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PubMedDate not supplied

AVP-independent high osmotic water permeability of frog urinary bladder and autacoids.

In the isolated frog urinary bladder a 20- to 50-fold increase of the osmotic water permeability has been revealed in the absence of arginine vasopressin (AVP) as a result of several successive changes of the serosal Ringer solution. This increase of the osmotic water permeability was of the same magnitude as that of the effect of 1 nM AVP. Similarly to the effect of AVP, the amount of adenosine 3',5'-cyclic monophosphate (cAMP) in the cells rose, and aggregates of intramembraneous particles were formed in the apical plasma membrane of granular cells (as shown by the freeze-fracture method). Immunocytochemical studies using anti-actin monoclonal antibodies indicated depolymerization of F-actin following the AVP-independent change in water permeability. It was possible to decrease the high level of osmotic permeability to the initial level if 10 microl/ml of frog blood serum or a lipid extract of this blood serum, or 1 microM arachidonic acid or 1 nM prostaglandin E2 was added to the serosal Ringer solution. The rapid restoration of the osmotic water impermeability of the epithelium after the AVP- evoked effect was achieved by the addition to the serosal Ringer solution of Ringer solution in which intact frog urinary bladders had been previously incubated for 1 h. The data obtained indicate that the maintenance of the impermeability to water of the osmoregulating epithelium and the restoration of the initial low level of the osmotic permeability after the effect of AVP are due to participation of prostaglandin E2 and other autacoids as well as, probably, some physiologically active substances of a lipid nature that are present in the blood serum.

Animals↗
PubMed1982

Autacoid and autonomic reactivity of sheep lung parenchymal strip and its modification by antigenic sensitization.

Lung parenchymal strips (LPS) of horse plasma-sensitized and control sheep were studied isometrically in isolated organ baths and their responses to autacoid and autonomic agents were compared. Control LPS responded with contractions to histamine greater than carbachol greater than 5HT and relaxed to isoproterenol greater than adrenaline greater than phenylephrine. In sensitized LPS, adrenaline and phenylephrine-induced relaxations were converted to contractions and a new order of potency and efficacy for spasmogens was observed i.e. histamine greater than carbachol greater than adrenaline greater than phenylephrine greater than 5HT. Isoproterenol was also significantly (P less than 0.05) less potent and less effective in relaxing sensitized LPS compared to controls. Mepyramine, atropine and propranolol competitively antagonized their respective agonists (i.e. histamine, carbachol and isoproterenol) confirming the presence of H1-histaminergic, muscarinic-cholinergic and beta-adrenergic receptors respectively. The conversion of the relaxant effect of adrenaline and phenylephrine to a contraction supplemented by a significant reduction in isoproterenol activity suggests an impairment in the effective ratio of beta: alpha adrenoceptors in ovine LPS subsequent to antigenic sensitization.

Animals↗
PubMed2000

Changes in renal autacoids and hemodynamics associated with aging and isolated systolic hypertension.

The aging kidney is characterized by a decrease in renal blood flow and glomerular filtration rate mainly due to glomerulosclerosis. Nevertheless, even in the presence of these changes, the kidney maintains its functionality until advanced age. However, there is a tendency towards greater renal vasoconstriction in the elderly as compared with young individuals. This occurs either in physiological circumstances such as physical exercise, or in disease manifestations, such as the effective circulatory volume depletion that develops, for example, in heart failure. This tendency may be secondary to the reduction of renal autacoid modulatory capacity, particularly at the vasodilating prostaglandin level. In an acute experimental model we could demonstrate that, in the healthy elderly, the renal response to adrenergic activation by mental stress is characterized by a prolonged and pronounced vasoconstriction. In addition to this, in elderly patients affected by isolated systolic hypertension, we demonstrated an impairment of renal hemodynamic and humoral adaptation capacity in response to adrenergic activation and blood pressure increase. In the presence of sudden blood pressure increase, the kidney of these patients responds with a passive vasodilation and a glomerular filtration rate increase without any activation of humoral modulatory substances. The impairment in renal adaptation capacity may predispose these patients to renal injury, particularly in the presence of the many hypertensive peaks which characterize everyday life of elderly individuals. In conclusion, these results show that renal adaptation capacity of elderly patients with isolated systolic hypertension is completely lost. Further studies will elucidate whether antihypertensive treatment per se, or specific classes of antihypertensive drugs, are able to revert this impairment.

