Abstract
The characteristics of uterine receptors for angiotensin II and their regulation during the estrous cycle and after gonadal steroid treatment were investigated in the rat and rabbit. Binding of [125I]iodoangiotensin II to rat uterine particles was temperature dependent and saturable, and Scatchard analysis showed a single population of binding sites with Ka of about 109m−1. The concentration of uterine angiotensin II receptors changed markedly during the estrous cycle of the rat and after treatment with gonadal steroids. During the ovarian cycle, the concentration of angiotensin II receptors was about 4 times higher at proestrus than at diestrus II. Similar changes were observed when estrous cycles were induced in immature rats by a single injection of PMS gonadotropin. Ovariectomy was followed by a progressive decrease in uterine angiotensin II receptors, reaching 50% of the control values 8 days after castration. Conversely, injection of 17β-estradiol caused a dose-dependent increase in angiotensin II receptors measured 24 h after steroid treatment. Similarly, short term infusion of 17β-estradiol caused a progressive increase in angiotensin II receptors, which reached a maximum of 4- to 6-fold above control values at 36 h. However, after long term infusion of estradiol for 5–8 days, angiotensin receptors returned to or below the control values. Progesterone infusion for 7 days caused uterine angiotensin II receptors decrease by 93%. When immature rabbits were primed with estrogen, a 4-fold increase in the concentration of uterine angiotensin II receptors was measured. In progesterone-primed uteri, angiotensin II receptor concentration was no longer augmented by estrogen. No effects of steroids upon the affinity of the receptors for angiotensin II were detected, all changes in binding being due to alterations in the tissue content of receptor sites. These studies have revealed marked changes in the concentration of angiotensin receptors during the estrous cycle and after steroid treatment. Thus, receptors for angiotensin II are regulated by estrogen in manner similar to the control of receptors for other oxytocic hormones. These findings may explain the increased contractile sensitivity of estrogen-primed uteri to angiotensin II and suggest a role for angiotensin II in the physiological control of myometrial activity. (Endocrinology106: 5, 1980)
Published Version
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