Role of Endothelium-Derived Metabolites of Arachidonic Acid in Enhanced Pulmonary Artery Contractions in Female Rabbits

Hypertension ◽  
1996 ◽  
Vol 27 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Sandra L. Pfister ◽  
William B. Campbell
Keyword(s):  
Arachidonic Acid ◽  
Pulmonary Artery

Role of Arachidonic Acid Metabolites in Hypoxic Contractions of Isolated Porcine Pulmonary Artery and Vein

1989 ◽  
Vol 15 (2) ◽  
pp. 213-222 ◽  
Author(s):  
D. S. Miller ◽  
A. Yaghi ◽  
J. T. Hamilton ◽  
N. A. M. Paterson
Keyword(s):  
Arachidonic Acid ◽  
Pulmonary Artery ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Porcine Pulmonary Artery

Testosterone Potentiation of Ionophore and ADP Induced Platelet Aggregation : Relationship to Arachidonic Acid Metabolism

1981 ◽  
Vol 46 (02) ◽  
pp. 538-542 ◽  
Author(s):  
R Pilo ◽  
D Aharony ◽  
A Raz
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Unsaturated Fatty Acids ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Arachidonic Acid Metabolism ◽  
Ionophore A23187 ◽  
Low Concentrations ◽  
Induced Aggregation

SummaryThe role of arachidonic acid oxygenated products in human platelet aggregation induced by the ionophore A23187 was investigated. The ionophore produced an increased release of both saturated and unsaturated fatty acids and a concomitant increased formation of TxA2 and other arachidonate products. TxA2 (and possibly other cyclo oxygenase products) appears to have a significant role in ionophore-induced aggregation only when low concentrations (<1 μM) of the ionophore are employed.Testosterone added to rat or human platelet-rich plasma (PRP) was shown previously to potentiate platelet aggregation induced by ADP, adrenaline, collagen and arachidonic acid (1, 2). We show that testosterone also potentiates ionophore induced aggregation in washed platelets and in PRP. This potentiation was dose and time dependent and resulted from increased lipolysis and concomitant generation of TxA2 and other prostaglandin products. The testosterone potentiating effect was abolished by preincubation of the platelets with indomethacin.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

The Role of TRPV4 Cation Channels in Regulation of Phenylephrine-Induced Contraction of Rat Pulmonary Artery

2017 ◽  
Vol 8 (2) ◽  
pp. 121-130
Author(s):  
Dariia Dryn ◽  
Mariia Melnyk ◽  
Ihor Kizub ◽  
Hongzhen Hu ◽  
Anatoly I. Soloviev ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Cation Channels

Heart failure in an elderly man: where is that coronary?

2021 ◽  
pp. 1-4
Author(s):  
Charlie J. Sang ◽  
Stephen A. Clarkson ◽  
Elizabeth A. Jackson ◽  
Firas Al Solaiman ◽  
Marc G. Cribbs
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Medical Therapy ◽  
Coronary Arteries ◽  
Right Coronary Artery ◽  
Adult Population ◽  
Anomalous Coronary ◽  
Anomalous Coronary Arteries

Abstract Anomalous coronary arteries from the pulmonary artery are uncommon causes of heart failure in the adult population. This case demonstrates the unusual presentation in a patient with anomalous right coronary artery from the pulmonary artery and discusses the complex pathophysiology of this lesion and the role of guideline-directed medical therapy in the management of these patients.

scholarly journals The role of the arachidonic acid cascade in the hypotensive activity of N-(dibenzyloxyphosphinoyl)-L-alanyl-L-prolyl-L-proline

1986 ◽  
Vol 40 ◽  
pp. 233
Author(s):  
Ryota Yoshimoto ◽  
Toshihiko Ishimitsu ◽  
Yoshikatsu Koyama ◽  
Shigebumi Hashimoto ◽  
Hiroaki Matsuoka ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Hypotensive Activity ◽  
Arachidonic Acid Cascade
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