Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isocapnic dry gas hyperpnea-induced bronchoconstriction (HIB) in the guinea-pig is mediated by both tachykinin release from airway sensory nerve C-type fiber terminals and secondary synthesis of cysteinyl-leukotrienes, in particular LTD(4). Beta (beta)(2)-agonists are potent bronchodilators but potentially could also inhibit the airway response to hyperpnea challenge via effects on the release of LTD(4)from airway cells in vivo. The purpose of this study was to test the hypothesis that beta(2)agonists attenuate HIB in guinea-pigs, in part, by reduction in LTD(4)release in vivo. Twenty-six guinea-pigs (400-550 g) were anesthetized with xylazine (7 mg/kg) and pentobarbital (65 mg/kg), tracheotomized and mechanically ventilated with a small animal ventilator using a tidal volume of 3 ml and a breathing frequency of 60 breaths/min. Dry gas (95%O(2)/5%CO(2)) with a 4 ml tidal volume and a breathing frequency of 150/min was used for hyperpnea challenge. Challenge with isocapnic dry gas triggered a significant increase in pulmonary resistance (0.3 +/- 0.02 vs. 0.57 +/- 0.06 cmH(2)O/ml per s; P=0. 017; n=13) and excretion of LTD(4)in the bile (baseline: 2.43 vs. HIB: 4.66 pmol/h; P=0.04). Salbutamol pretreatment completely blocked the airway response to the challenge (0.3+/-0.02 vs. 0.3+/-0. 05 cmH(2)O/ml per s; n=13) and reduced the biliary excretion of LTD(4)(baseline: 2.42 pmol/h; vs. HIB: 2.40 pmol/h). We conclude that salbutamol inhibited the airway responses to dry gas hyperpnea challenge and LTD(4)synthesis by the airway cells.
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PMID:The beta(2)-agonist salbutamol inhibits bronchoconstriction and leukotriene D(4) synthesis after dry gas hyperpnea in the guinea-pig. 1054 87

The unitary postsynaptic mechanism underlying the influence of diverse neuromodulators on modification of excitatory and inhibitory inputs to granule, pyramidal and inhibitory hippocampal cells is suggested. According to this mechanism, the effect of dopamine, adenosine, acetylcholine, noradrenaline, serotonin, somatostatin, galanin, opioids, cannabinoids, neuropeptide Y on postsynaptic receptors, bound to Gi/0 proteins, should promote LTD of excitatory inputs and LTP of inhibitory inputs. The effect of dopamine, adenosine, acetylcholine, noradrenaline, serotonin, vasopressin, tachykinin, histamine on postsynaptic receptors, bound to Gs and Gq/11 proteins, should oppositively modulate the same inputs. Only synaptically activated excitatory and inhibitory inputs can by influenced by neuromodulators. The character of neuromodulatory influence on modification of hippocampal synaptic efficacy, implying from the suggested mechanism is in accordance with known experimental data.
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PMID:[A unified postsynaptic mechanism for the effect of various neuromodulators on modification of potentiated and depressed inputs to hippocampal cells (hypothesis)]. 1188 34

A mechanism of opioid and substance P-mediated modulation of a cortical signal transduction through the striatum is suggested. According to this mechanism, an activation of postsynaptic receptors, bound to Gi/0 proteins, should increase the magnitude of NMDA-dependent (NMDA-independent) LTD (LTP) of excitatory inputs and LTP (LTD) of inhibitory inputs to all types of striatal cells. An activation of postsynaptic receptors, bound to Gs or Gq/11 proteins, should oppositely modulate LTD and LTD in the same inputs. It follows from the model that the negative feedback loops can held the activity of a striatal output cells at the stable level due to recurrent activation by endogenous opioids of delta receptors on striatopallidal cells, mu and kappa receptors on striatonigral cells of striosomes and matrix, respectively, and subsequent suppression of the efficacy of corticostriatal inputs. Cholinergic interneurons, affected by enkephalin and substance P, are also involved in these feedback loops. We hypothesized that an activation of mu and delta receptors and/or inactivation of kappa receptors on striatal spiny cells might alleviate parkinsonian symptoms and recover locomotor activity.
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PMID:[Mechanism of opioid and substance P-mediated modulation of cortical signal transduction through the striatum]. 1465 3