Regulation of fetal vascular tone in the human placenta

1991 ◽  
Vol 3 (4) ◽  
pp. 475 ◽  
Author(s):  
WA Walters ◽  
AL Boura
Keyword(s):  
Smooth Muscle ◽  
Prostaglandin E1 ◽  
Vascular Tone ◽  
Thromboxane A2 ◽  
High Sensitivity ◽  
Human Platelets ◽  
Perfusion Technique ◽  
A2 Receptors

Using an in vitro placental lobule perfusion technique, the human fetal placental vasculature has been found to respond vigorously with high sensitivity to various vasoconstrictor substances, including angiotensin II, endothelins 1 and 3, prostaglandins F2 alpha, E2 and D2 and the thromboxane A2 agonist U46619. Thromboxane A2 receptors mediating vasoconstriction have been characterized in fetal placental vessels and appear to be identical to those on human platelets and pulmonary blood vessels. Although the isolated fetal placental vessels are largely unresponsive to exogenous vasodilatory stimuli, when preconstricted they respond by vasodilatation to several vasodilator substances, including arachidonate, prostacyclin, prostaglandin E1, theophylline and nitroglycerine. The resistance offered to flow in vitro by the villous vasculature is therefore low, as it is in vivo. Both intrinsic and extrinsic mechanisms probably operate to cause relaxation of the vascular smooth muscle with the vasodilatory effects of locally released autacoids dominating the effects of those having vasoconstrictor actions.

Increased in vitro airway responsiveness in sheep following repeated exposure to antigen in vivo

1985 ◽  
Vol 59 (6) ◽  
pp. 1874-1878 ◽  
Author(s):  
E. M. Wagner ◽  
S. R. Kleeberger ◽  
E. W. Spannhake ◽  
G. K. Adams
Keyword(s):  
Smooth Muscle ◽  
Thromboxane A2 ◽  
Airway Responsiveness ◽  
Tracheal Smooth Muscle ◽  
Prostaglandin F2 Alpha ◽  
Peripheral Airway ◽  
Exposure In Vivo ◽  
Thromboxane A2 Analogue

We have studied the effect of repeated in vivo antigen exposure on in vitro airway responsiveness in sensitized sheep. Fourteen sheep underwent five biweekly exposures to aerosolized Ascaris suum antigen or saline. Following this exposure regimen, the animals were killed and tracheal smooth muscle and lung parenchymal strips were prepared for in vitro studies of isometric contraction in response to histamine, methacholine, prostaglandin F2 alpha, and a thromboxane A2 analogue. No alteration in tracheal smooth muscle responsiveness was observed between saline- and antigen-exposed tissue. In contrast, by use of lung parenchymal strips as an index of peripheral airway responsiveness, significant increases in responsiveness to histamine and a thromboxane A2 analogue (10(-6) and 10(-5) M) were observed in antigen-exposed tissue compared with saline controls. These results demonstrate that repeated antigen exposure in vivo selectively increase the responsiveness of peripheral lung smooth muscle to certain chemical mediators of anaphylaxis.

Pharmacologic antagonism of thromboxane A2 receptors by trimetoquinol analogs in vitro and in vivo

Chirality ◽  
1991 ◽  
Vol 3 (2) ◽  
pp. 112-117 ◽  
Author(s):  
Yangmee Shin ◽  
Karl J. Romstedt ◽  
Kathrine Doyle ◽  
Marc W. Harrold ◽  
Mark A. Gerhardt ◽  
...  
Keyword(s):  
Thromboxane A2 ◽  
A2 Receptors

scholarly journals Intrinsic activity of the non-prostanoid thromboxane A2 receptor antagonist, daltroban (BM 13,505), in human platelets in vitro and in the rat vasculature in vivo

1995 ◽  
Vol 115 (1) ◽  
pp. 210-216 ◽  
Author(s):  
Frédéric Bertolino ◽  
Jean-Pierre Valentin ◽  
Myriam Maffre ◽  
Françoise Grelac ◽  
Anne-Marie Bessac ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Thromboxane A2 ◽  
Human Platelets ◽  
Intrinsic Activity ◽  
Thromboxane A2 Receptor

Stretch-dependent (myogenic) tone in rabbit ear resistance arteries

1986 ◽  
Vol 250 (1) ◽  
pp. H87-H95 ◽  
Author(s):  
J. J. Hwa ◽  
J. A. Bevan
Keyword(s):  
Smooth Muscle ◽  
Vascular Tone ◽  
Mechanical Stretch ◽  
Myogenic Tone ◽  
Resistance Arteries ◽  
Physiological Regulation ◽  
Rabbit Ear ◽  
Arterial Tone

