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Prostaglandins, but not sympathetic nervous system, modulate Renin/Prorrenin receptor expression during normal pregnancy and pregnancy‐induced hypertension in rats
Author(s) -
Lopez Pedro,
CortesTinajero Viridiana,
CardenazVega Rocio,
AnguianoRobledo Liliana
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.654.1
Subject(s) - endocrinology , medicine , pregnancy , sympathetic nervous system , renin–angiotensin system , blood pressure , metoprolol , receptor , angiotensin ii , biology , genetics
Pregnancy is associated with blunted response to contractile agents as angiotensin II (Ang II), catecholamines and prostaglandins (PG's). In contrast, their responses are increased in pregnancy‐induced hypertension (PIH). The renin‐angiotensin system (RAS) has become more complex with new components with cardiovascular functions. Renin/Prorenin receptor (RPR) is one of these components. The aim of this work was to elucidate if sympathetic nervous system (SNS) and/or PG's modulate RPR expression in normal and pregnancy‐induced hypertensive pregnant rats. We used a subrenal aorctic coarctation (SRAC) model. Using immunoblot, RT‐PCR and immunohistochemistry, we determined RPR expression in aorta and kidney from normal and PIH animals. Similar groups were treated with Prazosine (P, 2mg/Kg), Metoprolol (M, 5 mg/Kg), Indomethacine (I, 3 mg/Kg) or Celecoxib (C, 10 mg/Kg) during the third week of pregnancy. Neither P, M nor Cox inhibitors altered blood pressure. In normal pregnancy, RPR increased its expression significantly. RPR expression during PIH decreased even lower than control levels. Adrenergic blockers did not affect RPR expression significantly. I and C, in contrast, normalized RPR expression during non‐complicated pregnancy and increased it to higher levels during PIH. These results suggest that PG's, but no SNS, modulates RPR expression. Supported by SIP‐IPN 20120122 and 20120929 grants