Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown by microelectrode techniques and microcytofluorometry that fragments of the substance P and L-vasopressin--low molecular physiologically active peptides of wide regulatory action--bind to the receptors on the surface of plasma membranes outside the region of high permeable gap contact in unimolar concentrations and cause an increase in the rate of intracellular diffusion exchange of inorganic ions and fluorescein molecules in the salivary gland cells of Drosophila larva. The growth of intracellular contact permeability induced by low peptide concentrations is blocked by carbodiimide--a reagent cross-linking the membrane proteins. On the basis of the previous data it is suggested that the functions of intracellular contacts are regulated by the distant action mechanism involving the generalized structural rearrangements of plasma membranes.
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PMID:[Structural-membrane regulation of intercellular contacts of low-molecular weight peptides]. 171 61

Autoradiographic analysis has been performed to determine whether or not platelets and megakaryocytes can take up in vitro vasoactive neuropeptides such as [3H]angiotensin II, [3H]neuropeptide Y, [3H]substance P and [3H]vasopressin. Light microscope autoradiography has revealed the active uptake of [3H]angiotensin II by megakaryocytes. [3H]angiotensin II uptake by platelets has also been confirmed by electron microscope autoradiography. Silver grains are preferentially associated with the dense bodies of platelets. Neither megakaryocytes nor platelets show any active uptake of [3H]neuropeptide Y or [3H]substance P. Megakaryocytes are slightly labelled after incubation with [3H]vasopressin.
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PMID:Autoradiographic analysis of vasoactive neuropeptide uptake by rabbit megakaryocytes and platelets. 171 18

The effects of angiotensin-converting-enzyme (ACE) inhibitors on circulatory regulating mechanisms in congestive heart failure (CHF) were studied by comparison of plasma levels of catecholamines, neuropeptide Y-like immunoreactivity (NPY-LI), substance P (SP-LI), calcitonin gene-related peptide (CGRP-LI), vasopressin (ADH-LI), atrial natriuretic peptide (ANP-LI) and renin activity (PRA) in patients with severe CHF (NYHA III-IV) with (n = 15) or without (n = 17) ACE inhibitors in addition to digoxin and diuretic therapy. Data were also compared with those for healthy subjects (n = 31) and patients with moderate CHF (NYHA I-II). Catecholamines and NPY-LI were increased to the same extent in both groups with severe CHF. CGRP-LI showed no changes relative to controls in any of the patient groups, and was not affected by ACE inhibitors. The SP-LI level was significantly increased in all patient groups. Patients with severe CHF on ACE inhibition had a SP-LI level of 4.05 +/- 0.79 pmol l-1, compared to a concentration of 2.28 +/- 0.30 pmol l-1 (P less than 0.05) in the patient group with a comparable degree of CHF but without ACE inhibition. In the latter group, an inverse relationship appeared between the SP-LI and the serum sodium levels (r = -0.68, P less than 0.05). The patients with severe CHF who received ACE inhibitors had significantly lower ADH-LI levels than the patients with a comparable degree of CHF who were not treated with ACE inhibitors, while the ANP-LI levels was increased to a similar extent in both groups.
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PMID:Increased plasma level of substance P in patients with severe congestive heart failure treated with ACE inhibitors. 171 29

Investigations have shown the presence of a cardiodepressant factor in the fluid incubating the posterior pituitary lobe "in situ", which decreased contraction frequency of the isolated heart auricle (Acta Physiol. Pol., 1984, 35: 460-468). The influence on the spontaneous contraction frequency of the isolated heart auricle of the following synthetic neuropeptides was determined: substance P, leu-enkephalin, met-enkephalin, angiotensin II, arg-vasopressin, oxytocin, delta sleep-inducing peptide and atrial natriuretic factor. It was found that the investigated neuropeptides had no effect on the contraction frequency of the isolated auricle of the heart right atrium of two-day-old rat in a concentration from 2.1 x 10(-7) to 1 x 10(-3) mol/l in the bathing medium and it was concluded that their biological properties differ from the cardiodepressant factor.
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PMID:The lack of influence of some neuropeptides present in the posterior pituitary lobe on the frequency of spontaneous contraction of the isolated heart auricle. 172 1

