The Na+/H+ exchange is required for platelet aggregation induced by AVP (arginine-vasopressin)

Toledo, Teresa; Palomo, F; Hockaday, T. D. R.

doi:10.1016/0049-3848(89)90071-6

Cited by 3 publications

(3 citation statements)

References 10 publications

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“…Here, we hypothesize that AVP-evoked phosphatidylserine exposure can be mediated by the Na þ influx produced by activated NHE. This is based on the following findings: AVP activates the NHE in platelets [3,7] (Fig. 1); AVPevoked phosphatidylserine exposure was strongly reduced following inhibition of the NHE by EIPA or genistein ( Table 2); and artificially evoked Na þ -H þ antiport is associated with phosphatidylserine exposure (Table 2).…”

Section: Discussionmentioning

confidence: 96%

“…It has also been reported that, in platelets stimulated by collagen, sodium influx mediated by activated NHE may result in the generation of procoagulant activity [12,13]. Taking into account that AVP is a strong activator of NHE in human platelets [6,7], one can expect that the treatment of platelets with this hormone may result in a procoagulant response. This is consistent with the finding that an analog of AVP, desmopressin (DDAVP; Rhone-Poulenc Rorer Pharmaceuticals.…”

Section: Introductionmentioning

confidence: 94%

“…AVP treatment of platelets is also associated with strong activation of Na þ /H þ exchanger (NHE) [6,7]. NHEs are ubiquitous integral plasma membrane proteins that exchange extracellular Na þ for intracellular H þ with the stoichiometry of one per one [8].…”

Section: Introductionmentioning

confidence: 99%

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Vasopressin acts on platelets to generate procoagulant activity

Tomasiak

Stelmach²,

Rusak³

et al. 2008

Blood Coagulation &Amp; Fibrinolysis

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The aim of our study was to examine whether arginine vasopressin (AVP) is able to evoke in human platelets a procoagulant response due to activation of an Na+/H+ exchanger. It was found that treatment of platelets with AVP (20-100 nmol/l) results in generation of a weak calcium signal, activation of Na+/H+ exchanger, aggregation, and development of a procoagulant response. The AVP-evoked procoagulant response was dose and time dependent, weaker than that produced by collagen or monensin (mimics Na+/H+ exchanger), and less pronounced following the inhibition of Na+/H+ exchanger by 5-(N-ethyl-N-isopropyl) amiloride or genistein. Flow cytometry studies reveal that in-vitro platelet treatment with AVP results in an unimodal left shift in the forward and side scatter of the entire platelet population, indicating morphological changes on the plasma membrane. The shift was dose related, weaker than that evoked by collagen, similar to that produced by monensin and strongly reduced in the presence of 5-(N-ethyl-N-isopropyl) amiloride or genistein. Using flow cytometry, we demonstrated enhanced expression of phosphatidylserine on the AVP-treated platelets. AVP-evoked phosphatidylserine exposure was dose dependent, inhibited by 5-(N-ethyl-N-isopropyl) amiloride or genistein and weaker than that produced by collagen. AVP in a dose-dependent manner produced a rise in platelet volume. The swelling was inhibited by 5-(N-ethyl-N-isopropyl) amiloride, and its kinetics was similar to that observed in the presence of monensin. We conclude that prolonged treatment of platelets with AVP results in a procoagulant response, which may occur as a consequence of Na+ influx mediated by Na+/H+ exchanger.

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Section: Discussionmentioning

confidence: 96%