Investigation of the negative inotropic effects of 17β‐oestradiol in human isolated myocardial tissues

Sitzler, Gerhard; Lenz, Olaf; Kilter, Heiko; Rosée, Karl La; Böhm, Michael

doi:10.1111/j.1476-5381.1996.tb15675.x

Cited by 35 publications

(23 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another new finding of the present investigation was the demonstration that progesterone infusion did not significantly affect left ventricular dPÏdtmax, which in the absence of changes in heart rate, arterial blood pressure and filling pressures of the heart indicated no change in ventricular contractility (Furnival et al 1970). This finding is also supported by previous reports showing that progesterone or its derivatives had no significant effect on contractility of isolated human heart muscles (Sitzler et al 1996) or guinea-pig atria (Temma et al 1983). However, one report in isolated rabbit heart found that progesterone induced coronary vasoconstriction and a negative inotropic effect (Raddino et al 1989).…”

Section: Discussionsupporting

confidence: 89%

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Molinari

Battaglia

Grossini

et al. 2001

Experimental Physiology

View full text Add to dashboard Cite

The present study was designed to investigate the effect of progesterone on the coronary circulation and to determine the mechanisms involved. In pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous infusion of progesterone at constant heart rate and arterial blood pressure were assessed using an electromagnetic flowmeter. In 14 pigs, infusion of 1 mg h−1 of progesterone caused an increase in coronary blood flow without affecting left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In a further four pigs, this vasodilatory coronary effect was enhanced by graded increases in the dose of the hormone of between 1, 2 and 3 mg h−1. The mechanisms of the above response were studied in the 14 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the coronary vasodilatation caused by progesterone. In the remaining eight pigs, this response was abolished by intracoronary injection of Nω‐nitro‐L‐arginine methyl ester (L‐NAME) even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L‐NAME with continuous intravenous infusion of papaverine. The present study showed that intravenous infusion of progesterone primarily caused coronary vasodilatation. The mechanism of this response was shown to involve the endothelial release of nitric oxide.

show abstract

Section: Discussionsupporting

confidence: 89%

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Molinari

Battaglia

Grossini

et al. 2001

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…Coronary dilation may also explain the antiischemic effect of 17β-estradiol in women (Rosano et al 1993). The heart muscle may also be a target organ for estrogens (Jiang et al 1992b;Eckstein et al 1994;Sitzler et al 1996). In male guinea-pig cardiac myocytes an inhibition of calcium inward current and a shortening of action potentials occurs (Jiang et al 1992b).…”

Section: Introductionmentioning

confidence: 99%

“…In male guinea-pig cardiac myocytes an inhibition of calcium inward current and a shortening of action potentials occurs (Jiang et al 1992b). In human atrial and ventricular preparations a negative inotropic effect of 17β-estradiol has been reported (Sitzler et al 1996). We examined male rat ventricular myocytes and focussed our investigations on 17β-estradiol-induced effects on outward currents.…”

Section: Introductionmentioning

confidence: 99%

Effects of 17β-estradiol on action potentials and ionic currents in male rat ventricular myocytes

Berger

Borchard

Häfner

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

This study describes electrophysiological effects of estrogens in isolated male rat ventricular myocytes. According to the literature these cells do not express the nuclear estrogen receptor. Action potentials or membrane currents were recorded in the whole-cell configuration with standard techniques. Action potential durations (APD) measured at a level of 0 mV (APD 0) and -70 mV (APD -70) were prolonged by 17beta-estradiol (0.5 Hz stimulation frequency, 24-26 degrees C). Threshold concentration was 1 micromol/l. At the highest concentration used (30 micromol/l) no saturation of the response was reached and APD 0 was 162% and APD -70 was 230% of the respective control. The resting potential remained unaffected in most cells. The prolongation induced by 17beta-estradiol developed fast and reached a steady state 10 min after start of hormone superfusion. Effects of estrogen were completely reversible during 10-15 min wash-out with hormone-free solution. The extent of prolongation (10 micromol/l 17beta-estradiol) was frequency dependent. Expressed as percentage of the respective control APD 0 (or APD -70) was 115% (188%) at 0.05 Hz, 118% (163%) at 0.5 Hz and 99% (129%) at 5 Hz stimulation frequency. The response was stereoselective, because 30 micromol/l 17alpha-estradiol did not prolong action potentials (APD 0: 101%, APD -70: 104% of the respective control, 0.5 Hz stimulation frequency). The endogenous estrogens estrone and estriol were less effective than 17beta-estradiol. With 30 micromol/l estrone (0.5 Hz stimulation frequency) APD 0 was 103% and ADP-70 148% of control and with 30 micromol/l estriol APD 0 was 135% and APD -70 137% of control. The prolongation of action potentials can be explained by inhibition of transient outward current which, in rat ventricle, is composed of fast (i[to,f]) and slowly (i[to,s]) inactivating components. At 30 micromol/l 17beta-estradiol i(to,f) was reduced to 50% and i(to,s) to 43% of their maximal amplitudes. The voltage sensor of i(to,f) or i(to,s) was hardly affected. Additionally, 17beta-estradiol decreased the calcium current (i[Ca,L]) to 76% (10 micromol/l) and 38% at 30 micromol/l. The inwardly rectifying potassium current (i[K1]) was reduced partly with 30 micromol/l 17beta-estradiol and its amplitude was 72% of control at -90 mV (inward current flow) and 65% at -40 mV (outward current flow). These results show that 17beta-estradiol is active in cardiac cells which do not express the nuclear estrogen receptor. The hormone exerts class III activity and reduces calcium inward current. These effects, however, occur in vitro with concentrations above the physiological level and therefore may be without significance in vivo.

