scholarly journals Cardiac effects of prostaglandins E1 and F1α

1981 ◽  
Vol 59 (5) ◽  
pp. 473-478 ◽  
Author(s):  
Rao V. S. V. Vadlamudi ◽  
John H. McNheill

The effects of prostaglandin E1 (PGE1) and prostaglandin F1α (PGF1α) were studied on perfused rat hearts and isolated rat atria. Both PGE1 and PGF1α produced dose-dependent increases in right atrial rate but had no effect on left atrial tension development. PGE1 (10−4 M) increased right atrial cyclic AMP content without changing phosphorylase a activity. PGF1α (10−4 M) did not change right atrial cyclic AMP or cyclic GMP content. Both prostaglandins had no effect on left atrial cyclic nucleotide content. When infused at a rate of 1 μg/min, PGE1 produced a time-dependent increase in cyclic AMP content in the Langendorff perfused hearts but did not alter contractile force development or phosphorylase a activity. An infusion of PGF1α produced a dose-dependent increase in tension development which was secondary to a negative chronotropic effect. PGF1α (1 μg/min) did not produce any changes in cyclic nucleotide levels or phosphorylase a activity in the Langendorff perfused hearts. These results show that PGE1 can selectively increase myocardial cyclic AMP content without altering contractile force or phosphorylase activity and that PGF1α does not increase rat cardiac AMP levels.

1969 ◽  
Vol 47 (10) ◽  
pp. 871-879 ◽  
Author(s):  
D. Kadar ◽  
F. A. Sunahara

The effects of prostaglandins on the isolated mesenteric vein and artery of the dog were investigated. Prostaglandin E1 (PGE1) inhibited spontaneous contractions of the tissue whereas prostaglandin F1α (PGF1α) and prostaglandin F2α (PGF2α) stimulated them. The effects of prostaglandins were not influenced by pretreatment with atropine, phenoxybenzamine, propranolol, or tetrodotoxin. The norepinephrine-induced contractions were inhibited by PGE1 and enhanced by PGF1α and PGF2α Both these contrasting effects were enhanced in a low concentration of K+ (1.2 mM) and diminished when the media contained K+ in high concentration (23.2 mM). Pretreatment of the tissue with ouabain in sufficiently high concentration (1.5 × 10−5 M) produced an initial contracture followed by relaxation. PGE1 and PGF1α had no effect on the ouabain-treated tissue but PGF2α still induced dose-dependent contractions. In the ouabain-treated tissue the effects of PGE1 and PGF1α on the norepinephrine-induced contraction were also absent. From these experiments it is concluded that the transport enzyme (Na+ + K+)-dependent ATPase is necessary for PGE1 and PGF1α to elicit their action on vascular tissue. The PGF2α effect is probably mediated by an enzyme which is not sensitive to ouabain.


1983 ◽  
Vol 61 (6) ◽  
pp. 608-613 ◽  
Author(s):  
A. K. Goff ◽  
D. T. Armstrong

The changes in responsiveness of granulosa cells to either FSH or prostaglandin E2 (PGE2), during culture of the cells, have been examined. In freshly isolated cells, FSH and PGE2 stimulated both cyclic AMP and progesterone production in a dose–dependent manner. In these cells, FSH stimulated cyclic AMP production to a greater extent than did PGE2. After the cells had been cultured for 2 days, neither FSH nor PGE2 stimulated progesterone production to any detectable extent. In these cells the ability of FSH to stimulate cyclic AMP was decreased, and that of PGE2 was increased markedly, such that PGE2 was far more effective than FSH in stimulating cyclic AMP. After culture of the cells for a further 2 days (4 days total), the FSH stimulation of cyclic AMP returned to that seen in freshly isolated cells, whereas the stimulation by PGE2 remained elevated. The acute stimulation of progesterone production could be restored by chronic exposure of the cells to either FSH or PGE2. These results demonstrate that dramatic changes in responsiveness of granulosa cells take place during culture. The results also suggest that some stimulating factor must be present to maintain the steroidogenic capabilities of the cells. Without this, although the cells are able to produce cyclic AMP in response to FSH, they cannot produce progesterone.


