ISSN:
1440-1681
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
1. Systolic blood pressure (SBP), bodyweight, organ weight, renal β-adrenoceptor and myocardial β- and myocardial α1-adrenoceptor characteristics were investigated in female Sprague-Dawley rats after chronic subcutaneous (s.c.) administration of ethynyloestradiol (EE2, 0.2 μg/day), levonorgestrel (NG, 2.0 μg/day) separately and in combination (EE2/NG).2. EE2 caused a sustained increase in SBP from 6 weeks (maximum at 14 weeks, +22 mmHg compared to control) which was accompanied by increased kidney and ventricle weight after 12 weeks. EE2/NG-treated rats also demonstrated a gradual rise in SBP (maximum at 9 weeks, +18 mmHg compared with control) with renal and ventricular hypertrophy, but were normotensive by week 17 of treatment. In contrast, NG induced only transient SBP increases (maxima at 5 and 10 weeks, + 14 mmHg compared with control), unaccompanied by organ hypertrophy. Norethisterone (2 μg/day) also produced transient increases (weeks 6–8, + 13 mmHg) in SBP.3. α1- and β-adrenoceptors were investigated using [3H]-prazosin and (-)- [125I]-iodocyanopindolol (ICYP), respectively. Myocardial α- and β-adrenoceptors were unaffected by steroid contraceptive administration for up to 12 weeks. Renal β-adrenoceptor affinity was markedly reduced in 12 week EE2-treated rats (equilibrium dissociation constant, KD, 53±7 pmol/L) compared with controls (KD, 31±4 pmol/L), an effect which was prevented by co-administration of NG (KD, 34±8 pmol/L). Renal β-adrenoceptor number was not altered by any treatment.4. The relatively late onset of organ hypertrophy and β-adrenoceptor changes appear to result from, rather than cause, EE2-induced hypertension.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1440-1681.1990.tb01357.x
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