Effects of Progesterone and Four Synthetic Progestagens on Sodium Balance and the Renin-Aldosterone System in Man*†

Oelkers, W.; Schöneshöfer, M.; Blümel, A.

doi:10.1210/jcem-39-5-882

Cited by 109 publications

(42 citation statements)

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“…In addition, another study showed that increases in levels of progesterone were positively correlated with decreases in blood pressure in the progression of pregnancy 9 . On the other hand, some reports show that administration of a progesterone derivatives also exerts effect on blood pressure; for example, there are reports which indicate that medroxyprogesterone acetate induce changes in blood pressure in postmenopausal women receiving estrogen replacement therapy; this phenomenon, possibly depends the stimulation of sodium retention 10 . However, there are data from clinical studies which provide evidence that sequential administration of medroxyprogesterone acetate or progestogene norethisterone acetate does not alter blood pressure 11,12 .…”

Section: Introductionmentioning

confidence: 99%

Effect of progesterone-carbachol derivative on perfusion pressure and coronary resistance in isolated rat heart: via activation of the M<sub>2</sub> muscarinic receptor

Figueroa‐Valverde¹,

Díaz-Cedillo²,

Elodia³

et al. 2014

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Aim. The present study was designed to investigate the effects of progesterone-carbachol derivative on perfusion pressure and coronary resistance in rats. An additional aim was to identify the molecular mechanisms involved. Methods. The Langendorff model was used to measure perfusion pressure and coronary resistance changes in isolated rat heart after progesterone-carbachol derivative alone and after the following compounds; mifepristone (progesterone receptor blocker), yohimbine (α 2 adreno-receptor antagonist), ICI 118,551 (selective β 2 receptor blocker), atropine (non-selective muscarinic receptor antagonist), methoctramine (antagonist of M 2 receptor) and L-NAME (inhibitor of nitric oxide synthase). Results. The results show that progesterone-carbachol derivative [10 -9 mM] significantly decreased perfusion pressure (P=0.005) and coronary resistance (P=0.006) in isolated rat heart. Additionally, the effect of progesterone-carbachol on perfusion pressure [10 -9 to 10 -4 mM] was only blocked in the presence of methoctramine and L-NAME. Conclusions. These data suggest that progesterone derivative exert its effect on perfusion pressure via activation of the M 2 muscarinic. In addition, this phenomenon involves stimulation of nitric oxide synthase (NOS).

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Section: Introductionmentioning

confidence: 99%

Effect of progesterone-carbachol derivative on perfusion pressure and coronary resistance in isolated rat heart: via activation of the M<sub>2</sub> muscarinic receptor

Figueroa‐Valverde¹,

Díaz-Cedillo²,

Elodia³

et al. 2014

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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“…Within the context of water regulation, for example, progesterone has a high affinity for the mineralocorticoid receptor and competes with aldosterone for this receptor. It is primarily through this mechanism that progesterone increases sodium excretion in men [13][14][15][16][17] and can prevent water retention associated with estrogens.14 Most progestins do not possess this antimineralocorticoid effect so have little impact on the water and sodium retention properties of estrogens. Our studies in young women have demonstrated this contrast comparing osmotic regulation of AVP as well as sodium and water regulation during combined oral contraceptives containing norethindrone versus the mid-luteal phase of the menstrual cycle.…”

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confidence: 99%

Hormonal Changes During Menopause and the Impact on Fluid Regulation

Stachenfeld

2014

Reprod. Sci.

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Reproductive surgeries leave women more susceptible to postoperative hypervolemic hyponatremia because during this period women can retain water at an accelerated pace and much faster than they do sodium. This review proposes that estrogen and progestogen exposure play an important role in the increased risk of hyponatremia in menopausal women. Estrogen and progesterone exposure have important effects on both body fluid regulation and cardiovascular function and both of these reproductive hormones impact blood pressure responses to sodium loads. This article provides information on the effects of female reproductive hormones and hormone therapy (HT) on fluid regulation and cardiovascular function during menopause. Thirst-and fluid-regulating hormones respond to both osmotic and volume stimuli. Aging women maintain thirst sensitivity to osmotic stimuli but lose some thirst sensitivity to changes in central body fluid volume. Thus, older adults are more at risk of dehydration because they may replenish fluids at a slower rate. Estrogen therapy increases osmotic sensitivity for mechanisms to retain body water so may help menopausal women control body fluids and avoid dehydration. Some progestogens can mitigate estradiol effects on water and sodium retention through competition with aldosterone for the mineralocorticoid receptor and attenuating aldosterone-mediated sodium retention in the distal tubule. However, some progestogens can increase cardiovascular risks. Appropriate balance of these hormones within HT is important to avoid the negative consequences of body fluid and sodium retention, including edema and hypertension.Keywords hormone therapy, estrogen, progesterone, body fluid regulation, arginine vasopressin Reproductive surgeries leave women more susceptible to postoperative hypervolemic hyponatremia because women retain water at a faster rate than sodium during this period, 1-5 especially after reproductive surgeries. 4,7 Indeed, women are at high risk of postoperative hyponatremia even after relatively low-risk surgeries such as operative hysteroscopy. In such surgeries, glycine solution (lacking electrolytes) is used as a distension medium and can cause intravascular volume retention, increasing the risk of hyponatremia, cerebral and/or pulmonary edema, psychological disturbances, and even death. 4,[8][9] A combination of anesthesia, nausea, and the postsurgical experience tends to increase arginine vasopressin (AVP). This hormone, the primary hormone involved in free water retention, is also associated with altered astroglia volume regulation in both pre-and postmenopausal (PM) women. 3,5,10,11 Studies in animals support an important role for estradiol in increasing astroglia volume in women with hyponatremia, suggesting a role for female reproductive hormones in the dire consequences that can be associated with postoperative hyponatremia in both young and PM women. 6,12 Hormones During MenopauseThe stages of the menopause transition are classified by changes in menstrual bleeding, concomitant...