Author(s):  
M.K. Tripathi ◽  
S. Mondal ◽  
I.J. Reddy ◽  
A. Mor

Background: Corpus luteum plays key role in embryonic survival. Prostaglandins are the important regulator controlling the life span of corpus luteum. The present study investigated the effect of various doses of TNFα on in vitro PGF2α and PGE2 production and expression profiling of PGFS and PGES mRNA in buffalo Corpus Luteum (CL).Methods: Buffalo ovaries with mid-luteal phase CL were collected from the abattoir and CL were enucleated from surrounding tissues. Corpus luteum were finely chopped, rinsed with HBSS (Hanks Balanced Salt Solution) medium; supplemented with gentamycin and 0.1% BSA and incubated at 37°C for 1 hr in HBSS containing 0.1% collagenase. The cell suspension following filtration was washed by HBBS supplemented with gentamycin and 0.1% BSA (bovine serum albumin) and was treated with increasing doses of TNFα (0.1, 0.5 and 1.0 nM) and cultured at 38.5°C, 5% CO2 level for 24 hr. Result: There was dose dependent increase in concentrations of PGF2α and PGE2 with increasing doses of TNFα. The PGFS (prostaglandin F synthase) mRNA expression increased with increasing doses of TNFα. However, there was decrease in PGES (prostaglandin E synthase) mRNA expression at 0.1 nM and 0.5 nM TNFα but PGES mRNA expression increased at 1.0 nM TNFα as compared to control. It can be concluded that TNFα may alter PGES and PGFS mRNA expression and prostaglandin secretion in buffalo CL. 


1957 ◽  
Vol 192 (1) ◽  
pp. 114-120 ◽  
Author(s):  
Marion deV. Cotten ◽  
Phyllis E. Stopp

Ouabain induces a moderate increase in the contractility of the nonfailing heart of the dog with a complete circulatory system in doses which do not produce electrocardiographic signs of digitalis intoxication. The increased contractility was demonstrated both by the increase in ventricular contractile force and by the higher ventricular function curves obtained after administration of ouabain. The drug also increased systemic peripheral resistance and blood pressure, decreased systemic output, heart rate, left and right atrial pressures, and produced only small, variable changes in left ventricular stroke work. The reduction in systemic output and left atrial pressure and the absence of substantial changes in stroke work after ouabain appeared to be the result of a decrease in venous return to the heart. Evidence for this interpretation was obtained from experiments in which left atrial pressure was kept constant during the actions of ouabain by infusing 100–300 cc of whole blood. Under these conditions, ouabain brought about moderate increases in systemic output and left ventricular stroke work as well as in contractile force even though the changes in heart rate and blood pressure were comparable to those obtained in experiments in which left atrial pressure was uncontrolled. The data presented indicate that ouabain has two primary hemodynamic effects in the normal animal, namely, a direct cardiac stimulant action and a peripheral action resulting in a decreased venous return. The relationship of these findings to the mechanism of action of digitalis in congestive heart failure is discussed.


1988 ◽  
Vol 26 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Ichiro Nagata ◽  
Kenichi Furuya ◽  
Eiji Imaizumi ◽  
Katsuyoshi Seki ◽  
Noriko Makimura ◽  
...  

1982 ◽  
Vol 93 (1) ◽  
pp. 1-9 ◽  
Author(s):  
D. Dumas ◽  
B. Charrier ◽  
A. Margotat ◽  
J. Mauchamp

Thyroid cell cyclic AMP synthesis is stimulated by β-adrenergic agonists. We have characterized this sensitivity on cultured porcine thyroid cells and have studied its modulation by chronic treatment with thyrotrophin. The synthesis of cyclic AMP in intact porcine thyroid cells in primary culture was stimulated by the β-adrenergic agonist, isoproterenol. This stimulation was dose-dependent and was inhibited by the β-adrenergic antagonists propranolol and alprenolol. The cell responsiveness (i.e. the response elicited by 5 μm-isoproterenol after 5-min stimulation) was increased when the cells were cultured in the absence of thyrotrophin. Thyrotrophin, when present in the culture medium at the onset of culturing, inhibited this increase. A concentration of 100 μu. thyrotrophin/ml was sufficient to reduce the cyclic AMP response to 15% of its control value. Prostaglandin E2 or dibutyryl cyclic AMP did not mimic the effect of thyrotrophin. The low sensitivity of thyrotrophin-treated cells to β-adrenergic agonists could be explained by a decreased number of β-adrenergic receptors. [125I]Iodohydroxybenzyl pindolol specific binding was ten times greater in membrane preparations of control cells than in membranes derived from thyrotrophin-treated cells. The β-adrenergic sensitivity of cultured thyroid cells was also decreased after long-term treatment by terbutaline. A time- and dose-dependent desensitization was observed.