Rabbit ear resistance arteries are vessels with three to six layers of smooth muscle cells and an unstretched lumen diameter of 75-150 micron. Ring segments of these arteries, in response to mechanical stretch in vitro, developed a maintained tonic contraction. The stretch-dependent contraction achieved a plateau within 10-30 min. Smooth muscle relaxants, such as NaNO2 and papaverine, substitution of extracellular Ca2+ by subthreshold Ca2+ (25 microM), or exposure to the Ca2+ influx antagonist Mn2+ abolished the stretch-dependent tone. The extent of the tone was dependent on the level of the applied stretch and the extracellular Ca2+ concentration ( [Ca2+]o). The maximal tone developed at optimal stretch, and [Ca2+]o in the bath solution was 18.1 +/- 4.6% of the maximal contraction of the vessel to histamine. This level of tone is comparable to neurogenic tone developed in response to nerve stimulation within the physiological frequency range. The stretch-dependent tone is considered probably myogenic in origin, since it was present in arterial segments that had been chronically denervated by surgical sympathectomy, mechanically deprived of the endothelium, and multireceptor blocked (phenoxybenzamine, 10(-6) M). Our findings suggest first that the stretch-dependent tone is myogenic and may be similar to basal vascular tone arising from the stretch of arterial pressure and its changes in vivo. Second, the magnitude of myogenic tone is a function of the applied stretch and the [Ca2+]o. Finally, myogenic tone is important in the physiological regulation of arterial tone in the rabbit ear resistance arteries.

In vivo attenuation of endothelium-dependent pulmonary vasodilation by methylene blue

1991 ◽  
Vol 71 (2) ◽  
pp. 735-741 ◽  
Author(s):  
J. R. Fineman ◽  
M. R. Crowley ◽  
M. A. Heymann ◽  
S. J. Soifer
Keyword(s):  
Methylene Blue ◽  
Smooth Muscle ◽  
Arterial Pressure ◽  
Guanylate Cyclase ◽  
Vascular Tone ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Vasodilation ◽  
Pulmonary Arterial

In vitro evidence suggests that resting pulmonary vascular tone and endothelium-dependent pulmonary vasodilation are mediated by changes in vascular smooth muscle concentrations of guanosine 3′,5′-cyclic monophosphate (cGMP). We investigated this hypothesis in vivo in 19 mechanically ventilated intact lambs by determining the hemodynamic effects of methylene blue (a guanylate cyclase inhibitor) and then by comparing the hemodynamic response to five vasodilators during pulmonary hypertension induced by the infusion of U-46619 (a thromboxane A2 mimic) or methylene blue. Methylene blue caused a significant time-dependent increase in pulmonary arterial pressure. During U-46619 infusions, acetylcholine, ATP-MgCl2, sodium nitroprusside, isoproterenol, and 8-bromo-cGMP decreased pulmonary arterial pressure. During methylene blue infusions, the decreases in pulmonary arterial pressure caused by acetylcholine and ATP-MgCl2 (endothelium-dependent vasodilators) and sodium nitroprusside (an endothelium-independent guanylate cyclase-dependent vasodilator) were attenuated by greater than 50%. The decreases in pulmonary arterial pressure caused by isoproterenol and 8-bromo-cGMP (endothelium-independent vasodilators) were unchanged. This study in intact lambs supports the in vitro evidence that changes in vascular smooth muscle cell concentrations of cGMP in part mediate resting pulmonary vascular tone and endothelium-dependent pulmonary vasodilation.

scholarly journals EFFECTS OF PROSTAGLANDIN E1 ON CANINE GASTROINTESTINAL MOTILITY IN VIVO AND HUMAN ISOLATED SMOOTH MUSCLE IN VITRO.

1973 ◽  
Vol 9 (2) ◽  
pp. 69-77 ◽  
Author(s):  
Shuichi OHASHI ◽  
Suguru OHMURO ◽  
Ichiro SUGAWARA ◽  
Keiji KUWATA ◽  
Eizo OKAMOTO
Keyword(s):  
Smooth Muscle ◽  
Gastrointestinal Motility ◽  
Prostaglandin E1

scholarly journals Endothelium-Derived Hyperpolarizing Factor and Myoendothelial Coupling: The in vivo Perspective

2020 ◽  
Vol 11 ◽  
Author(s):  
Kjestine Schmidt ◽  
Cor de Wit
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Tone ◽  
Radial Spread ◽  
Distinct Features ◽  
Type Response ◽  
Chemical Mediators

The endothelium controls vascular tone adopting blood flow to tissue needs. It releases chemical mediators [e.g., nitric oxide (NO), prostaglandins (PG)] and exerts appreciable dilation through smooth muscle hyperpolarization, thus termed endothelium-dependent hyperpolarization (EDH). Initially, EDH was attributed to release of a factor, but later it was suggested that smooth muscle hyperpolarization might be derived from radial spread of an initial endothelial hyperpolarization through heterocellular channels coupling these vascular cells. The channels are indeed present and formed by connexins that enrich in gap junctions (GJ). In vitro data suggest that myoendothelial coupling underlies EDH-type dilations as evidenced by blocking experiments as well as simultaneous, merely identical membrane potential changes in endothelial and smooth muscle cells (SMCs), which is indicative of coupling through ohmic resistors. However, connexin-deficient animals do not display any attenuation of EDH-type dilations in vivo, and endothelial and SMCs exhibit distinct and barely superimposable membrane potential changes exerted by different means in vivo. Even if studied in the exact same artery EDH-type dilation exhibits distinct features in vitro and in vivo: in isometrically mounted vessels, it is rather weak and depends on myoendothelial coupling through connexin40 (Cx40), whereas in vivo as well as in vitro under isobaric conditions it is powerful and independent of myoendothelial coupling through Cx40. It is concluded that EDH-type dilations are distinct and a significant dependence on myoendothelial coupling in vitro does not reflect the situation under physiologic conditions in vivo. Myoendothelial coupling may act as a backup mechanism that is uncovered in the absence of the powerful EDH-type response and possibly reflects a situation in a pathophysiologic environment.

