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)

Changes in epithelial cell morphology, especially at the apical plasma membrane, are frequently cited as initial evidence for antidiuretic hormone (ADH)-induced increase in membrane permeability. The effects of ADH and agents that alter and modify calcium and prostaglandin concentrations on the morphology and cytology of the epithelial cells of frog (Rana pipiens) urinary bladder are presented using the techniques of transmission and scanning electron microscopy. It was found that, like ADH, calcium ionophore, A23187, produce intense microvilli formation, microfilament mobilization and an increase in the density of granules and membrane associated vesicles, suggesting a prominent role of calcium in these processes. Moreover, our results suggest that these membrane and cytosolic transformations may be mediated in part through prostaglandin formation, as exogenous PGE2 mimicked these effects, and indomethacin, a prostaglandin synthesis inhibitor, attenuated ionophore's effect on luminal cytomorphology. However, unlike ADH, prostaglandins and ionophore inhibit hormonal-induced increase in transepithelial water flow. These results suggest that other components more distal to the luminal membrane, perhaps the basolateral membrane, may be rate-limiting for transepithelial water flow and possibly are regulated by either changes in calcium concentrations or prostaglandins.
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PMID:Morphometric analysis of epithelial cells of frog urinary bladder. I. Effect of antidiuretic hormone, calcium ionophore (A23187) and PGE2. 311 95

Synthesis of prostaglandins (PGs) was characterized in the lateral wall (LW) of guinea-pig cochlea. Basal synthesis at 37 degrees C was about 480 pg/LW (12.8 ng X mg-1 protein) for PGI2 and 85 pg/LW (2.3 ng X mg-1 protein) for PGE2, levelling out after 10 min of incubation. Incubation with arachidonic acid (10(-5) M) increased PGI2 and PGE2 synthesis by 44% and 1020%, respectively, showing that arachidonic acid availability is a synthesis-limiting factor. The stimulating effect of the Ca++ ionophore A23187 (5 X 10(-6) M) on PG synthesis was weak (about +50%) but was enhanced (about +140%) by preincubation with arachidonic acid. Angiotensin II (10(-6) M), vasopressin (5 X 10(-7) M), and furosemide (10(-8) to 10(-3) M) did not alter PG secretion. Neither aspirin nor indomethacin prevented the development of furosemide ototoxicity (endocochlear potential) in the rat. Perfusion with PGI2 influenced the furosemide effect in some instances.
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PMID:Strial prostaglandins and leukotrienes. Biochemical characteristics and interrelationship with furosemide. 311 70

Urinary excretion of prostaglandin E2 (PGE2 and F2 alpha (PGF2 alpha) and plasma concentration of arginine vasopressin (AVP) were determined during urinary concentrating and diluting tests in renal transplant recipients and control subjects. During the concentrating test PGE2 and PGF2 alpha remained unchanged in the renal transplant recipients, whereas both PGE2 and PGF2 alpha were significantly reduced in the control subjects. During the diluting test PGE2 and PGF2 alpha increased in both groups but, contrary to PGF2 alpha, PGE2 was significantly higher in all periods in the transplant recipients compared to the controls. However, the prostaglandin excretion rates per kidney were significantly higher in the renal transplant recipients than control subjects, for all periods during both the concentrating and the diluting test. Arginine vasopressin was significantly higher in renal transplant recipients than control subjects during basal conditions, increased to a significantly higher level in the transplant recipients after thirst, but was reduced to the same levels in the two groups during the diluting test. It is concluded that the increased excretion of prostaglandins in renal transplant recipients may be a compensatory phenomenon representing an adaptation to a reduced renal mass in order to maintain adequate renal water excretion. Although a direct relationship between the prostaglandin excretions of PGE2 and PGF2 alpha and AVP does not seem to exist, it is possible that the higher prostaglandin excretion in the renal transplant recipients may be a counterbalancing mechanism to the higher AVP level, which most likely is secondary to a decreased responsiveness to vasopressin of the renal collecting ducts in the transplanted kidney.
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PMID:Relationship between urinary prostaglandin E2 and F2 alpha excretion and plasma arginine vasopressin during renal concentrating and diluting tests in renal transplant recipients. 312 47

