Premium
The Effects of AT1 Receptor Blockade on Skin Microcirculatory Blood Flow and Thromboxane A2 (TXA2) Production in Young Healthy Women
Author(s) -
Cavka Ana,
Grizelj Ivana,
Cosic Anita,
Koller Akos,
Jelakovic Bojan,
Lombard Julian H,
Phillips Shane A,
Drenjancevic Ines
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.898.14
Subject(s) - losartan , thromboxane a2 , medicine , angiotensin ii receptor type 1 , endocrinology , thromboxane , angiotensin ii , plasma renin activity , vasodilation , blockade , receptor , microcirculation , renin–angiotensin system , chemistry , blood pressure , platelet
AT1 receptor activation has an important role in maintaining the vascular release of prostaglandins responsible for mediating hypoxic dilation in skeletal muscle microvessels in normotensive rats. High salt diet leads to impairment of vasodilator responses that could be restored by infusion of subpressor dose of ANG II via its interaction with AT1 receptors. In addition to AT1 receptors blockade, losartan blocks thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptor. The aim of this study was to determine the effect of one week AT1 receptor blockade by losartan in 10 healthy normotensive women (20±2 years old) on law salt diet (LSD) on post occlusive hyperemic blood flow response in skin microcirculation by Laser Doppler Flowmetry (LDF) and to determine the plasma renin activity (PRA) and plasma thromboxane A2 (TXA2) concentration. Participants maintained LSD (<40 mmol of Na/day) and took 50 mg of losartan/day for 7 days. After one week of losartan administration the post occlusive hyperemic tissue blood flow was unchanged. However, plasma PRA and TXA2 levels were significantly increased compared to pre‐losartan values. Our results indicate that although one week of AT1 receptor blockade increases the plasma TXA2 concentration and PRA, the skin microcirculatory blood flow remained unchanged, possibly due to losartan blockade of TXA2 receptors and ANG II interaction with AT2 receptors.