Role of Thromboxane A2 as a Mediator of Platelet-Activating-Factor-Induced Aggregation of Human Platelets

1989 ◽  
Vol 77 (1) ◽  
pp. 99-103 ◽  
Author(s):  
R. K. McCulloch ◽  
J. Summers ◽  
R. Vandongen ◽  
I. L. Rouse
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activating Factor ◽  
Thromboxane A2 ◽  
Human Platelets ◽  
Minor Role ◽  
A Minor ◽  
Induced Aggregation

1. At present it is unclear whether platelet-activating-factor (PAF)-induced aggregation is mediated by thromboxane. To obtain further information about this event we have compared the affects of aspirin on platelet aggregation and secretion induced by PAF and collagen. 2. Collagen and PAF induced aggregation and secretion in human platelets in a dose-related manner. 3. Aspirin inhibited the magnitude of both platelet aggregation and secretion induced by PAF and collagen, but the degree of inhibition was much greater for collagen. 4. Aspirin strongly inhibited the aggregation rate of collagen-induced platelet aggregation, but had no measurable effect on the rate of PAF-induced aggregation. 5. Inconsistencies reported in previous studies of the effect of aspirin on PAF-induced platelet aggregation may be explained, in part, by the doses of PAF used and the method of inactivating cyclo-oxygenase (in vitro compared with in vivo). 6. Our results suggest that the initial events of PAF-induced aggregation are independent of thromboxane A2 formation and that thromboxane A2 plays only a minor role in the later phase of PAF-induced aggregation.

The Effects of Brinolase (Fibrinolytic Enzyme from Aspergillus Oryzae) on Platelet Aggregation of Dog and Man

1972 ◽  
Vol 28 (01) ◽  
pp. 031-048 ◽  
Author(s):  
W. H. E Roschlau ◽  
R Gage
Keyword(s):  
Platelet Aggregation ◽  
Aspergillus Oryzae ◽  
Degradation Products ◽  
Blood Platelet ◽  
Human Platelets ◽  
Fibrinolytic Enzyme ◽  
Inhibitory Effects ◽  
Blood Platelet Aggregation

SummaryInhibition of blood platelet aggregation by brinolase (fibrinolytic enzyme from Aspergillus oryzae) has been demonstrated with human platelets in vitro and with dog platelets in vivo and in vitro, using both ADP and collagen as aggregating stimuli. It is suggested that the optimal inhibitory effects of brinolase occur indirectly through the generation of plasma fibrinogen degradation products, without compromising platelet viability, rather than by direct proteolysis of platelet structures.

The Filter Loop Technique as a Method of Measuring Platelet Aggregation in the Flowing Blood of the Rat; the Inhibitory Activity of 5-oxo-l-cyclopentene-l-heptanoic Acid (AY-16,804) on Platelet Aggregation

1973 ◽  
Vol 30 (01) ◽  
pp. 138-147 ◽  
Author(s):  
Christopher R. Muirhead
Keyword(s):  
Platelet Aggregation ◽  
Prostaglandin E1 ◽  
Suitable Model ◽  
Heptanoic Acid ◽  
Simple Method ◽  
Loop Technique ◽  
Flowing Blood ◽  
Filter Loop

SummaryThe filter loop technique which measures platelet aggregation in vivo in the flowing-blood of the rat was compared to the optical density technique of Born which is carried out in vitro with platelet rich plasma. Using these two experimental models the effect on platelet aggregation of three known inhibitors sulfinpyrazone, dipyridamole and prostaglandin E1, and a novel compound 5-oxo-l-cyclopentene-l-heptanoic acid (AY-16, 804) was determined.The effects on platelet aggregation of the known inhibitors were consistent with information in the literature. Prostaglandin E1 was the most potent inhibitor in both techniques; sulfinpyrazone inhibited aggregation in both models but was less potent than prostaglandin E1. AY-16, 804 exhibited activity in vitro and in vivo similar to that of sulfinpyrazone. Dipyridamole did not inhibit platelet aggregation in vivo and did not inhibit aggregation in vitro in concentrations at which it remained soluble.The filter loop technique is a suitable model for measuring platelet aggregation in the flowing blood of the rat. It is a relatively simple method of determining aggregation and easily adapted to other species.

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