Aged↗
PubMed1988

Alteration of fate of vasoactive autacoids in pulmonary circulation following monocrotaline-induced lung vascular injury in rats.

1. To learn how pulmonary vascular injury alters the ability of the lung to metabolize vasoactive autacoids, lung vascular lesions were produced in rats by a single subcutaneous injection of monocrotaline (90 mg kg-1), and the blood pressure responses to angiotensin I (AI), angiotensin II (AII), bradykinin, prostaglandin E2 (PGE2) and substance P were examined. Vasoactive agents were given intravenously or intra-arterially. 2. On histological examination of the lung at 3 weeks after monocrotaline treatment, degeneration or necrotization of endothelial cells was evident. 3. The conversion of AI to AII was only slightly depressed by monocrotaline treatment. On the other hand, the depressor response to intravenously injected bradykinin was enhanced in monocrotaline-treated rats. When the rats were pretreated with indomethacin the depressor response to intravenous bradykinin was the same for both control and monocrotaline-treated groups which suggests that endogenous prostaglandins are involved in the enhancement of the response to bradykinin. 4. In monocrotaline-treated rats the depressor response to intravenous PGE2 was significantly enhanced depending on the period following the treatment, while that to the intra-arterial injection did not differ from control. 5. The data suggest that monocrotaline-induced lung injury impairs the metabolism of PGE2 during pulmonary circulation but has little effect on the conversion of AI to AII and the degradation of bradykinin in rats.

Angiotensin I↗
PubMed1986

Effects of vasoactive autacoids on different segments of human umbilicoplacental vessels.

Effects of serotonin, prostaglandin E2, prostaglandin F2 alpha, U 46619 (a thromboxane A2 mimetic) and angiotensin I and II on the perfusion pressure were studied on vessel segments from human umbilical arteries, placental arteries and the umbilical vein during in vitro perfusions. All drugs were found to induce vasoconstriction. Serotonin displayed strong vasoconstrictor potencies in all vessel segments, whereas the responsiveness to the other autacoids differed greatly in the various segments. In the umbilical artery prostanoids were most potent in the juxtafetal segment, whereas angiotensin I and II displayed greatest effects in the juxtaplacental segment. The results lend additional support to the concept that angiotensins and prostanoids are of importance in the regulation of fetal extracorporeal blood flow.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Formation of biologically active autacoids is regulated by calcium influx in endothelial cells.

The blocker of receptor-mediated calcium entry SK&F 96365 was used to evaluate the contribution of calcium influx to the formation of biologically active endothelial prostanoids and endothelium-derived relaxing factor (EDRF). SK&F 96365 inhibited histamine-stimulated calcium entry into human umbilical vein endothelial cells but not its discharge from intracellular stores as determined spectrofluorometrically by changes of intracellular calcium concentration in fura-2-loaded cells. Concordantly, SK&F 96365 inhibited histamine-induced endothelial synthesis of 6-keto-prostaglandin F1 alpha and thromboxane B2 in a dose-dependent manner. To assess the functional significance of endothelial formation of prostacyclin and EDRF to platelets, the cAMP- and cGMP-dependent phosphorylation of two platelet proteins, rap1B and a 50-kD vasodilator-stimulated phosphoprotein (VASP), was analyzed in coincubation experiments of endothelial cells with platelets. Autacoids released by histamine-stimulated endothelial cells caused the phosphorylation of rap1B and VASP in platelets, which was only partly inhibited by either indomethacin or NG-monomethyl-L-arginine but was almost completely suppressed by SK&F 96365. The concomitant endothelial release of thromboxane A2 had no effect on protein kinase C- and calcium-dependent phosphorylation of platelet proteins. The results demonstrate that blockade of receptor-mediated calcium entry by SK&F 96365 markedly reduced the release of biologically active prostacyclin and EDRF from endothelial cells. Thus, calcium influx but not calcium release from intracellular stores plays a critical role in the receptor-stimulated formation and liberation of prostacyclin and EDRF in endothelial cells.

