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

The distribution of substance P(SP)-like immunoreactivity was studied in the habenulo-interpeduncular (HAB-ITP) complex of the frog Rana esculenta by means of the immunohistochemical peroxidase-antiperoxidase (PAP) method. The HAB of the frog were subdivided into dorsal and ventral nuclei, corresponding to the medial and lateral HAB of mammals respectively. In addition, the dorsal HAB of the frog were morphologically asymmetric, since only the left has a lateral and a medial subnucleus. SP-like immunoreactive cells were found in the right dorsal HAB, in the lateral subnucleus of the left dorsal HAB and in a nucleus of scattered cells located rostrodorsally to the ITP. However, the medial subnucleus of the left dorsal HAB and a portion of the right dorsal HAB facing the 3rd ventricle, did not show SP immunoreactivity. Immunoreactive fibers were found in the medial subnucleus of the left dorsal HAB, in the two fasciculi retroflexes and in the ITP. Moreover, immunoreactive terminals were observed in the ventral HAB of both sides, in the ITP and on the blood vessels which cross the ITP. It is assumed that a portion of fibers connecting the various structures of the HAB-ITP complex belongs to the SP peptidergic system as suggested for mammals. However, in contrast to the mammals, the results on the frog are in favour of an histochemical asymmetry of the SP-like immunoreactivity, since a different distribution of this peptide was found between the right and left side of the brain. Such histochemical asymmetry was less pronounced than the morphological asymmetry and its functional meaning is unknown.
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PMID:The distribution of substance P in the habenulo-interpeduncular system of the frog shown by an immunohistochemical method. 608 86

Rat brain cortex membranes bind to a conjugate of substance P and 125I-labeled Bolton-Hunter reagent, and this binding can be inhibited by a low concentration of substance P (Kd = 1.2 +/- 0.4 X 10(-8) M). This binding is reversible and saturable (0.5 +/- 0.1 pmol of binding sites/mg of protein). Fragments of substance P as small as the carboxyl-terminal hexapeptide can inhibit the binding although their potency decreases with the decrease in the length of the peptides. The binding affinities of smaller peptides or peptides in which the carboxyl-terminal amide or amino acids are removed are drastically reduced. Biologically active analogs of substance P, physalaemin, eledoisin, substance P methyl ester, [D-Ala0]hepta(5-11)substance P, kassinin, and the eledoisin-related hexapeptide also can inhibit the binding. However, the binding is not inhibited by polypeptides structurally unrelated to substance P or by amine hormones/neurotransmitters. The binding affinities of biologically active peptides to rat brain cortex membranes are almost identical with their affinities for rat parotid cells which we previously determined. Furthermore, the recently described substance P antagonist, [D-Pro, D-Trp]substance P, inhibits the binding of the 125I-labeled substance P derivative to brain cortex membranes and to parotid cells equally well. These results suggest that the substance P receptors in the brain cortex and the parotid gland are similar. The brain cortex membrane binding of the 125I-labeled substance P derivative can be inhibited by micromolar concentrations of GTP, GDP, and their analogs. ITP and IDP were less active. Adenine and pyridine nucleotides were inactive.
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PMID:Characterization of the substance P receptor in rat brain cortex membranes and the inhibition of radioligand binding by guanine nucleotides. 618 45

Nitric oxide (NO) exerts several effects on myocardial contraction, including enhancement of relaxation and diastolic function, modulation of beta-adrenergic inotropic responses, and inotropic effects in the absence of agonist pre-stimulation. Different effects have been observed in different species and preparations, and it is unclear whether they are species- or preparation-specific, or whether they represent a range of responses that can manifest in most mammalian species. We therefore examined the effects of NO on the inotropic response to beta-adrenergic stimulation in the isolated guinea-pig heart, a species in which we have previously shown that NO enhances basal left ventricular (LV) relaxation and modulates the Frank-Starling response. Isolated ejecting hearts were perfused with Krebs buffer at constant placed heart rate (1 microM) indomethacin, 37 degrees C, constant loading conditions), and high fidelity LV pressure was monitored by an apical 2 F Millar catheter. All hearts were initially treated with dobutamine (0.1 microM) and then, once the peak inotropic and chronotropic response had been established, with either (a) no further treatment (n = 6), (b) the NO donor sodium nitroprusside (1 microM, n = 6; 10 microM, n = 6), or (c) the specific agonist for NO release, substance P (0.1 microM, n = 6). Dobutamine (0.1 microM) produced a rapid positive inotropic and chronotropic response, associated with a fall in LV end-diastolic pressure (LVEDP) and a rise in coronary flow. The positive inotropic effect of dobutamine declined over 20-28 minutes, while the chronotropic response persisted over this period. Low dose sodium nitroprusside (1 microM) delayed the decline in the inotropic response to dobutamine and exaggerated the fall in LVEDP. Similar effects were observed with substance P (0.1 microM). In contrast, a higher dose of sodium nitroprusside (10 microM) did not alter the response to dobutamine. These data indicate that "low dose" NO augments the inotropic response to beta-adrenergic stimulation in the isolated ejecting guinea-pig heart, in addition to its previously reported effects on basal LV relaxation in the same preparation.
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PMID:Nitric oxide enhances the inotropic response to beta-adrenergic stimulation in the isolated guinea-pig heart. 978 70