The production of prostaglandins by rat renal tubular cells and by rat vascular smooth muscle cells (VSMC) in response to vasoactive hormones was examined. A superfusion technique was used to stimulate collagenase-dispersed renal cortical or medullary tubular cells and trypsinized rat aortic smooth muscle cells with vasoactive hormones and ANF. All cell types responded promptly to the stimuli in a dose-dependent manner. Renal tubular cells produced mainly PGE2, less PGF2 alpha and no 6-keto-PGF1 alpha, while VSMC produced exclusively 6-keto-PGF1 alpha. This production of PG was strictly dependent on the presence of extracellular Ca2+ and was not inhibited by antagonists of voltage-dependent Ca2+-channels. Angiotensin II (Ang II) was active on cortical tubular cells and VSMC. Sar1-Ala8-angiotensin II blocked this action. Arginine-vasopressin (AVP acted on medullary tubular cells and VSMC and its effect was inhibited by selective V1-antagonists. The V2-agonist dDAVP had no effect on PG production. A clear distinction between V1-receptor mediated PG release and V2-receptor mediated cAMP extrusion was observed in medullary tubular cells. Bradykinin was a weak agonist on medullary tubular cell. The synthetic (1-24) atrial natriuretic peptide did not prevent 6-keto-PGF1 alpha release induced by Ang II or AVP in VSMC nor the PGE2 release in cortical tubular cells induced by Ang II.
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PMID:The regulation of prostaglandins by vasoactive hormones in renal tubular and vascular smooth muscle cells. 312 55

It has been postulated that fetal hormonal signals act upon amnion to trigger labor via prostaglandin (PG) production. Human amnion epithelial cell cultures were established to test the effects of potential activators of the inositol phospholipid-protein kinase-C effector system on intracellular inositol phosphate turnover, intracellular free calcium ([ Ca2+]i), and PGE2 production. Oxytocin provoked 3-, 2.5-, and 4-fold increases in inositol triphosphate, inositol bisphosphate, and inositol monophosphate, respectively. [Ca2+]i, measured with the fluorescent dye fura-2, was stimulated by oxytocin and vasopressin (oxytocin greater than vasopressin) in a dose-dependent manner. The [Ca2+]i transient produced by oxytocin reached a peak in 15 sec, followed by a slow return to baseline over 10 min. Preincubation with phorbol 12-myristate-13 acetate (PMA) markedly blunted the oxytocin-induced transient. No [Ca2+]i transient was seen with leukotrienes, PG, serotonin, angiotensin, or alpha- or beta-adrenergic agents. PGE2 production increased 30- to 50-fold with phospholipase-C and PMA, and 10-fold with the calcium ionophore A23187. Oxytocin and vasopressin produced 10- and 3-fold PGE2 increases, respectively. Increased PGE2 production induced by PMA, oxytocin, and A23187 was first seen after 8 hr of incubation and reached maximal levels at 24 h. Minimal PGE2 stimulation occurred with agents that produced no [Ca2+]i transient. Direct activators of the inositol phospholipid-protein kinase-C system in human amnion induce large increases in PGE2 in human amnion cells. Oxytocin and vasopressin are hormonal activators of this system in these cells, as demonstrated by their effects on inositol phosphate turnover and [Ca2+]i. These hormones also increase PGE2 production and may influence labor by stimulating PGE2 production in amnion through the inositol phospholipid-protein kinase-C system.
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PMID:Oxytocin activates the inositol-phospholipid-protein kinase-C system and stimulates prostaglandin production in human amnion cells. 313 2

In four boys with congenital nephrogenic diabetes insipidus, plasma arginine-vasopressin (AVP) and urinary excretion of prostaglandins were studied in response to treatment with hydrochlorothiazide and indomethacin. An abnormal relationship between AVP and urine osmolality was demonstrated in all patients. In the first patient, treatment with indomethacin (3 mg/kg per day) resulted in a drop of the insulin and paraminohippurate clearances. In the other three patients urinary excretion of PGE2 was raised, and fell during treatment with hydrochlorothiazide (2 mg/kg per day) and indomethacin (2 mg/kg per day). Urine flow, free water clearance and osmolar clearance decreased during treatment. A combination of both drugs is more effective than hydrochlorothiazide alone and the effect appears to be additive.
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PMID:Congenital nephrogenic diabetes insipidus-vasopressin and prostaglandins in response to treatment with hydrochlorothiazide and indomethacin. 315 21