Animals↗
PubMed1987

Changes in autacoid and neuropeptide contents of lung cells in asbestos-induced pulmonary fibrosis.

The purpose of this study was to determine if asbestos-induced pulmonary fibrosis in the rat can affect the levels of autacoids and peptides in freshly isolated lung cells. Lung fibrosis was experimentally induced in rats by a single intratracheal instillation of 5 mg UICC Canadian chrysotile B fibers. Isolated lung cells were prepared from normal and from asbestos-exposed rats. These cells were also fractionated on bovine serum albumin (BSA) gradients. The contents of serotonin (5-HT), histamine (HIST), vasoactive intestinal peptide (VIP), and bombesin (BN) were measured in isolated total cell preparations as well as in density-fractionated cell populations from normal and from asbestos-exposed rats. Analysis of total lung cell preparation showed the presence of heterogeneous populations in normal rat lung. After asbestos exposure, there were significant changes in these cell populations as evidenced by significant increases in lymphocyte and mast cell numbers. In addition, increased levels of 5-HT, HIST, and VIP were observed in isolated lung cells obtained from rats exposed to asbestos 1, 3, and 6 months after instillation. BN content was unchanged 3 months after treatment, but was significantly increased at the 6 month-interval, suggesting a different pattern of response for this neuropeptide. Density fractionation of various cell populations further showed selective changes in specific cell fractions of lung after asbestos exposure. At 6 months, increased levels of 5-HT, HIST, and VIP were associated with cell fraction 7, whereas changes in BN content were found in cell fractions 2 and 3. Similarly, there was a significant increase of mast cells in fraction 7 at the 6-month interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

In vitro effects of hormones and autacoids on the hydrogen peroxide production and the morphology of endotoxin-activated rat peritoneal macrophages.

Peritoneal macrophages activated in vitro by endotoxin exhibit alterations of their capability to produce hydrogen peroxide after phorbol ester stimulation when certain hormones or autacoids are present in the culture medium. They also show morphological changes, mainly concerning cell size and nuclear appearance. Agents known to increase the intracellular levels of cyclic AMP, e.g. adrenalin and PGE2 reduce the hydrogen peroxide production. Insulin, which is known to decrease cyclic AMP levels, produces opposite results. Agents postulated to act via phospholipase C, e.g. serotonin, augment the production of hydrogen peroxide. We assume that this form of modulation may represent a regulatory mechanism of macrophage activation.

Animals↗
PubMed2000

Changes in renal autacoids in aged human hypertensives.

The aging process determines several modifications of the kidney, that, however, do not provoke any dysfunction in normal conditions. But in the elderly--in the presence of stressful situations and particularly when adrenergic activation is present--the kidney is more vulnerable than in the young, and renal failure may arise. Variations typical of the aging kidney are accelerated when hypertension overlaps the physiological renal process, because both senescence and hypertension weight on the same structures, i.e. glomeruli. We studied renal hemodynamic adaptation capacity both in the healthy elderly and in patients affected by isolated systolic hypertension, in an acute experiment which requires the application of a mental stress-induced adrenergic activation. In hypertensive patients we have already demonstrated a total lack of renal adaptation capacity. In fact, while the elderly normotensives react with a prolonged and pronounced vasoconstriction, in those with isolated systolic hypertension, adrenergic activation induces a passive renal vasodilation and glomerular hyperfiltration. The anomalous adaptation capacity of renal hemodynamics is probably due to an impairment in the paracrine response of renal vasculature. Indeed in the hypertensive elderly, unlike in the normotensive one, no variations of autacoid production occur during the adrenergic activation. Following on from this, pattients affected by isolated systolic hypertension passively suffer the many hypertensive peaks which characterize their every day life. The altered renal autoregulation of the elderly with isolated systolic hypertension may explain the accelerated glomerulosclerosis and the greater incidence of renal damage and end-stage renal disease which characterize this condition. These aspects underline the primary role of the antihypertensive treatment of isolated systolic hypertension, not only for the prevention of cardiovascular mortality but also of renal damage and/or end-stage renal disease.

