Sex differences in mouse platelet aggregation.

A P Torres Duarte; P Ramwell; A Myers

doi:10.1016/0049-3848(86)90042-3

Home/Archive/PubMed

PubMed · 3088759

Sex differences in mouse platelet aggregation.

A P Torres Duarte·P Ramwell·A Myers

View original source ↗Export metadata ↓

Abstract

The role of platelets in the sex difference observed in mouse thrombosis models was evaluated by examining platelet diminution in vivo after thrombotic challenge, and aggregation of mouse platelets in PRP. A fall in platelet count was observed in both sexes after i.v. injection of either arachidonic acid or the thromboxane agonist, U46619. Platelet diminution induced by high dose arachidonate (50 mg/kg) was significantly greater in males compared to female mice. Responses to U46619 were similar in both sexes. In PRP, male platelets exhibited a greater response than female platelets to both ADP (15 uM) and arachidonate (0.3 mM), but not to U46619 (4.6 and 6.9 uM). These results suggest that the gender difference in arachidonate-induced sudden death, in which males are more susceptible than females, is related to a sex difference in mouse platelet function.

Explore related subjects

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid Adenosine Diphosphate Animals Arachidonic Acid Arachidonic Acids Dose-Response Relationship, Drug Female Hematocrit Injections, Intravenous Male Mice Mice, Inbred Strains Platelet Aggregation Platelet Count Prostaglandin Endoperoxides, Synthetic Sex Characteristics Comparative Study Journal Article Research Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

A P Torres Duarte, P Ramwell, A Myers. 1986-07-01. Sex differences in mouse platelet aggregation.. https://doi.org/10.1016/0049-3848(86)90042-3

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Involvement of Na+-Ca2+ exchanger in cAMP-mediated relaxation in mice aorta: evaluation using transgenic mice.

BACKGROUND AND PURPOSE: Although vascular smooth muscle cells are known to express the Na+-Ca2+ exchanger (NCX), its functional role has remained unclear, mainly because of its relatively low expression. We thus investigated the involvement of NCX in the mechanism for the forskolin-induced vaso-relaxation, using wild type (WT) and transgenic (TG) mice that specifically over-express NCX1.3 in smooth muscle. EXPERIMENTAL APPROACH: We examined the relaxing effect of forskolin during the pre-contraction induced by 100 nM U46619, a thromboxane A2 analogue in the mouse isolated thoracic aorta. We also measured the intracellular Ca2+ concentration ([Ca2+]i) in fura-PE3-loaded aortic strips. KEY RESULTS: The forskolin-induced decreases in [Ca2+]i and tension were much greater in aortas from TG mice than in those from WT mice. In a low Na+ solution, forskolin-induced decreases in [Ca2+]i and tension were greatly inhibited in both groups of aortas. In WT aortas, the presence of 100 nM SEA0400, an NCX inhibitor, had only a little effect on the forskolin-induced decreases in [Ca2+]i, but inhibited the forskolin-induced relaxation. However, in TG aortas, the presence of SEA0400 greatly inhibited the forskolin-induced decreases in [Ca2+]i and tension. CONCLUSIONS AND IMPLICATIONS: The NCX was involved in the forskolin-induced reduction of [Ca2+]i and tension in the mouse thoracic aorta. Measurement of [Ca2+]i and tension in aortas of the TG mouse is thus considered to be a useful tool for evaluating the role of NCX in vascular tissue.

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

PubMed2007

Differential effects of nitric oxide synthase inhibitors on endothelium-dependent and nitrergic nerve-mediated vasodilatation in the bovine ciliary artery.

BACKGROUND AND PURPOSE: We have previously demonstrated that L-NMMA (NG-monomethyl-L-arginine) selectively inhibits vasodilatation produced by endothelium-derived nitric oxide but not nitrergic nerves in the bovine penile artery. The present study investigated whether L-NMMA had a similar selective action in the bovine ciliary artery. We also investigated whether two recently introduced inhibitors of neuronal nitric oxide synthase (nNOS), AAAN (N-(4S)-4-amino-5-[aminoethyl]aminopentyl-N'-nitroguanidine) and L-NPA (NG-propyl-L-arginine), produced selective blockade of vasodilatation induced by nitrergic nerves but not endothelium-derived nitric oxide. EXPERIMENTAL APPROACH: Rings of bovine ciliary artery were suspended in a wire myograph for tension recording. Neurogenic (nitrergic) vasodilatation was elicited by electrical field stimulation, and endothelium-dependent, nitric oxide-mediated dilatation was evoked using bradykinin. KEY RESULTS: L-NMMA inhibited vasodilatation induced by endothelium-derived nitric oxide but not the nitrergic nerves. In fact, L-NMMA, acted like L-arginine in protecting nitrergic vasodilatation against inhibition by L-NAME (NG-nitro-L-arginine methyl ester). AAAN had no effect on vasodilatation induced by either nitrergic nerves or endothelium-derived nitric oxide, but L-NPA inhibited both with equal potency. CONCLUSIONS AND IMPLICATIONS: In the bovine ciliary artery, L-NMMA acts as a selective inhibitor of the vasodilatation induced via endothelial NOS, without affecting that operating via nNOS. Furthermore, the putative nNOS inhibitors, AAAN and L-NPA failed to produce the expected selective inhibition of nitrergic vasodilatation in this artery.

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

PubMed2007

Contractile and relaxant properties of rat-isolated pulmonary veins related to localization and histology.

The aim of this study was to investigate the in vitro vasomotor properties of rat extra-and intralobar pulmonary veins (PVs) related to their localization and to assess the modulatory role of endothelium on these properties. Segments from PVs were mounted in small vessel myograph and stretched at various diameters (D(10), D(20), D(30)) corresponding to intraluminal pressures of 10, 20 or 30 mmHg. At D(10) or D(20), contractile responses to phenylephrine, U46619 and angiotensin II of distal intralobar part of PVs were smaller compared with those of proximal extralobar part, but no longer different when distal part was stretched at D(30). When submitted to an NO donor, sodium nitroprusside, distal part of PV relaxed more strongly when stretched at D(30) compared with D(10). Acetylcholine and bradykinin were devoid of relaxing effect on distal parts stretched at D(10), but in contrast to acetylcholine, bradykinin slightly relaxed preparations stretched at D(30). Isoprenaline strongly relaxed PVs ( approximately 80% of initial precontraction), with the distal part exhibiting a higher sensitivity to the agonist compared with the proximal part. This relaxation was also observed with salbutamol and suppressed with ICI 118551, which is in favour of the involvement of beta(2)-adrenoceptors in this effect. Preincubation of the preparations with N(G)-nitro-l-arginine methyl ester (10(-4) m) and indomethacin (10(-5) m) did not modify the contractile responses to U46619, nor the relaxing response to isoprenaline, which support that endothelium does not appear to play a significant modulatory role in these responses. Histological and electron microscopical examinations of proximal and distal sections of the same vein show that the layers of smooth muscle cells and cardiomyocytes were thicker in the proximal compared with the distal part. This study shows that, because of morphological heterogeneity of the PVs, the site of dissection and the initial condition of tension can play a significant role upon the sensitivity and the magnitude of the responses to both contractile and relaxing agonists.

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