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

An immunocytochemical investigation was carried out on round and spreading hemocytes of Planorbarius corneus by using 20 antisera to vertebrate bioactive peptides. The immunotests showed the presence of alpha 1-antichymotrypsin-bombesin-, calcitonin-, CCK-8 (INC)-, CCK-39-, gastrin-, glucagon-, Met-enkephalin-, neurotensin-, oxytocin-, somatostatin-, substance P-, VIP-, and vasopressin-immunoreactive molecules in the spreading hemocytes. The round hemocytes were only positive to anti-bombesin, anticalcitonin, anti-CCK-8 (INC), anti-CCK-39, anti-neurotensin, anti-oxytocin, anti-substance P and anti-vasopressin antibodies. No immunostaining was observed with anti-CCK-8 (Peninsula), anti-insulin, anti-prolactin, anti-thyroglobulin and anti-thyroxin (T4) antibodies. As probably in vertebrates, these bioactive peptides may modulate immuno cell function.
 ...
PMID:Immunocytochemical evidence of vertebrate bioactive peptide-like molecules in the immuno cell types of the freshwater snail Planorbarius corneus (L.) (Gastropoda, Pulmonata). 169 11

Recent studies have demonstrated that in vivo administration of 1-deamino-8-D-arginine-vasopressin, an analog of arginine-8-vasopressin, induces homologous desensitization to vasopressin in the thick ascending limb of the loop of Henle. Desensitization has been documented by a decreased physiological response to vasopressin in vivo and by a reduced cAMP accumulation in the cortical thick ascending limb (CTAL). By measuring cAMP content in single isolated medullary thick ascending limbs (MTALs), we now report that desensitization can occur all along the thick ascending limb and, more importantly, that it can also be induced in vitro. In a first series of experiments, we observed that 1 hr after in vivo injection of 1-deamino-8-D-arginine-vasopressin, MTALs were desensitized by 80% to vasopressin, whereas the effects of the other hormones acting on the same cyclase pool (glucagon, calcitonin) were fully maintained. In a second set of experiments, desensitization was induced in vitro by vasopressin, the natural hormone. A 60-min preincubation of MTALs with vasopressin caused a marked (up to 86%) and highly reproducible desensitization. The process was dose and time dependent. The apparent Ka for desensitization was 0.2 nM, and the half-maximal effect was obtained within 20 min. The desensitization induced in vitro by vasopressin was again essentially homologous in nature, with 80% of the maximal stimulation of cAMP accumulation being obtained in the presence of glucagon. Desensitization to vasopressin was observed in the presence and absence of indomethacin, indicating that it is independent of prostaglandin synthesis. It is concluded that (i) vasopressin and its analog 1-deamino-8-D-arginine-vasopressin cause marked desensitization in the CTAL and MTAL and (ii) the low vasopressin concentrations required to induce desensitization and the rapid onset of the process suggest that it has a physiological significance.
 ...
PMID:In vitro desensitization of isolated nephron segments to vasopressin. 169 29

Outside diameter of isolated submucosal arterioles in guinea pig colon were monitored to examine vasodilator innervation to these gastrointestinal microvessels. Electrical stimulation of intrinsic submucosal ganglia dilated submucosal arterioles that had been preconstricted with vasopressin or norepinephrine. In approximately 50% of arterioles examined, the muscarinic receptor antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, 10 nM) abolished nerve-evoked vasodilations; 4-DAMP (500 nM) only partially inhibited the response in the other 50%. No significant differences in the nerve-evoked vasodilations were observed after extrinsic denervation of sympathetic and sensory fibers and removal of myenteric neurons by surgical myectomy. Immunohistochemistry demonstrated both substance P (SP) and vasoactive intestinal polypeptide (VIP) fiber projections to arterioles after sensory denervation and myectomy. Superfusion with muscarine and SP, but not with VIP or calcitonin gene-related peptide (CGRP), also dilated the arterioles; concentrations of muscarine and SP producing half-maximal responses were 35 and 6 nM, respectively. However, local pressure ejection of both CGRP and VIP dilated the arterioles. The SP receptor antagonist [D-Arg1,D-Phe5,D-Trp7,9,Leu11]SP reduced vasodilations in response to ganglionic stimulation as well as to pressure ejection of both SP and VIP. This study demonstrates that submucosal arterioles in the guinea pig distal colon receive a cholinergic as well as a noncholinergic vasodilator input from neurons in the submucosal plexus. SP and VIP are both likely candidates as the noncholinergic vasodilator transmitter to colonic gastrointestinal microvessels.
 ...
PMID:Cholinergic and noncholinergic submucosal neurons dilate arterioles in guinea pig colon. 171 16