Aging↗
PubMed2002

Inhibitory role of Syzygium cumini on autacoid-induced inflammation in rats.

The ethanolic extract of Syzygium cumini bark has been reported to possess anti-inflammatory activity in our previous studies. The present study is an attempt to elucidate the anti-inflammatory activity of S. Cumini bark against inflammation induced by individual autacoid insult. Histamine (1 mg/ml), 5-HT (1 mg/ml), bradykinin (0.02 mg/ml) and PGE2 (0.001 mg/ml) were used as inflammogens. One of these agents (0.1 ml) was injected s.c. into the right hind paw of each rat. The ethanolic extract of S. cumini bark was tested at the doses of 100, 300 and 1000 mg/kg, p.o. The results indicated the anti-inflammatory activity of S. cumini bark in histamine, 5-HT and PGE2-induced rat paw oedema. However, there was no such significant inhibition of oedema volume observed in bradykinin-induced rat paw oedema at any dose level. Thus, it is concluded that S. cumini exhibits inhibitory role on inflammatory response to histamine, 5-HT and PGE2.

Animals↗
PubMed1991

[Contractile responsiveness of the isolated guinea pig oviduct to autacoids at different phases of the sexual cycle or under ovarian steroid treatment].

Contraction of the longitudinal smooth muscle of the isolated guinea pig oviduct in response to autacoids was examined at different phases of the sex cycle or during ovarian steroid treatments. Isolated strips from isthmic smooth muscle of the female guinea pig (body weight; 300-900 g) oviduct were mounted in an organ bath and their isotonic responses were measured in the longitudinal direction. Histamine (greater than or equal to 3 X 10(-8) M) produced a concentration-dependent contraction of the oviductal smooth muscle, which was unaffected by the sex cycle. Noradrenaline and adrenaline (greater than or equal to 10(-8) M) produced a contraction mediated by alpha-adrenoceptors and a relaxation mediated by beta-adrenoceptor. During proestrus and metestrus (high estrogen), the contractile response was reduced but relaxation was increased, compared with those observed during diestrus. Prostaglandin E2 and F2 alpha (greater than or equal to 10(-10)M and greater than or equal to 10(-9)M, respectively) produced a concentration-dependent contraction and their maximum responses were about 50% of that induced by histamine (10(-4)M). These contractile responses were unaffected by the sex cycle. On the other hand, acetylcholine did not modify the smooth muscle tone of the isolated guinea pig oviduct in the concentration range from 10(-7)M to 3 X 10(-4)M. The contractile response of the oviductal smooth muscle to adrenaline after bilateral ovariectomy was inhibited by estrogen treatment, while relaxation was inhibited by progesterone treatment.

Animals↗
PubMed1995

Three autacoids--endogenous digitalis-like factor, clonidine-displacing substance, and quinidine-like immunoreactivity.

The existence of endogenous ligands of opioid receptors prompted research of a potential endogenous digitalis-like factor (DLF) and of endogenous clonidine-displacing substance (CDS). Within eleven years of research, endogenous ouabaine was identified as DLF. It originates in the adrenal cortex. Its physiological role is not yet clear. Most probably, endogenous ouabaine is primarily active in regulation of natriuresis and of blood pressure. The CDS originates in the brain and is active in regulation of blood pressure as well. Its chemical formula was recently identified as agmatine. The potential presence of further autacoids like, e.g. endogenous quinidine-like substance remains to be clarified.

Animals↗
PubMed1990

Endothelial cells as part of a vascular oxygen-sensing system: hypoxia-induced release of autacoids.

