Antibody to marinobufagenin lowers blood pressure in pregnant rats on a high NaCl intake

Федорова, О. В.; Kolodkin, Nikolai I.; Agalakova, Natalia I.; Namikas, Alexandra R; Bzhelyansky, Anton; St‐Louis, Jean; Lakatta, Edward G.; Bagrov, Alexei Y.

doi:10.1097/01.hjh.0000163153.27954.33

Cited by 81 publications

(108 citation statements)

References 31 publications

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“…149 Administration of an anti-marinobufagenin antibody resulted in a 28 mmHg decrease in blood pressure and a simultaneous increase in the activity of the Na + /K + -ATPase in thoracic aortae. 149 In pregnant rats rendered hypertensive by deoxycorticosterone acetate and salt supplementation, uterine arteries exhibited enhanced sensitivity to the vasoconstrictor action of marinobufagenin, and an antimarinobufagenin antibody had an antihypertensive effect. 150 Thus, it appears that increases in circulating marinobufagenin levels are responsible for the Na + /K + -ATPase inhibition induced by preeclampsia and contribute to the pathogenesis of pre-eclampsia.…”

Section: Role Of Cardiotonic Steroids In Pre-eclampsiamentioning

confidence: 99%

Endogenous digitalis: pathophysiologic roles and therapeutic applications

2008

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SUMMARYEndogenous digitalis-like factors, also called cardiotonic steroids, have been thought for nearly half a century to have important roles in health and disease. The endogenous cardiotonic steroids ouabain and marinobufagenin have been identified in humans, and an effector mechanism has been delineated by which these hormones signal through the sodium/potassium-transporting ATPase. These findings have increased interest in this field substantially. Although cardiotonic steroids were first considered important in the regulation of renal sodium transport and arterial pressure, subsequent work has implicated these hormones in the control of cell growth, apoptosis and fibrosis, among other processes. This Review focuses on the role of endogenous cardiotonic steroids in the pathophysiology of essential hypertension, congestive heart failure, end-stage renal disease and pre-eclampsia. We also discuss potential therapeutic strategies that have emerged as a result of the increased understanding of the regulation and actions of cardiotonic steroids.

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Section: Role Of Cardiotonic Steroids In Pre-eclampsiamentioning

confidence: 99%

Endogenous digitalis: pathophysiologic roles and therapeutic applications

2008

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“…The placentas were removed and placental and fetal weights determined. Blood was collected for Na,K-ATPase measurements in erythrocytes [14], and for plasma MBG measurements [13].…”

Section: Experimental Protocolmentioning

confidence: 99%

“…In patients with PE and in pregnant rats with PE-like symptoms, however, levels of MBG become substantially elevated and accompany inhibition of the NKA [11,13,15]. Accordingly, in rats with PE-like symptoms, in vivo administration of anti-MBG antibody reduced blood pressure and restored activity of the sodium pump in vascular sarcolemma [13]. Likewise, in patients with PE, anti-MBG antibody ex vivo restore activity of erythrocyte NKA [15].…”

Section: Introductionmentioning

confidence: 99%

“…Pregnancy is associated with renal sodium retention [12,13], a major stimulus for MBG production [14]. In normal pregnancy, moderatly elevated levels of MBG do not alter vascular tone [10,13]. In patients with PE and in pregnant rats with PE-like symptoms, however, levels of MBG become substantially elevated and accompany inhibition of the NKA [11,13,15].…”

Section: Introductionmentioning

confidence: 99%

“…One of the factors contributing to the pathogenesis of PE are CTS [3,10,11]. Pregnancy is associated with renal sodium retention [12,13], a major stimulus for MBG production [14]. In normal pregnancy, moderatly elevated levels of MBG do not alter vascular tone [10,13].…”

Section: Introductionmentioning

confidence: 99%

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Endogenous sodium pump inhibitors, diabetes mellitus and preeclampsia

et al. 2007

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Endogenous inhibitors of the Na/K-ATPase (NKA) and diabetes mellitus (DM) are both risk factors for preeclampsia and NaCl sensitive hypertension. Our goal was to test the hypothesis that NaCl supplementation, induces preeclampsia-like symptoms in pregnant rats with DM via stimulation of marinobufagenin (MBG), a natriuretic and vasoconstrictor inhibitor of the NKA. Type 2 DM in female Sprague-Dawley rats was induced by administration of 65 mg/kg streptozotocin at day 4 post partum. In intact rats, pregnancy was associated with a 2-fold increase in MBG levels and a mild impairment in glucose tolerance. Pregnant rats with DM exhibited fetal macrosomia, greater impairment of glucose tolerance, and higher levels of MBG as compared to that in normal pregnant rats. As compared to intact pregnant rats, NaCl supplementation of diabetic pregnant rats (drinking 1.8% NaCl during days 12-19 of pregnancy) was associated with an increase in systolic blood pressure, decreased fetal and placental weight, five-fold elevation of MBG excretion, and 42% inhibition of NKA in erythrocytes. In nonpregnant rats, in vivo pretreatment with anti-MBG antibody produced an exaggerated response of plasma levels of glucose and insulin in oral glucose tolerance test. These results suggest that MBG is a common factor in the pathogenesis of DM and preeclampsia, and that regulation of glucose tolerance may be one of the physiological functions of endogenous cardiotonic steroids.

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