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)

Everted sacs of the rat jejunum change the accumulation of [3H]leucine when beta-casomorphins (BCMs) or synthetic analogs, in a concentration range of 10(-8) mol/l, are coincubated with the amino acid. BCM5 (BCM fragment 1-5, Tyr-Pro-Phe-Pro-Gly) and [D-Ala2]-BCM5-NH2 (Tyr-D-Ala-Phe-Pro-Gly) increase, whereas [D-Pro4]-BCM5 (Tyr-Pro-Phe-D-Pro-Gly) decreases the leucine accumulation and [Arg8]-vasopressin has no effect. No effect of BCM5 could be observed on the accumulation of the space marker [14C]inulin. Specific binding sites for casomorphins were detected microautoradiographically, exclusively at the epithelial cell layer using [3H][D-Pro4]-BCM5 in competition studies as a model. HPLC analysis revealed that under the experimental conditions about 50% of the studied [D-Pro4]-BCM5 was enzymatically degraded and no intact peptide is accumulated within the samples of everted sacs. From the results we postulate a brush-border receptor contact of the BCMs which induces an alteration of the amino acid uptake. A contraluminal binding of the chemical signals is not likely, because there is no evidence for a transepithelial transport of intact BCMs. The observed effects of the BCMs demonstrate as yet unknown peptide-receptor interactions, probably at the brush-border membrane, with subsequent effects on the nutrient supply. Furthermore, the results support the general hypothesis of distinct peptide-receptor interactions in those types of epithelia in which the cells are connected by tight junctions.
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PMID:beta-Casomorphins alter the intestinal accumulation of L-leucine. 254 74

Binding of the opiate antagonists [3H]diprenorphine and [3H]naloxone and of the opioid agonists [3H]Met-enkephalin and [3H]dynorphin(1-8) was studied in a fraction of the rat neurohypophysis containing disconnected oxytocin and vasopressin nerve endings ('neurosecretosomes'). There was specific binding of [3H]diprenorphine in the fraction enriched with neurosecretosomes. This binding was only partially displaceable by naloxone; naloxone binding was stereospecific. Intact and unoxidized [3H]Met-enkephalin was found in the neurosecretosome pellet; binding of the analogue D-Ala-D-Leu-enkephalin was very low. Our data favour the assumption of a direct action of endogenous opioids at the neurosecretory nerve endings.
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PMID:Opioid binding in a rat neurohypophysial fraction enriched in oxytocin and vasopressin nerve endings. 286 4

In order to clarify the effects of endogenous opiate peptides on the vasopressin system, we have investigated the presence of different opiate receptor subtypes in the neurohypophysis by radioreceptor assay and autoradiography. [3H]-etorphine binding to membrane preparations revealed the presence of high- and low-affinity binding sites (KD, 1.2 nM and 8.1 nM). Displacement of [3H]-etorphine by opiate receptor subtype-specific ligands gave the following results: the preferential mu agonists DAGO (Tyr-D-Ala-Gly-NMe-Phe-Gly-oL) and the tetrapeptide morphiceptin did not displace etorphine; the preferential sigma receptor agonists DADLE (D-Ala2,D-Leu5-enkephalin) or DSTLE (D-Ser2,Leu5,Thr6-enkephalin) and beta-endorphin, a preferential agonist of the epsilon receptor, displaced [3H]-etorphine from its low-affinity site only, and dynorphin 1-8, a preferential kappa agonist, displaced [3H]-etorphine from its high-affinity binding site. Film autoradiography of neurohypophyseal sections incubated with [3H]-etorphine showed a displacement of 30% of the labeled ligand by unlabeled dynorphin 1-8. Exposure of rat neurointermediate lobes in organ culture to dynorphin 1-8 caused a small but significant stimulation of vasopressin release. These results demonstrate the existence of dynorphin 1-8 sensitive opiate receptors of the kappa subtype in the neurohypophysis and their possible involvement in vasopressin release.
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PMID:Dynorphin 1-8 binds to opiate kappa receptors in the neurohypophysis. 287 1