Higher developed organisms are equipped with many central and local control mechanisms, which enable an adequate blood and oxygen supply to tissues over a wide range of demands. Global adaptive responses include changes in the circulatory and ventilatory system as well as increases in the oxygen carrying capacity of the blood. At the level of the specialized organs there exist additional control systems for the regulation of local blood flow. Most systems make use of highly specialized cells which are able to sense the oxygen partial pressure of the transport medium, blood, and within the tissues. In the past years, it has been shown that the vascular endothelium lining the entire circulatory system can actively modulate the vascular tone and platelet functions by the release of autacoids, among them prostacyclin and endothelium-derived nitric oxide (EDRF). Recent experiments demonstrate that the release of EDRF is PO2-dependent, which suggests that endothelial cells may act as functional local oxygen sensors within the vascular system.

Adenine Nucleotides↗
PubMed1986

Prostacyclin and thromboxane formation in human umbilical arteries following stimulation with vasoactive autacoids.

The formation of prostacyclin (PGI2) and thromboxane A2 (TXA2) (measured as the stable metabolites 6-keto-PGF1 alpha and TXB2) during stimulation with vasoactive autacoids was registered in human umbilical arteries perfused in vitro. Responses were registered within 3-4 minutes after addition of the substances. Both angiotensin I and II were found to increase the formation of PGI2 while depressing that of TXA2. Serotonin increased the formation of TXA2 but not that of PGI2. Both PGE2 and PGF2 alpha stimulated the PGI2 formation. The TXA2 mimetic U46619, increased PGI2 production, whereas PGI2 slightly increased the formation of TXA2. All responses were found to be completely inhibited by indomethacin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Indomethacin enhances endothelial NO release--evidence for a role of PGI2 in the autocrine control of calcium-dependent autacoid production.

OBJECTIVE: We studied whether NO or prostacyclin (PGI2), which are continuously released by endothelial cells, have autocrine/paracrine effects on the calcium-dependent autacoid production by modulating the intracellular Ca2+ concentration ([Ca2+]i). METHODS: Histamine(His)-induced [Ca2+]i increases (Fura 2-method) and NO-dependent cGMP increase were measured in human umbilical vein endothelial cell (HUVECs) before and after cyclooxygenase inhibition or application of cAMP- and cGMP-elevating drugs. RESULTS: 0.3 microM His increased endothelial [Ca2+]i from 77 +/- 2 nM to 418 +/- 59 nM. The His-induced [Ca2+]i increases were significantly attenuated following treatment with PGI2 (by 23%) and forskolin (by 33%), both increasing the cAMP release from HUVECs (by 49% and 66%). The His-induced [Ca2+]i increases were inhibited by the protein kinase A-activator cBIMPS (by 61%) which also abolished the His-induced PGI2 release. Conversely, inhibition of the PGI2 production with indomethacin significantly augmented the His-induced [Ca2+]i increases (by 32%), resulting in a significantly augmented NO production as indicated by an enhanced LNNA-sensitive cGMP increase in HUVECs. In contrast, neither increases of cGMP (basal 0.4 +/- 0.1 pmol/mg) elicited by 10 microM SNP (21 +/- 2 pmol/mg) or 10 microM C-type natriuretic peptide (CNP, 4.6 +/- 1.6 pmol/mg) nor its reduction by 30 microM LNNA had any effect on the His-induced [Ca2+]i increases. CONCLUSION: PGI2 attenuates agonist-induced [Ca2+]i increases by a cAMP-dependent mechanism, thereby modulating not only its own synthesis via a negative feedback but also that of NO. Consequently, reduced PGI2 levels result in an increased NO production. NO which does not cause a negative feedback control by cGMP might therefore compensate for the lack of PGI2.

Autocrine Communication↗
PubMed1994

Renal autacoids are involved in the stimulation of renin gene expression by low perfusion pressure.