1976 ◽  
Vol 50 (6) ◽  
pp. 487-491
Author(s):  
K. Siddle ◽  
C. J. Davies ◽  
K. J. Shetty ◽  
R. S. Elkeles

1. The action of insulin on plasma cyclic nucleotide concentrations in normal human subjects has been studied after intravenous injection, alone and in combination with glucagon. 2. After injection of insulin alone there was an initial small, though not significant, decrease in plasma cyclic AMP at 15 min followed by an increase to more than twice the initial concentration at 30 min. The increase was absent when hypoglycaemia was lessened by infusion of glucose after insulin injection. 3. Injection of insulin caused no significant change in plasma cyclic GMP concentration, whether or not glucose was infused after the hormone. 4. Glucagon (3–300 nmol, 10–1000 μg), caused a dose-dependent increase in plasma cyclic AMP concentration. The rise in plasma cyclic AMP produced by 3 or 30 nmol of glucagon was not significantly modified by simultaneous injection of insulin (44 nmol; 6 units).


1989 ◽  
Vol 121 (3) ◽  
pp. 395-400 ◽  
Author(s):  
Werner Schlegel ◽  
Dieter Daniels

Abstract. Luteal cells were isolated from pseudopregnant rabbits on days 3, 6, 9, 12 and 15 post ovulation. Prostaglandin concentration and the activities of the enzymes prostaglandin E-2-9-ketoreductase and prostaglandin-15-hydroxydehydrogenase were determined. Luteal cells from day 7 and 12 of pseudopregnancy were maintained in culture for 24 h and then exposed to a mixture of [1-14C]PGE2 (70 μmol/l) in the presence or absence of estradiol-17β. After a 24 h incubation period, the culture medium was adjusted to pH 3.5, immediately extracted and analysed for PG. Cultured luteal cells were able to convert exogenously applied PGE2 to PGF2α and to metabolize both PGs. Primary PGs as well as their metabolites 15-keto PGE2, 15-keto PGF2α, 13,14 dihydro15-keto PGE2, and 13,14 dihydro-15-keto PGF2α were detected in the culture medium and in the cells. The addition of estradiol-17β together with PGE2 caused a significant reduction in the PGE2-9-ketoreductase mediated PGF2α synthesis, whereas the metabolism of PGE2 remained unchanged. This inhibitory effect of estradiol-17β was dose-dependent on day 12 of pseudopregnancy. The results demonstrate that isolated rabbit luteal cells are able to synthesize and metabolize the luteolytic factor PGF2α. Whether the inhibitory effect of estradiol-17β may have any physiological relevance has to be examined in further studies.


1980 ◽  
Vol 93 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Naokazu Nagata ◽  
Yuriko Ono ◽  
Narimichi Kimura

Abstract. The interaction between parathyroid hormone (PTH) and prostaglandin E1 (PGE1) in influencing cyclic AMP metabolism in rat renal cortical tissue was examined. PTH and PGE1 stimulated additively the adenylate cyclase activity in the homogenate of the tissue. Both PTH and PGE1 enhanced the level of cyclic AMP in the incubated renal cortical tissue, but the effect of their simultaneous addition did not exceed the effect induced by PTH alone. Cyclic AMP accumulated in the incubation medium by stimulation by PTH was decreased by the simultaneous addition of PGE1. When the tissue was pre-incubated for 30 min with 2 to 10 μg/ml of PGE1, the magnitude of the increase of cyclic AMP caused by PTH subsequently added was lessened. However, the response to PTH of adenylate cyclase preparation obtained from the homogenate of PGE1-pre-treated tissue was not decreased. When first PTH was added to the incubating renal cortical tissue, the subsequent addition of PGE1 accelerated the decrease of cyclic AMP content in the tissue and decreased the amount of cyclic AMP released from the tissue. The interaction of PTH and PGE1 on cyclic AMP metabolism in the renal cortical tissue was in contrast to that seen in newborn rat calvaria where PGE1 and PTH acted additively in enhancing the level of cyclic AMP.


Author(s):  
M Medvedev, M.V. Kubrina, O.S. Zarubina et all

Two cases of prenatal ultrasound diagnosis of left atrial isomerism in the second trimester of gestation is presented. These two cases were in combination with pulmonary atresia and right aortic arch. Left atrial isomerism was identify by the digit-like shape of the left and right atrial appendages. The pulmonary atresia was identified on the basis of reverse flow in small pulmonary artery. A right aortic was identified by “U”-shaped confluence of aorta and ductus arteriosus in view of three vessels and trachea. The trachea was located between the vessels. The pregnancies were terminated and prenatal diagnosis was conformed at autopsy


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