We examined opioid binding in fractions with disconnected nerve endings (secretosomes) which were prepared from porcine neurohypophyses by centrifugation in a discontinuous Percoll gradient. Specific (= displaceable) binding was observed with 3H-etorphine and with 3H-diprenorphine, two ligands with low selectivity for distinct opiate receptor subclasses. No displaceable binding was found with the prototypic mu- and delta-ligands 3H-dihydromorphine and 3H-(D-Ala, D-Leu) enkephalin. Displacement of 3H-diprenorphine binding was almost absent with the selective mu- and delta-ligands morphiceptin and ICI-174864. Partial displacement occurred with the selective kappa-ligand U-50488 and with dynorphin. Binding of 3H-etorphine was stereo-specific. 3H-diprenorphine binding was saturable with a KD between 2 and 4 nM. Maximum of opiate binding activity was detected in the fractions with accumulated secretosomes. By autoradiography specific 3H-diprenorphine binding is shown to be mainly associated with secretosomes. In imunocytochemical preparations an oxytocin antibody was immunoreactive in 85% of the secretosomes in the fraction with highest opiate binding. These fractions in radioimmunoassays exhibited the largest contents in oxytocin and low vasopressin levels. The data therefore suggest that in the porcine neurohypophysis opioid binding sites of the kappa-type occur in secretory endings presumably of the oxytocin type.
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PMID:Opiate binding differentially associated with oxytocin and vasopressin nerve endings from porcine neurohypophyses. 340 60

A previous report described the existence of substantial amounts of enkephalin immunoreactivity and the occurrence of nerve terminals containing an enkephalin-like material in the pars nervosa of rat pituitary. It was suggested that an enkephalin innervation of the pars nervosa originating from the magnocellular hypothalamic nuclei might regulate the secretion of neurohypophyseal hormones. The results of the present studies support this hypothesis, as we find that a stable enkephalin analogue (D-Ala 2,D-Leu5-enkephalin) inhibits the calcium-dependent release of vasopressin evoked by electrical stimulation of the rat pituitary stalk in vitro. A similar inhibition of the stimulus-evoked vasopressin release is caused by morphine and beta-endorphin, and the inhibitory effects of the enkephalin analogue can be reversed by naloxone. These findings suggest the possible existence of inhibitory opiate receptors on the terminals of vasopressin fibres in the pars nervosa.
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PMID:Opiate receptors influence vasopressin release from nerve terminals in rat neurohypophysis. 624 3

The ability of the neurohypophyseal hormones and related synthetic peptides to potentiate the action of synthetic ovine corticotropin releasing factor (CRF-41) was examined using male rats whose endogenous CRF release was blocked with chlorpromazine, morphine and nembutal. CRF potency was clearly related to the pressor activity of the analogues. However, the threshold dose for eliciting a significant corticosterone response with the neurohypophyseal hormones was greater than with CRF-41. When arginine vasopressin (AVP) was coadministered with CRF-41 at subthreshold doses of both peptides, a significant corticosterone response was observed. When the neurohypophyseal hormone analogues were compared with regard to intrinsic CRF bioactivity, it was observed that an L-basic residue in sequence position 8 is necessary for high intrinsic activity. With one exception, l-Deamino-(9-D-Ala) arginine vasopressin, the ability to potentiate the effect of CRF-41 was related to the intrinsic CRF potency of the analogues. These results support previous reports of in vitro potentiation of CRF-41 by AVP and point out the complexity of CRF-neurohypophyseal hormone interaction in vivo.
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PMID:In vivo potentiation of corticotropin releasing factor activity by vasopressin analogues. 633 65

The cardiovascular effects of opioid peptides have been studied. Leucine-enkephalin (Leu-ENK) produced blood pressure (BP) increases following administration into the lateral brain ventricles (i.v.t.), into the cisterna magna (i.c.i.), and following intravenous (i.v.) administration. Heart rate (HR) increases were observed following all routes of administration (threshold for BP and HR effects at 0.3 nmole, maximum at 360 nmoles). The cardiovascular effects were independent of generalized seizures, which may occur at higher doses of enkephalins (ENK). D-alanine-enkephalin (D-Ala-ENK) attenuated the vagal component of the baroreceptor reflex in cats. This was indicated by the findings that HR did not decrease following D-Ala-ENK-induced BP increases and that the compensatory decreases in HR following i.v. pressor doses of angiotensin II (ANG II) were markedly attenuated in cats treated with i.v.t. D-Ala-ENK. Naloxone inhibited the BP and HR effects following i.c.i. and i.v., but not following i.v.t., administration of Leu-ENK. The i.v.t. Leu-ENK effect were inhibited by beta-adrenergic receptor blockade. Bratteboro rats homozygous for hereditary diabetes insipidus with total absence of antidiuretic hormone (ADH) synthesis responded with BP decreases following i.v.t. Leu-ENK, while BP increases were observed in control Long-Evans rats. Blood pressure increases to i.v.t. Leu-ENK were markedly greater in spontaneously hypertensive rats of the stroke-prone strain (SHR-sp) than in normotensive control rats; SHR-sp exhibit a humoral pattern of increased ADH, ACTH, and catecholamines, presumably due to central peptidergic stimulation. The known effects of opioid peptides on these hormones and the observed cardiovascular responses suggest a possible participation of this peptide system in the maintenance of high BP in the SHR-sp.
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PMID:Enkephalin effects on blood pressure, heart rate, and baroreceptor reflex. 739 23