A novel "cAMP-resistant" variant of LLC-PK1 renal epithelial cells which is impaired in in vivo down-regulation of response following hormonal stimulation of adenylate cyclase (AC) is described. Compared to parental cells, the BIB27 mutant exhibited markedly higher in vivo activation of cAMP-dependent protein kinase (cAMP-PK) in response to the hormones salmon calcitonin (SCT) or [Arg8]-vasopressin (AVP) or the AC activator forskolin. The activation of cAMP-PK subsequent to agonist stimulation also persisted much longer in the mutant than in LLC-PK1 cells, although the cAMP-PK of BIB27 cells was normal in terms of both absolute levels and regulation by cAMP in vitro. Intracellular cAMP accumulation was also much higher in BIB27 than in LLC-PK1 cells following agonist stimulation. Production of cAMP could be detected in BIB27 cells even 12 h after treatment with AVP or SCT, whereas cAMP production in LLC-PK1 had returned to basal within 1 and 8 h, respectively. High levels of free cAMP-PK catalytic (C) subunit in BIB27 persisted even 12 h after hormone addition, meaning that the higher cAMP production in BIB27 did not result in the normal down-regulation of cAMP-PK C subunit levels. In vitro AC activity in BIB27 cell homogenates could be stimulated by hormones or receptor-independent agonists, but to a lesser extent than in LLC-PK1 cell homogenates. The SCT and AVP concentrations promoting half-maximal AC activation in BIB27 cells were about 10- and 3-fold higher than parental, respectively. BIB27 accordingly appeared to possess a mutation in AC responsible for the impairment of both in vitro response to agonists and the normal in vivo down-regulation processes following hormonal stimulation.
 ...
PMID:A novel LLC-PK1 renal epithelial cell mutant impaired in in vivo down-regulation of cAMP-mediated hormonal response. 171 64

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.
 ...
PMID:Increased plasma level of substance P in patients with severe congestive heart failure treated with ACE inhibitors. 171 29

The cellular signaling mechanism of adenosine action has been studied in highly purified populations of cultured cells from the rabbit medullary thick ascending limb of Henle's loop (MTAL). The effects of specific adenosine-receptor agonists 5'(N-ethylcarboxamido)adenosine (NECA; A2) and N6-cyclohexyladenosine (CHA; A1) on basal and hormone-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production, cytosolic free calcium concentration ([Ca2+]f), and formation of inositol phosphates were examined. Production of cAMP was stimulated by high doses of NECA and was inhibited by low doses of CHA. The inhibitory effect of CHA was observed in cells in which cAMP production was first stimulated with vasopressin, isoproterenol, prostaglandin E2 (10(-6) M), or calcitonin (100 ng/ml) and was abolished by pretreating the cells with pertussis toxin (PT) for 12-20 h. A highly selective adenosine A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine (CPX), also abolished the inhibitory effect of CHA. Both NECA and CHA induced a rapid (10 s) and transient increase in [Ca2+]f, and this was associated with an increased inositol trisphosphate (IP3) production. Single-cell [Ca2+]f measurements indicated that all MTAL cells responded to CHA. The removal of extracellular Ca2+ failed to inhibit these responses. Pretreatment with PT or administration of CPX abolished both the increase in [Ca2+]f and the formation of IP3 occurring in response to CHA and NECA. Our results suggest that both adenylate cyclase-coupled inhibitory (A1) and stimulatory (A2) adenosine receptors are present in pure populations of cultured MTAL cells. Moreover, activation of an adenosine receptor coupled to a PT substrate results in the increased production of inositol phosphate and elevation of [Ca2+]f.
 ...
PMID:Effects of adenosine on cAMP production and cytosolic Ca2+ in cultured rabbit medullary thick limb cells. 184 67