This study aimed to examine the role of local autacoids for the regulation of renin secretion and renin gene expression by the renal perfusion pressure. To this end the effects of unilateral reduction of renal perfusion by 0.2 mm clips on plasma renin activity and on renal renin mRNA levels were examined in rats treated with the cyclooxygenase inhibitor meclofenamate (8 mg/kg body wt, twice a day), with the NO-synthase inhibitor nitro-L-arginine-methylester (L-NAME, 40 mg/kg body wt, twice a day) or with a combination of both. L-NAME alone decreased basal PRA values from 9.9 to 5.4 ng Ang I/hr x ml, while meclofenamate alone and the combination meclofenamate/L-NAME had no consistent effect on basal PRA. Unilateral renal artery clipping increased PRA values from 9.9 ng Ang I/hr x ml to 34, 27, and 16 ng Ang I/hr x ml in vehicle, meclofenamate, and L-NAME treated animals, respectively, but did not increase PRA in meclofenamate/L-NAME treated rats (9.5 ng Ang I/hr x ml). Renal renin mRNA levels in the clipped kidneys increased 4.8-, 2.6-, 2.5- and 1.8-fold in the clipped kidneys in vehicle, meclofenamate, L-NAME and meclofenamate/L-NAME injected animals, respectively. These findings indicate that both the inhibition of prostaglandin synthesis and of the formation of endothelium-derived relaxing factor (EDRF) attenuate the increase of renin gene expression and of renin secretion in response to acute unilateral renal hypoperfusion and that the effects of both maneuvers are additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Selective inhibition of agonist-induced but not shear stress-dependent release of endothelial autacoids by thapsigargin.

1. The effects of the Ca(2+)-ATPase inhibitor, thapsigargin, on the shear stress-dependent and on the agonist-stimulated release of endothelium-derived relaxing factor, i.e. nitric oxide (NO), and prostacyclin (PGI2) were studied in bovine and human cultured endothelial cells as well as in endothelium-intact arterial segments of the rabbit. 2. Preincubation with thapsigargin (1 microM for 10 min) had no effect on the shear stress-dependent release of NO from bovine aortic endothelial cells grown on beads, but abolished the release of NO induced by ADP, bradykinin, ionomycin or poly-L-lysine. Similarly, thapsigargin completely abrogated the agonist-stimulated PGI2 release from these cells, but had no effect on the shear stress-dependent release of PGI2. 3. The acetylcholine-induced release of NO from the luminally perfused thoracic aorta and femoral artery of the rabbit was suppressed by pretreatment with thapsigargin (1 microM). In contrast, thapsigargin did not affect the shear stress-dependent release of NO from the femoral artery. 4. Administration of thapsigargin to these vascular preparations or to cultured endothelial cells alone produced a substantial release of both NO and PGI2. This release declined towards previous values after washout of thapsigargin. 5. In human and bovine cultured endothelial cells, thapsigargin (1-1000 nM) caused a dose-dependent sustained rise in [Ca2+]i, an effect that was abolished in the absence of extracellular Ca2+. Stimulation of these cells with bradykinin, histamine, ADP or ionomycin after previous exposure to thapsigargin (30-1000 nM) no longer caused an increase in [Ca2+]i. of the release of these endothelial autacoids caused by shear stress or receptor-dependent and independent agonists.

Adenosine Diphosphate↗
PubMed1990

Effects of some autacoids on breathing and perfusion flow in the isolated perfused rat lung.

The effects of three autacoids [5-hydroxytryptamine (5-HT), bradykinin and acetylcholine (Ach)) on breathing and pulmonary circulation were studied in the isolated perfused and ventilated rat lung after intravascular injection or intrabronchial instillation. 5-HT, bradykinin and Ach all caused a dose related reduction in breathing, after injection into the pulmonary artery, with Ach being the most potent. With regard to effects on the pulmonary circulation, a dose-related reduction in perfusate flow was noted with bradykinin and 5-HT with bradykinin being about 10 times more potent than 5-HT. Ach did not reduce or increase perfusate flow. After intrabronchial instillation only 5-HT caused reduced perfusate flow. Effects on breathing were difficult to evaluate with this route of administration. The isolated perfused and ventilated lung seems to be a usable model to simultaneously study effects on respiration and pulmonary circulation.

Acetylcholine↗