Opioid peptides have profound inhibitory effects on the production of oxytocin and vasopressin, but their direct effects on magnocellular neuroendocrine neurons appear to be relatively weak. We tested whether a presynaptic mechanism is involved in this inhibition. The effects of mu-opioid receptor agonist D-Ala(2), N-CH(3)-Phe(4), Gly(5)-ol-enkephalin (DAGO) on excitatory and inhibitory transmission were studied in supraoptic nucleus (SON) neurons from rat hypothalamic slices using whole cell recording. DAGO reduced the amplitude of evoked glutamatergic excitatory postsynaptic currents (EPSCs) in a dose-dependent manner. In the presence of tetrodotoxin (TTX) to block spike activity, DAGO also reduced the frequency of spontaneous miniature EPSCs without altering their amplitude distribution, rising time, or decaying time constant. The above effects of DAGO were reversed by wash out, or by addition of opioid receptor antagonist naloxone or selective mu-antagonist Cys(2)-Tyr(3)-Orn(5)-Pen(7)-NH(2) (CTOP). In contrast, DAGO had no significant effect on the evoked and spontaneous miniature GABAergic inhibitory postsynaptic currents (IPSCs) in most SON neurons. A direct membrane hyperpolarization of SON neurons was not detected in the presence of DAGO. These results indicate that mu-opioid receptor activation selectively inhibits excitatory activity in SON neurons via a presynaptic mechanism.
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PMID:Selective modulation of excitatory transmission by mu-opioid receptor activation in rat supraoptic neurons. 1060 35

Abstract To clarify the effects of opioid peptides, and in particular the effects of kappa-receptor agonists on the activity of supraoptic neurons, extracellular recordings were made from 71 spontaneously firing neurons in the rat hypothalamic slice preparation. Of 71 neurons, 28 showed a phasic firing pattern (phasic neurons: putative vasopressin neurons). The mean firing rate of phasic neurons was 2.6 spikes/s (intraburst firing rate 5.4 +/- 2.2 spikes/s). The mean firing rate of neurons classified as non-phasic neurons (putative oxytocin neurons) was 4.5 spikes/s. Following bath application of leumorphin (LM) at 10(-7) M, which has potent opioid activity at kappa-receptors, 17 (61%) of 28 phasic neurons were inhibited and 22 (51%) of 43 non-phasic neurons were inhibited. Excitation was observed in only one non-phasic neuron. The dose-dependence of the response to LM was tested in five supraoptic neurons. There was an inverse relationship between LM concentration and percent change in firing rate. The threshold concentration of LM was approximately 10(-8) M. The relatively selective kappa-receptor antagonist, MR-2266, completely blocked the LM-induced responses. Its effects were long-lasting and only partial recovery was observed 2 h after the application of MR-2266. Dynorphin had similar inhibitory effects on supraoptic neurons to those obtained with LM when tested on the same neurons. In another series of experiments the mu-receptor agonist morphine and the delta-receptor agonist [D-Ala, D-leu]-enkephalin (DADLE) were applied to 28 supraoptic neurons (12 phasic and 16 non-phasic neurons) at 10(-7) M and their actions compared directly with that of LM. Only two of 12 phasic neurons tested were inhibited by DADLE and none of five phasic neurons tested was inhibited by morphine, while eight of the 12 neurons tested were inhibited by LM. By contrast the non-phasic neurons tested were inhibited by application of each of the peptides; seven of 16 neurons tested were not only inhibited by LM, but also five of 11 neurons by DADLE and seven of 15 by morphine. The magnitude of the responses varied from cell to cell. These results suggest that LM acts at the same receptors as dynorphin, and that opioids acting preferentially at kappa-receptors inhibit both vasopressin and oxytocin neurons while delta- and mu-receptor agonists inhibit primarily oxytocin neurons.
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PMID:Kappa-selective opioid receptor agonists leumorphin and dynorphin inhibit supraoptic neurons in rat hypothalamic slice preparations. 1921 65