An endopeptidase was isolated from Xenopus laevis skin secretions. This enzyme, which has an apparent molecular mass of 100 kDa, performs a selective cleavage at the Xaa-Phe, Xaa-Leu, or Xaa-Ile bond (Xaa = Ser, Phe, Tyr, His, or Gly) of a number of peptide hormones, including atrial natriuretic factor, substance P, angiotensin II, bradykinin, somatostatin, neuromedins B and C, and litorin. The peptidase exhibited optimal activity at pH 7.5 and a Km in the micromolar range. No cleavage was produced in vasopressin, ocytocin, minigastrin I, and [Leu5]enkephalin, which include in their sequence an Xaa-Phe, Xaa-Leu, or Xaa-Ile motif. The endopeptidase activity was inhibited by divalent cation chelators and by phosphoramidon only at high concentrations (IC50 = 50 microM), whereas it was insensitive to classical inhibitors of chymotrypsin, angiotensin convertase, and serine and cysteine peptidases, as well as carboxypeptidases. It is hypothesized that this enzyme, which is distinct from neutral endopeptidase (EC 3.4.24.11), constitutes the prototype of a family of related metalloendopeptidases that inactivate peptide substrates by cleavage at the Xaa-Phe, Xaa-Leu, or Xaa-Ile bond.
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PMID:A peptide-hormone-inactivating endopeptidase in Xenopus laevis skin secretion. 172 23

1. In anaesthetized rats, an i.v. injection of endothelin-1 (0.25 nmol kg-1) evoked a rapidly appearing (maximal effect within 15 s) and short lasting (3 min) fall in blood pressure with tachyphylaxis occurring so that it was reduced by 50% by the last of 4 injections given 10 min apart. This property was also shared by endothelin-2, endothelin-3 and vasoactive intestinal contractor (VIC). 2. Cross tachyphylaxis between the isopeptides occurred. However, under the same experimental conditions the hypotensive effects of acetylcholine, adenosine, atrial natriuretic peptide (ANP) and substance P were reproducible and not modified in animals in which endothelin-1 no longer lowered blood pressure. Thus, the mechanism of the hypotensive action of endothelin peptides is different from that of acetylcholine, adenosine, ANP, and substance P. 3. In pithed rats, endothelin-1 (0.25 nmol kg-1) and its precursor human proendothelin (h-proendothelin) (0.5 nmol kg-1) induced pressor responses of a similar magnitude, which for h-proendothelin (up to 5.0 nmol kg-1) were not preceded by a hypotensive phase. The pressor effects of endothelin-1, like those of vasopressin, were reproducible upon repeated i.v. injections. 4. Rats given a 10 min infusion (0.1 nmol kg-1 min-1) of endothelin-1 showed no hypotensive response to an i.v. bolus injection of endothelin-1, whereas animals pretreated with an equipressor infusion of h-proendothelin did not develop tachyphylaxis to endothelin-1. 5. In pitched rats, endothelin-1, at a dose inducing the same maximal increase in blood pressure as h-proendothelin, was approximately 3 fold more potent as a mesenteric vasoconstrictor than h-proendothelin. These results suggest that if h-proendothelin is processed to endothelin-1, this transformation is not uniform throughout the vascular system. 6. The pressor response of h-proendothelin in pithed rats was dose-dependently inhibited by phosphoramidon (2.5-5.0mgkg '). However, this compound did not antagonize the effects of endothelin-1(0.25 nmol kg- ) or those of h-proendothelin (0.5 nmol kg- ) once developed. 7. Although some of these results may suggest that h-proendothelin does not undergo in vivo conversion to endothelin-1, the results obtained with phosphoramidon suggest that h-proendothelin is converted into endothelin-1. Therefore, the amount of endothelin-1 so produced can elicit pressor responses or regional vasoconstriction, but is insufficient to lower blood pressure and to inhibit endothelin-1-induced hypotension. 8. The mechanism of the tachyphylaxis does not appear to be depletion of endothelium-derived relaxing factor, since agents coupled to the latter endogenous vasorelaxant substance do not exhibit crosstachyphylaxis with endothelin-1. It is suggested that upon repeated or sustained exposure to endothelin-1, the endothelin-1 receptors mediating hypotension decrease in number and/or undergo conformational changes making them refractory to activation. Alternatively, the depletion of a blood-borne agent responsible for the hypotension could be involved.
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PMID:Cross tachyphylaxis to endothelin isopeptide-induced hypotension: a phenomenon not seen with proendothelin. 178 22

