Premium
RENAL AND MYOCARDIAL ADRENOCEPTORS IN STEROID CONTRACEPTIVE‐INDUCED HYPERTENSION IN RATS
Author(s) -
Geraghty Dominic P.,
Byrne K. Bruce,
McPherson Grant A.,
Burcher Elizabeth
Publication year - 1990
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1990.tb01357.x
Subject(s) - steroid , medicine , endocrinology , pharmacology , hormone
SUMMARY 1. Systolic blood pressure (SBP), bodyweight, organ weight, renal β‐adrenoceptor and myocardial β‐ and myocardial α 1 ‐adrenoceptor characteristics were investigated in female Sprague‐Dawley rats after chronic subcutaneous (s.c.) administration of ethynyloestradiol (EE 2 , 0.2 μg/day), levonorgestrel (NG, 2.0 μg/day) separately and in combination (EE 2 /NG). 2. EE 2 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. EE 2 /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. α 1 ‐ and β‐adrenoceptors were investigated using [ 3 H]‐prazosin and (‐)‐ [ 125 I]‐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 EE 2 ‐treated rats (equilibrium dissociation constant, K D , 53±7 pmol/L) compared with controls (K D , 31±4 pmol/L), an effect which was prevented by co‐administration of NG (K D , 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, EE 2 ‐induced hypertension.