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At least 433 records · Page 24Linked to original sources
PubMed1979

Effects of an angiotensin II antagonist; [sarcosine 1, isoleucine 8] angiotensin II, on blood pressure, plasma renin activity and plasma aldosterone concentration in hypertensive and normotensive subjects taking oral contraceptives.

To examine the involvement of renin-angiotensin-aldosterone system in the etiology of oral contraceptive induced hypertension, normal women (Group I), normotensive (Group II) and hypertensive (Group III) women taking Ovulen (R) were infused with a competitive angiotensin II (AII) antagonist, [1-sarcosine, 8-isoleucine] angiotensin II. The angiotensin II antagonist was infused at a rate of 600 ng/kg/min for 30 min 1.5 hrs after intravenous injection of 40 mg of furosemide. Blood pressure was monitored and pre-infusion and post-infusion plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were determined. Pre-infusion PRA and PAC showed no significant differences among these three groups. In response to the AII antagonist infusion blood pressure rose in Groups I and II, but blood pressure responses in Group III were variable. Four out of the total 6 subjects had pressor responses and only one subject had a significant blood pressure reduction. In both Groups I and II, PRA decreased and PAC rose after infusion of the antagonist. In Group III, PRA decreased to a lesser degree and PAC showed no consistent change. These data suggest that the renin-angiotensin-aldosterone system in hypertensive women or oral contraceptives is different from that of the normotensive users. However, the pathophysiology of oral contraceptive induced hypertension is not homogenous and angiotensinogenic hypertension is uncommon.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1975

Interaction of contraceptive progestins and related compounds with the oestrogen receptor. Part I: Effect on (3H)oestradiol distribution pattern in the ovariectomized rat.

The distribution pattern of oestradiol in ovariectomized rats as a function of time has been studied following intravenous adminstration of the tritiated hormone. Oestrogen specific binding with limited capacity was observed in the uterus, vagina, anterior pituitary, adrenals, preoptic area, hypothalamus, amygdala, septum and tractus diagonalis. Maximal uptake of oestradiol in the pituitary occurred within 5 min, in the uterus 60 min after injection, and remained almost unchanged at this level for more than two hours. The binding capacity per mg tissue decreased in the order pituitary, uterus, vagina, preoptic area, adrenals, hypothalamus, amygdala, spetum and tractus diagonalis. The hormone concentration in these tissues one hour after (3H)oestradiol injection was lowered by previous administration of ethinodiol, norethinodrel, lynestrenol and norethindrone, whereas medroxyprogesterone, chlormadinone, megestrol and methyllynestrenol had no effect. The same results were obtained, when instead of the steroid alcohols the corresponding acetate esters were administered. For norgestrel, oestrenol and nortestosterone the effect in the dose range studied was limited to the pituitary and preoptic area. For lynestrenol the inhibition of oestradiol binding in the target tissues was almost the same when the progestin was given 60 and 5 min before oestradiol, whereas in the case of administration 30 min after oestradiol no inhibition was observed. The reduction of oestrogen binding appeared to be dose-dependent, but the dose required to obtain a certain effect for the uterus was four times as high as for the pituitary. Discrepancies between previous studies and the implications of the present findings for the mechanism of action of ovulation inhibition by these progestins are discussed.

Adrenal Glands↗
PubMed1988

Investigations upon the mechanism of inhibition of spermatogenesis in the rat by a dimeric ethynodiol-testosterone ester.

The combination of androgens and progestogens has been shown to be a suitable male contraceptive. Previous experiments revealed that injection of a dimeric testosterone-ethynodiol ester into rats and monkeys induces azoospermia for several weeks. In order to investigate the mechanism of action, we compared the endocrine effects of a single injection of 10 mg of the dimeric ester into intact male rats with that of 6 mg of norethisterone enanthate + 6 mg of testosterone enanthate. After the injection of the dimer there was a transitory reduction of serum FSH and a strong suppression of serum LH and testosterone, of testicular testosterone and of androgen-binding protein (ABP) in the testis and epididymis for at least 8 weeks, whereas spermatogenesis was totally depressed between the 4th and 8th week. Contrary to this, the enanthates caused only a slight suppression of spermatogenesis, although serum LH, testicular testosterone and ABP were profoundly reduced. The only conspicuous difference in the endocrine pattern of both groups during the first 4 weeks was in the serum testosterone level which remained normal in the rats treated with the enanthates. The results suggest that testicular testosterone and ABP concentrations are of minor significance for an intact spermatogenesis, and that some other factors produced by Sertoli cells might be involved and possibly maintained by normal serum testosterone levels.

Androgen-Binding Protein↗