The knowledge on the neuronal inputs to the locus coeruleus (LC) and their roles in regulating noradrenergic (NA) cellular activity is quite advanced. In recent years, however, about ten neuropeptides were found to be localized in the area of the rodent LC; peptides which may be considered as potential transmitters or modulators acting in this area. Electrophysiological studies performed in vivo and in vitro have revealed that many of these peptides are able to alter LC neuronal activity. Stimulatory effects have been described with vasopressin, substance P, adrenocorticotropin hormone and corticotropin-releasing factor. Depressant effects were seen with galanin, somatostatin, neuropeptide Y and enkephalin. Variable actions were observed in the case of neurotensin. While these findings point to a possible regulatory function of these peptides in this area, precise roles remain unclear. Important information is lacking that would conclusively demonstrate their regulatory functions. It should be determined whether the stimulation of peptidergic cells elicits synaptic effects identical to the ones observed with local exogenous peptide applications. By studying the action of blockers of these transmitter and modulator candidates, we would probably begin to understand their importance in the regulation of tonic and phasic activity components. The LC is generally considered to consist of a homogenous group of neurons. The recent observation that subpopulations of these cells contain peptides as in the case of neuropeptide Y, galanin and vasopressin, points to the possible existence of subgroups of neurons having different functions.
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PMID:Responses of locus coeruleus neurons to neuropeptides. 181 23

This review summarizes the revolutionary impact of brain peptides on our understanding of the nervous system and then discusses the localization, distribution, synthesis, receptor sites, and possible function of 32 brain peptides. The peptides are discussed in three subgroups: I) the opioid peptides, which include beta-endorphin, the enkephalins, and dynorphin; II) the pituitary releasing hormones, most of which are wide-spread in the brain and include corticotropin-releasing hormone, luteinizing hormone-releasing hormone, somatostatin, and thyrotropin-releasing hormone; and III) a selection of 12 other peptides potentially important for neurological function, including vasopressin, oxytocin, substance P, cholecystokinin, bombesin, neurotensin, renin, angiotensin, vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and calcitonin. Within each individual peptide section, the possible physiological roles in anterior pituitary hormone release, blood-flow regulation, feeding behavior, temperature regulation, nociception, memory and learning, and movement are reviewed. Further, where noted, the peptide findings in Huntington's, Alzheimer's, Parkinson's and psychiatric diseases are emphasized.
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PMID:Neuropeptides. 187 Jul 24

The effects of various neuroactive substances on the intracellular free Ca2+ concentration ([Ca2+]i) in cultured type-2 astrocytes were examined by fura-2-based microfluorometry. Type-2 astrocytes showed [Ca2+]i elevation in response to all the substances examined, i.e. carbachol (10(-4) M), histamine (10(-4) M), noradrenaline (10(-4) M), serotonin (10(-4) M), substance P (10(-6) M), vasopressin (10(-6) M) and glutamate (10(-4) M). Not all type-2 astrocytes, however, responded to these substances at the concentrations tested, and the percentages of astrocytes showing a Ca2+ response differed depending on the substance. These results indicate that type-2 astrocytes are potential targets for widely diverse neuroactive substances and heterogeneous in response to them.
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PMID:Type-2 astrocytes show intracellular Ca2+ elevation in response to various neuroactive substances. 194 45

The modulation of Ca2+ currents by neurotransmitters was studied in freshly dissociated rat spinal cord neurons, using the whole-cell patch-clamp technique. GABA, baclofen, adenosine, ATP, serotonin, norepinephrine, somatostatin, and dynorphin A inhibited the current through Ca2+ channels in a substantial fraction of cells, while substance P, vasoactive intestinal polypeptide, [D-ala2,d-leu5]-enkephalin, cholecystokinin-8 (sulfated), calcitonin gene-related peptide, angiotensin II, neurotensin, vasopressin, and thyrotropin-releasing hormone had no effect. In the case of baclofen, the inhibition is mediated, at least in part, by a GTP-binding protein. Suppression of Ca2+ current by neurotransmitters may represent a mechanism of presynaptic inhibition in the spinal cord.
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PMID:Neurotransmitter modulation of calcium current in rat spinal cord neurons. 196 36


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