Increase by oestrogen of calcium entry and calcium channel density in uterine smooth muscle

Batra, Satish

doi:10.1111/j.1476-5381.1987.tb11335.x

Cited by 58 publications

(31 citation statements)

References 13 publications

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“…Estrogen treatment of rats and rabbits usually lead to an increase in contractility in the reproductive organs. 24,25 Considering the calcium channel blocking effect of estradiol that is already known, it is assumed that the changes of clitoris and vaginal tissues after oophorectomy and estrogen replacement reported by other authors is not the sole effect of the change in NOS production, but is the ®nal consequence of many other factors affecting in a complex way. 17 ± 19,26 Furthermore, depending on the tissue, there is diversity in the mechanism by which ovarian steroids can in¯uence the smooth muscle function.…”

Section: Discussionmentioning

confidence: 99%

Effects of estrogen on nitric oxide synthase and histological composition in the rabbit clitoris and vagina

et al. 2001

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We investigated the functional and histological changes after oophorectomy in the rabbit clitoris and vagina to determine the mechanism responsible for the development of arousal disorder in postmenopausal women. Twenty mature female New Zealand white rabbits were randomly divided into three groups: control; oophorectomy; and estrogen replacement after oophorectomy. We compared the nitric oxide synthase (NOS) activity and the degree of expression of neuronal (nNOS) and endothelial NOS (eNOS) using biochemical and Western blot analysis in clitoral and vaginal tissues. Histological change of smooth muscle and collagen contents in those tissues were also compared using Masson's trichrome staining. NOS activity and the expression of nNOS and eNOS were signi®cantly increased in the oophorectomized group while there was a decrease to the level of the control group in the estrogen replacement group. Histological examination showed that oophorectomy induced a signi®cant increase in collagen and decrease in muscle content in both clitoris and vagina, while the ratio of smooth muscle content was increased signi®cantly after the estrogen replacement. Our results clearly demonstrate that estrogen de®ciency induces compensatory NOS production which may be related to decreases in muscle to collagen ratio in female rabbit genital organs.

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Section: Discussionmentioning

confidence: 99%

Effects of estrogen on nitric oxide synthase and histological composition in the rabbit clitoris and vagina

et al. 2001

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“…An increase in potency of verapamil against uterine contractions in vitro has been observed in tissue from rats treated with oestrogen and progesterone, compared to uteri from untreated rats (Ishii et al, 1986), although the number of specific uterine binding sites for [3H]-nitrendipine did not differ between tissues from untreated and hormone-treated animals. Recently Batra (1987) has described an increase in the number of [3H]-nitrendipine binding sites in the uteri of oestrogen-treated rats.…”

Section: Selectivitymentioning

confidence: 99%

Nifedipine kinetics in the rat and relationship between its serum concentrations and uterine and cardiovascular effects

Downing¹,

Hollingsworth²

1988

British J Pharmacology

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1 The kinetics of nifedipine and the relationship between its serum concentration and uterine and cardiovascular effects were investigated in 3 groups of animals. These were ovariectomized (ovx) anaesthetized non-pregnant rats following bolus i.v. injection (400 yg kg-1) and during 300 min infusion (10pgkg-1 min-1) and ovx, progesterone-treated late pregnant rats during infusion. Also, the kinetics were determined in ovary-intact late pregnant rats following bolus i.v. injection (400 pg kg-1). 2 Measurement of serum nifedipine concentrations after bolus i.v. injection in ovx non-pregnant rats showed a biexponential decay with time from which the following parameters were calculated: Ve = 300 + 30mlkg-1; rate constants k12 = 0.51 + 0.18min-1; k21 = 0.07 + 0.02min-1; kel = 0.10 + 0.05 min1; elimination clearance = 2.4 + 0.2 (ml min 1)kg-1; t1/2_ = 2.5 + 1.0min; t 112, = 102 + 15 min. In intact pregnant rats, a biexponential decay of serum nifedipine concentrations with time was also observed after bolus i.v. administration with similar parameters to non-pregnant animals. These kinetic parameters, used to calculate serum nifedipine concentrations obtained during infusion, predicted values similar to experimental values for 180 min, but thereafter slightly underestimated experimental values. 3 Immediate reductions in uterine contractions, mean blood pressure and heart rate were observed following bolus i.v. injection of nifedipine to ovx non-pregnant rats, with returns towards control values as serum nifedipine concentrations declined. ICI5 values (15% change from baseline), calculated from log10 serum concentration-response curves, of 0.3 + 0.05 pg ml-I for inhibition of uterine contractions, 0.8 + 0.3pgml -1 for depression of blood pressure and 3.8 + 1.0 Yg ml1 for reduction in heart rate were obtained.4 In ovx non-pregnant rats, nifedipine infusion produced a maximum reduction in integral of uterine contractions of 70% by 120 min and a maximum reduction of 15% in heart rate. Mean blood pressure was not significantly different from vehicle-treated rats. IC1_ values were 0.7 + 0.1 pg ml1 and 2.8 + 0.6.pg ml-for inhibition of uterine contractions and heart rate respectively.5 In ovx, progesterone-treated late pregnant rats, nifedipine infusion produced similar serum concentrations to those of non-pregnant rats but completely abolished uterine contractions by 70min.Maximum reductions of 30% in heart rate and blood pressure were observed. IC1S values were 0.5 + 0.1ygml-1 for uterine contractions, 0.9 + 0.3lpgmlP1 for blood pressure and 1.2 ± 0.3 pg ml -1 for heart rate. 6 The findings suggest that the kinetics of nifedipine are similar in pregnant and non-pregnant rats and support the idea that the drug exerts a slight selectivity for uterine inhibition relative to cardiovascular effects. The uterus of the late pregnant rat appears to be more sensitive to nifedipine than that of the non-pregnant animal.

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“…The only references to the influence of sex hormones has been from the work of Ishii et al (1986), Batra (1987) and Ruzycky et al (1987) who reported that circulating oestrogens and progesterone can alter the binding characteristics of dihydropyridines in smooth muscle of female rats. However, to our knowledge, the possibility derived from the present results that male sex hormones also influence calcium channel regulation, has not been demonstrated previously.…”

mentioning

confidence: 99%

Low dihydropyridine receptor density in vasa deferentia of castrated rats

Castillo

Lafayette

Caricati‐Neto

et al. 1992

British J Pharmacology

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Increase by oestrogen of calcium entry and calcium channel density in uterine smooth muscle

Cited by 58 publications

References 13 publications

Effects of estrogen on nitric oxide synthase and histological composition in the rabbit clitoris and vagina

Effects of estrogen on nitric oxide synthase and histological composition in the rabbit clitoris and vagina

Nifedipine kinetics in the rat and relationship between its serum concentrations and uterine and cardiovascular effects

Low dihydropyridine receptor density in vasa deferentia of castrated rats

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