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“…The exercise test after 2 weeks of placebo treatment as well as after 4 and 8 weeks of therapy was conducted in a semireclining position on a bicycle ergometer (ERG 301 R, Robert Bosch, Berlin, West Germany) at 50 cycles/min, starting at 50 W and increasing by a 10-W increment every minute to a maximum of 100 W as submaximal exercise. 19 Blood samples for the determination of plasma norepinephrine and epinephrine (radioenzymatic method), 20 plasma renin activity (radioimmunoassay), 21 plasma aldosterone (radioimmunoassay), blood glucose (fluorometric method), serum insulin (radioimmunoassay), and blood lactate (enzymatic method) were collected from an antecubital vein after 30 minutes of rest in a supine position and during the sixth minute of exercise at a work load of 100 W before and after 4 and 8 weeks of therapy. The following measurements were done only at rest: total serum cholesterol (enzymatic method) 22 and triglycerides (coupled enzymatically) 23 ; serum lipoproteins (ultracentrifugation), 24 creatinine (autoanalyzer), sodium, and potassium (flame photometer); 24-hour urinary excretion of sodium and potassium; uric acid (enzymatic method); red and white blood cell count; serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase; alkaline phosphatase; and calcium.…”

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confidence: 99%

Antihypertensive and metabolic effects of diltiazem and nifedipine.

Schulte¹,

Meyer‐Sabellek²,

Haertenberger³

et al. 1986

Hypertension

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SUMMARY The antihypertensive effect of diltiazem (180-270 mg/day) and nifedipine (40-60 mg/day) in slow-release forms was assessed over 8 weeks in a double-blind parallel study in 40 subjects with essential hypertension at rest and during exercise. Blood pressure was comparably reduced in both groups at rest as well as during exercise. The responder rates (2:10% reduction in diastolic blood pressure) after 8 weeks of therapy were 53% at rest and 75% during exercise in the diltiazem group and 78% and 50%, respectively, in the nifedipine group. Diltiazem decreased heart rate by 8% (p<0.01), while nifedipine did not affect it. As a consequence, myocardial oxygen consumption, as judged by the pressure-rate product, was reduced by diltiazem. Resting plasma norepinephrine levels were increased significantly after 8 weeks of diltiazem therapy. Plasma epinephrine, renin, aldosterone, glucose, insulin, and lactate and routine laboratory parameters were unchanged at the end of the study. No significant changes in total cholesterol and triglyceride levels were observed after 8 weeks. Whereas therapy with diltiazem resulted in an 8% fall in low density lipoprotein cholesterol after 8 weeks (p<0.05), nifedipine induced a drop in very low density lipoprotein cholesterol (p<0.05) after 8 weeks of therapy. We conclude that both diltiazem and nifedipine are effective antihypertensive agents lacking undesirable metabolic side effects. Diltiazem, however, had the advantage of lowering heart rate and myocardial oxygen consumption. Therefore, the use of drugs with a direct dilating effect on the arterial wall is a logical treatment approach.2 As demonstrated more than 15 years ago by Bender 3 and Brittinger et al., 4 calcium entry blockers have an antihypertensive effect. All calcium entry blockers decrease the influx of extracellular Ca 2+ and promote systemic vasodilation. The effects on myocardium, cardiac cells, and vascular smooth muscle differ depending on the drug used. While verapamil and diltiazem act on myocardium, pacemaker cells, and vascular smooth muscle, nifedipine and its derivatives act mostly at the vascular site rather than on the cardiac pacemaker.5 "

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Effects of Progesterone and Four Synthetic Progestagens on Sodium Balance and the Renin-Aldosterone System in Man*†

Cited by 109 publications

References 0 publications

Effect of progesterone-carbachol derivative on perfusion pressure and coronary resistance in isolated rat heart: via activation of the M<sub>2</sub> muscarinic receptor

Effect of progesterone-carbachol derivative on perfusion pressure and coronary resistance in isolated rat heart: via activation of the M<sub>2</sub> muscarinic receptor

Hormonal Changes During Menopause and the Impact on Fluid Regulation

Antihypertensive and metabolic effects of diltiazem and nifedipine.

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