The effects of the pig calcitonin on the kidney excretory function in normotensive (NR) and spontaneously hypertensive rats (SHR) were examined. Calcitonin injection in the dose of 0.6 U/100 g of the body mass in NR and SHR in the conditions of 6-hour spontaneous diuresis caused the increase in the urination volume due to the inhibition of the tubular water reabsorption and growth of the glomerular filtration rate. The important role in the mechanism of the decrease in the water reabsorption in SHR plays the decrease in the content of vasopressin in the blood and urea in the kidney interstitium while in NR a more marked inhibition of the water reabsorption is caused by the decrease in the concentration of both urea and sodium in the kidney layers. The natriuretic effect of calcitonin was noticed only in NR.
 ...
PMID:[The effect of calcitonin on the mechanisms of urine formation and sodium excretion in normotensive and spontaneously hypertensive rats]. 185 46

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.
 ...
PMID:Neuropeptides. 187 Jul 24

The precise mechanistic role of the cAMP-dependent protein kinase (cAMP-PK) in cAMP-mediated gene induction remains unclear. Renal epithelial cell mutants were compared to the LLC-PK1 parental cell line for induction of the cAMP-responsive urokinase-type plasminogen activator (uPA) gene, as quantitated by the technique of mRNA solution hybridization. The FIB4 and FIB6 mutants, which possess less than 10% parental cAMP-PK catalytic (C) subunit activity, showed markedly diminished uPA mRNA induction in response to agents elevating intracellular cAMP such as the cAMP analogue 8-bromo-cAMP and the adenylate cyclase-stimulating hormones vasopressin and calcitonin. In contrast, the mutant cells responded to a similar or greater extent than the parental cells in terms of uPA mRNA induction following treatment with the Ca2+/phospholipid-dependent protein kinase activator phorbol 12-myristate 13-acetate (PMA). Elevation of intracellular cAMP was found to induce a translocation of the cAMP-PK C subunit from the perinuclear Golgi region to the nucleus in both parental and mutant cell lines, as shown by immunocytochemical techniques. Results argue for the role of the cAMP-PK C subunit activity and possibly nuclear translocation of the C subunit in cAMP-mediated uPA induction, which is mechanistically distinct from the PMA-stimulated response.
 ...
PMID:Mechanisms of cAMP-mediated gene induction: examination of renal epithelial cell mutants affected in the catalytic subunit of the cAMP-dependent protein kinase. 189 92

Our study investigates the distribution of neurophysins (Nph), proteins that are part of the precursors for vasopressin and oxytocin, and calcitonin gene-related peptide (CGRP) in the human brainstem by immunohistochemistry. Both peptides were found in discrete regions of the human hindbrain. Nph could be demonstrated exclusively in fibers and punctate perineural varicosities that were travelling within the mesencephalic central gray, substantia nigra, as well as locus coeruleus, medial longitudinal fascicle, raphe, nucleus of the solitary tract, lateral reticular nucleus and area postrema. A few varicosities were seen in the substantia gelatinosa of the spinal trigeminal tract and its continuation into the dorsal horn of the cervical spinal cord. In contrast to these observations. CGRP-immunoreactive fibers were found to be densest in the spinal tract of the trigeminal nerve and the dorsal horn of the spinal cord. In addition, fibers and varicosities could be demonstrated in numerous distinct brain regions, such as locus coeruleus and subcoeruleus, solitary tract, cuneate nucleus, raphe and periaqueductal gray. CGRP-immunoreactivity was also present in perikarya in the ventral horn of the spinal cord, as well as motor nuclei of cranial nerves, i.e., hypoglossal nucleus, ambiguous nucleus. Our results suggest that Nph-immunoreactivity in the human brainstem may be present predominantly within long fiber projections from hypothalamic neurosecretory nuclei, in analogy to data obtained from rodents, whereas CGRP may play a role in the branchiomotor system as well as in intrinsic or extrinsic projections involved in autonomic regulation and integration of sensory information.
 ...
PMID:Immunohistochemical mapping of neurophysins and calcitonin gene-related peptide in the human brainstem and cervical spinal cord. 193 Jul 49


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>