Previous studies in vitro have shown that prostaglandin (PG) E2 is formed in rat adenohypophysis upon stimulation by arginine-vasopressin (AVP) and synthetic ovine corticotropin-releasing factor (CRF-(1-41]. The aim of the present study was to examine whether long-term changes in the hypothalamic stimulation of the pituitary corticotrophs in vivo may influence PG synthesis in subsequent in vitro incubations of rat anterior pituitary quarters. The release of PGE2 from adenohypophyses obtained from adrenalectomized rats was increased to about 300% of controls both under basal conditions and after stimulation by AVP; by contrast, the release of PG D2 was changed neither by adrenalectomy nor by AVP. Simultaneously, basal release of beta-endorphin-like immunoreactivity (beta-EI) was increased after adrenalectomy to about 300% of controls, parallel to the increase in the tissue content, whereas AVP-induced beta-EI release was unchanged. Addition of PG E2 inhibited, whereas blockade of PG formation by indomethacin enhanced AVP-induced beta-EI release both in controls and after adrenalectomy. When anterior pituitary glands were taken from rats with lesions of the paraventricular nuclei, release of PG E2 was decreased as compared to controls both under basal conditions and after stimulation by AVP or CRF-(1-41). Simultaneously, basal and evoked release of beta-EI was unchanged. We conclude that the formation of PG E2 in the adenohypophysis varies according to long-term changes in the hypothalamic stimulation of adrenocorticotropin and beta-endorphin release supporting the view that PG E2 synthesis is related to, and may be involved in mechanisms controlling peptide hormone release from the corticotrophs.
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PMID:Release of prostaglandin E2 and beta-endorphin-like immunoreactivity from rat adenohypophysis in vitro: variations after adrenalectomy or lesions of the paraventricular nuclei. 315 85

The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and beta-endorphin-like immunoreactivity (beta-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2.8 and 28 mumol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of beta-EI was enhanced by indomethacin (28 mumol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of beta-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 mumol/l). Prostaglandin F2 alpha (5 mumol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 mumol/l) did not. Prostaglandin F2 alpha (5 mumol/l), D2 and I2 (1.5 mumol/l each) produced no effects on beta-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of beta-EI and, as can be inferred, alpha-MSH, by a direct action on intermediate lobe cells.
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PMID:Inhibition by prostaglandin E2 of the release of vasopressin and beta-endorphin from rat pituitary neurointermediate lobe or medial basal hypothalamus in vitro. 316 Aug 2

The relationship between natriuretic activity of neurohypophysial peptides and renal prostaglandins (PGs) was investigated in anesthetized rats under water diuresis and on kidney homogenates. Over the course of water diuresis, urinary sodium excretion increased steadily, reaching a 3.5-fold increase in 90 min, but there was no significant change in PGE2 and PGF2 alpha excretion. Inhibition of PG synthesis by naproxen sodium abolished the increase in sodium excretion. Oxytocin (OT) and vasopressin, in submaximal antidiuretic doses, produced marked natriuresis to 2139% and 345% of the control rate, respectively, without a concomitant increase in PG excretion. [Leu4]OT, which is devoid of antidiuretic activity, produced natriuresis and diuresis also without a significant effect on PG excretion. Inhibition of PG synthesis by naproxen attenuated the natriuretic response but enhanced the antidiuretic response to OT. Both the natriuretic and diuretic responses to [Leu4]OT were attenuated. Although the possibility that naproxen may have antinatriuretic activity independent of its PG synthesis inhibitory action cannot be excluded, the data obtained are consistent with our postulate that the natriuretic effect of OT-peptides may be mediated in part via a renal PG mechanism. This postulate is strengthened further by our findings that natriuretic peptides, OT, vasopressin and [Leu4]OT stimulated PG synthesis in kidney homogenates in a dose-dependent manner. Their order of potency is in the same order of their relative natriuretic potencies. [Penicillamine1,Phe(Methyl)2,Thr4,Orn8]OT, an OT antagonist and non-natriuretic, had no significant PG synthesis stimulating activity in the kidney homogenates.
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PMID:Renal prostaglandins and natriuretic action of oxytocin and vasopressin in rats. 316 43

Congestive heart failure is a complex clinical syndrome characterized by a number of neuroendocrine responses. These responses are probably an evolutionary vestige of mechanisms designed to defend volume and maintain circulatory homeostasis. Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and the release of vasopressin have been clearly documented in patients with heart failure. Unlike the normal ventricle, the failing ventricle responds to peripheral vasoconstriction and sodium retention with further hemodynamic embarrassment and circulatory congestion. Certain vasorelaxant natriuretic substances are also released during heart failure, perhaps in an attempt to offset excessive peripheral constriction and sodium retention. Prostaglandin E2, atrial natriuretic peptide (or atrial natriuretic factor) and plasma dopamine are found to be increased in some patients with heart failure. However, peripheral constriction and sodium retention appear to be dominant, particularly in the advanced stages of heart failure. An understanding of these neuroendocrine responses has led to new developments in therapy. Angiotensin-converting enzyme inhibitors have emerged as distinctly useful drugs in the treatment of heart failure. Agents designed to block excessive sympathetic drive and inhibit vasopressin are under investigation. Infusion of atrial natriuretic factors and the use of selective dopamine agonists are also undergoing clinical trials in patients with heart failure. Increased knowledge of the neuroendocrine responses will likely result in even newer and more imaginative therapy.
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PMID:Neuroendocrine manifestations of congestive heart failure. 329 96


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