express characteristics of differentiated pain sensory cells.

Baccaglini¹,

Hogan²

1983

Proc. Natl. Acad. Sci. U.S.A.

186

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Sensory neurons were dissociated from trigeminal ganglia or from dorsal root ganglia of rats, grown in culture, and examined for expression of properties of pain sensory cells. Many sensory neurons in culture are excited by low concentrations of capsaicin, reportedly a selective stimulus for pain sensory neurons. Many are excited by bradykinin, sensitized by prostaglandin E2, or specifically stained by an antiserum against substance P.These experiments provide a basis for the study of pain mechanisms in cell culture.Pain sensory neurons have been identified as a distinct class of sensory neurons in mammals (1-4). Pain sensory endings are activated or sensitized by painful mechanical stimulation, by painful heat, and by compounds that are released locally in damaged tissue (1,5,6). Bradykinin, prostaglandins, and amines are among the compounds that have been shown to activate or sensitize pain endings and are thought to have a role in the pain associated with injury and inflammation (5, 6).The action of these compounds on sensory endings has been studied in experimental animals (7-14), but the studies have encountered technical limitations. A major limitation is that the mechanisms that underlie excitation or sensitization ofpain sensory endings are not accessible to biophysical measurements. Other limitations are that the concentration of bradykinin, prostaglandins, or amines at the sensory endings is not accurately known; and that each of these compounds produces inflammatory changes in the tissue as well as release of other mediators, so that its actions are not evaluated in isolation. These difficulties would be alleviated if differentiated pain sensory neurons could be studied in cell culture. This alternative approach would allow more detailed pharmacological, biophysical, and biochemical studies of pain sensory neurons.As a first step toward the study ofpain mechanisms in culture, we have tested whether some characteristics of pain sensory neurons are expressed by sensory neurons in culture. We find that sensory cells grown in the absence of other cells express sensitivity to capsaicin (8-methyl-N-vanillyl-6-nonenamide), a property restricted to unmyelinated pain sensory fibers in adult animals (15-18), and in addition express other properties (7,8,10,11,19) of differentiated pain sensory neurons. METHODS Cell Culture. The portion of the trigeminal ganglion associated with the mandibular nerve was dissected from newborn rats (CD strain; Charles River Breeding Laboratories) and the cells were dissociated by treatment with dispase (grade 2; Boehringer Mannheim) and collagenase (type I; Worthington). Cells were plated on islands of collagen less than 1 mm in diameter (20) and grown in a modified L-15-CO2 growth medium (21) from which methocel and bovine serum albumin were omitted and in which glucose, penicillin, and streptomycin concentrations were reduced by half. Cultures were treated with 10 tkM 1-f3-D-arabinofuranosylcytosine (cytosine arabinoside) during the 4 days after plating to minimize gro...

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Section: Neuronsmentioning

confidence: 99%

Some rat sensory neurons in culture express characteristics of differentiated pain sensory cells.

Baccaglini¹,

Hogan²

1983

Proc. Natl. Acad. Sci. U.S.A.

186

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“…Antidromic trigeminal nerve stimulation has been shown to cause SP release from nerve terminals in the dental pulp (8,9) and eye (10). Furthermore, it has been shown that the antidromic vasodilation in the pulp (11) and the inflammation in the eye on IR irradiation (12) can be inhibited by SP antagonists. Recent studies suggest that capsaicin-sensitive sensory nerves of vagal origin can induce neurogenic inflammation and bronchoconstriction in the respiratory tract (13,14).…”

mentioning

confidence: 99%

A substance P antagonist inhibits vagally induced increase in vascular permeability and bronchial smooth muscle contraction in the guinea pig

Saria

Brodin

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

373

149

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“…In earlier both in vivo (Maggie et al, 1985(Maggie et al, , 1986) and in vitro (Erspamer et al, 1981;Sj6gren et al, 1982) studies similar excitatory motor effects of SP were demonstrated. The motor response of the bladder to SP observed in this study is suggested to be specific for the peptide, since the SP-analogue (D-Pro 2, D-Trp 7' 9)-SP, known to block SP-receptors Leander et al, 1981;Rosell et al, 1981), almost completely inhibited contraction. Furthermore, the bladder contraction induced by electrical stimulation of the preganglionic pelvic nerves was significantly reduced by high doses of the SP-analogue infused regionally via the superior vesical artery.…”

Section: Discussionmentioning

confidence: 82%

In vivo motor effects of substance P on the rat urinary bladder

Berggren

Ahlman

Dahlström³

et al. 1988

J. Neural Transmission

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Intravesical pressure recordings of the urinary bladder in anesthetized rats were performed and the role of substance P (SP) in the motor control of this organ was evaluated. Regional injection of SP (0.4 nmoles i.a.) into the superior vesical artery elicited a prompt bladder contraction; this motor response was dosedependent. The detrusor contraction could be completely inhibited by a SP-analogue, (D-Pro2, D-Trp7,9)-SP (45-90 nmoles i.a.). Furthermore, the detrusor contraction evoked by preganglionic stimulation of the pelvic nerves was partially inhibited by the same antagonist in a higher dose (65% reduction at a total dose of 150-300 nmoles). The contractile response to SP (0.5 nmoles i.a.) was also significantly reduced after blockade of muscarinic receptors with atropine (50% reduction at 1 mg/kg i.a.) or after ganglionic blockade with hexamethonium (75% reduction at 25 mg/kg i.v. + 50 mg/kg hr i.a.). Immunocytochemical studies demonstrated the occurrence of SP-immunopositive nerve terminals in the detrusor part of the rat urinary bladder. Based on these findings it is suggested that SP may act as a neurotransmitter/modulator in this organ. The mechanism of action for SP on the detrusor seems to be complex and may involve ganglionic transmission via both types of cholinoceptors as well as direct activation of smooth muscle.

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Inhibition of antidromic and substance P‐induced vasodilatation by a substance P antagonist

Cited by 142 publications

References 8 publications

Some rat sensory neurons in culture express characteristics of differentiated pain sensory cells.

Some rat sensory neurons in culture express characteristics of differentiated pain sensory cells.

A substance P antagonist inhibits vagally induced increase in vascular permeability and bronchial smooth muscle contraction in the guinea pig

In vivo motor effects of substance P on the rat urinary bladder

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