show abstract

“…In rabbit papillary muscle, the chronic administration of 17␤-estradiol at Ͻ10 Ϫ6 M, but not acute administration, reduced isometric force [17]. In contrast, the effects of acute dosage with high concentrations has been reported in the muscle: 10 Ϫ5 M for the reduction in cytosolic Ca 2ϩ and inward Ca 2ϩ current of guinea pig cardiac myocytes [18], and ϳ10 Ϫ6 M for the negative inotropic effect on human myocardium [19]. Also in the present experiments using isolated frog muscle, the effective concentration of 17␤-estradiol was 10 Ϫ5 M to allow the acute actions to be clearly observed.…”

Section: Discussionmentioning

confidence: 99%

Effects of 17.BETA.-Estradiol on Tension Responses and Fatigue in the Skeletal Twitch Muscle Fibers of Frog.

Hatae

2001

JJP

View full text Add to dashboard Cite

Estrogens, like other steroid hormones, initiate their action via specific intracellular receptors [1]. The presence of estrogen receptors in the skeletal muscle cell was demonstrated in bovine [2], rabbit [3,4], and rat [5]. Skeletal myoblasts also expressed functional estrogen receptors [6]. The effects of estrogen on skeletal muscle contractility have been diversely reported. A long-term treatment of the developing rat with estrogen reduced the tetanus tension of skeletal muscle [7]. In women, the supplement with a supraphysiological level of estrogen did not affect the contractile force and fatigue process of the first dorsal interosseus muscle [8]. Neither did the administration of estrogen significantly affect the fatigue of the estradiol-injected extensor digitorum longus muscle in rat [9]. In frog skeletal muscle, however, Rana temporaria, the presence of diethyl-stilboesterol, a nonsteroidal estrogen, markedly potentiated the twitch tension, but apparently not the tetanus tension [10], and it also potentiated the tension response of the fatigued Key words: skeletal muscle, contraction, fatigue, 17␤-estradiol. Abstract:The effects of 17␤-estradiol (10an active estrogen, on the tension and fatigue responses of single fiber or fiber bundle prepared from frog skeletal muscle were investigated. The administration of 17␤-estradiol caused a transient potentiation of tetanus tension by field stimulation at every minute. This potentiation was not affected by the presence of nicardipine, suggesting that the action of 17␤-estradiol would place the excitation-contraction (E-C) coupling beyond T-tubule depolarization. Fatigue was produced by repeated tetanic stimulation every second until tension declined to approximately 40% of the initial level. Fibers were then allowed to recover by having tetani given to them every minute. In the normal Ringer solution, the time to 50% of the initial tetanus tension was 41.7 s.With the presence of 17␤-estradiol, the time to 50% tension was faster than that of control. The presence of 17␣-estradiol, a stereoisomer, caused no potentiation of tetanic tension to be stimulated every minute, and the rate of decline of fatigued response was almost the same as that of control, suggesting the existence of specific estrogen receptors in the frog muscle. In fatigued muscle with or without estrogen, the tension to field stimulation was transient and not sustained. When the fatigued muscle was again treated with field stimulation at every minute after the more-frequent stimulation, the recovery rate was increased in 17␤-estradiol. A prompt reduction in temperature to 5°C, from 20°C, in the presence of caffeine elicited the tension response, a rapid cooling contracture (RCC). The presence of 17␤-estradiol inhibited peak tension and maximum rate of rise of the RCC only after the repetitive electrical stimuli. These results suggest that the potentiation of contraction upon the electrical stimulation by 17␤-estradiol was induced by the increase of myoplasmic-free Ca 2ϩ concentration via an activ...

show abstract

Investigation of the negative inotropic effects of 17β‐oestradiol in human isolated myocardial tissues

Cited by 35 publications

References 31 publications

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Effects of 17β-estradiol on action potentials and ionic currents in male rat ventricular myocytes

Effects of 17.BETA.-Estradiol on Tension Responses and Fatigue in the Skeletal Twitch Muscle Fibers of Frog.

Contact Info

Product

Resources

About