scholarly journals Progesterone increases plasma volume independent of estradiol

2005 ◽  
Vol 98 (6) ◽  
pp. 1991-1997 ◽  
Author(s):  
Nina S. Stachenfeld ◽  
Hugh S. Taylor
Keyword(s):  
Plasma Concentration ◽  
Plasma Volume ◽  
Gnrh Antagonist ◽  
Water Movement ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Escape Rate ◽  
Independent Effect ◽  
Transcapillary Escape Rate ◽  
Fluid Regulation

Adequate plasma volume (PV) and extracellular fluid (ECF) volume are essential for blood pressure and fluid regulation. We tested the hypotheses that combined progesterone (P4)-estrogen (E2) administration would increase ECF volume with proportional increases in PV, but that P4would have little independent effect on either PV or ECF volume. We further hypothesized that this P4-E2-induced fluid expansion would be a function of renin-angiotensin-aldosterone system stimulation. We suppressed P4and E2with a gonadotropin-releasing hormone (GnRH) antagonist in eight women (25 ± 2 yr) for 16 days; P4(200 mg/day) was added for days 5–16 (P4) and 17β-estradiol (2 × 0.1 mg/day patches) for days 13–16 (P4-E2). On days 2 (GnRH antagonist), 9 (P4), and 16 (P4-E2), we estimated ECF and PV. To determine the rate of protein and thus water movement across the ECF, we also measured transcapillary escape rate of albumin. In P4, [Formula: see text] increased from 2.5 ± 1.3 to 12.0 ± 2.8 ng/ml ( P < 0.05) with no change in [Formula: see text] (21.5 ± 9.4 to 8.6 ± 2.0 pg/ml). In P4-E2, plasma concentration of P4remained elevated (11.3 ± 2.7 ng/ml) and plasma concentration of E2increased to 254.1 ± 52.7 pg/ml ( P < 0.05). PV increased during P4(46.6 ± 2.5 ml/kg) and P4-E2(48.4 ± 3.9 ml/kg) compared with GnRH antagonist (43.3 ± 3.2 ml/kg; P < 0.05), as did ECF (206 ± 19, 244 ± 25, and 239 ± 27 ml/kg for GnRH antagonist, P4, and P4-E2, respectively; P < 0.05). Transcapillary escape rate of albumin was lowest during P4-E2(5.8 ± 1.3, 3.5 ± 1.7, and 2.2 ± 0.4%/h for GnRH antagonist, P4, and P4-E2, respectively; P < 0.05). Serum aldosterone increased during P4and P4-E2compared with GnRH antagonist (79 ± 17, 127 ± 13, and 171 ± 25 pg/ml for GnRH antagonist, P4, and P4-E2, respectively; P < 0.05), but plasma renin activity and plasma concentration of ANG II were only increased by P4-E2. This study is the first to isolate P4effects on ECF; however, the mechanisms for the ECF and PV expansion have not been clearly defined.

17α-HYDROXYLASE DEFICIENCY. A COMBINATION OF HYDROXYLATION DEFECT AND REVERSIBLE BLOCKADE IN ALDOSTERONE BIOSYNTHESIS

1979 ◽  
Vol 90 (3) ◽  
pp. 490-504 ◽  
Author(s):  
D. R. Rovner ◽  
J. W. Conn ◽  
E. L. Cohen ◽  
F. G. Berlinger ◽  
D. C. Kern ◽  
...  
Keyword(s):  
Plasma Concentration ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Hydroxyl Group ◽  
Side Chain ◽  
Hydroxylase Deficiency ◽  
Resultant Increase

ABSTRACT We have studied the hormonal secretion and excretion patterns in a patient with the XX type of 17α-hydroxylase deficiency. In the untreated state, the patient's urine contained only those steroids which do not require 17-hydroxylation in their biosynthesis. Aldosterone was not produced in the patient and the metabolic product of its immediate precursor, 18-hydroxy-11-dehydro-tetrahydrocorticosterone, was excreted in markedly elevated amounts. This apparent complete block in 18 oxidation was reversible upon long-term ACTH suppression within 27 days. Direct in vitro incubation of the patient's adrenal gland removed at operation demonstrated, 1) the complete lack of 17α-hydroxylase activity, 2) the functional block in the ability to oxidize the hydroxyl group at the 18 methyl side chain. The addition of physiological concentrations of angiotensin to the incubation medium further showed, 3) angiotensin mildly stimulated the entire aldosterone biosynthetic pathway, 4) angiotensin directly stimulated the conversion of 18-hydroxycorticosterone to aldosterone. We propose that in this patient, 17-hydroxylase deficiency produced a decreased plasma concentration of cortisol, followed by stimulation of deoxycorticosterone production by ACTH. The resultant increase in extracellular fluid volume suppressed plasma renin activity. This resulted in a low plasma concentration of angiotensin II which directly suppressed oxidation of 18-hydroxycorticosterone to aldosterone. This defect has been called corticosterone methyl oxidase defect type 2.

Effect of Catecholamines and Insulin on Plasma Volume and Intravascular Mass of Albumin in Man

1989 ◽  
Vol 77 (2) ◽  
pp. 149-155 ◽  
Author(s):  
J. Hilsted ◽  
N. J. Christensen ◽  
S. Larsen
Keyword(s):  
Cell Volume ◽  
Plasma Volume ◽  
Packed Cell Volume ◽  
Escape Rate ◽  
Intravenous Insulin ◽  
Transcapillary Escape Rate ◽  
Adrenaline Infusion ◽  
Combined Actions ◽  
Hyperinsulinaemic Euglycaemic Glucose Clamp ◽  
Healthy Males

1. The effect of intravenous catecholamine infusions and of intravenous insulin on plasma volume and intravascular mass of albumin was investigated in healthy males. 2. Physiological doses of adrenaline (0.5 μg/min and 3 μg/min) increased peripheral venous packed cell volume significantly; intravenous noradrenaline at 0.5 μg/min had no effect on packed cell volume, whereas packed cell volume increased significantly at 3 μg of noradrenaline/min. No significant change in packed cell volume was found during saline infusion. 3. During adrenaline infusion at 6 μg/min, packed cell volume increased, plasma volume decreased and intravascular mass of albumin decreased significantly. During noradrenaline infusion at 6 μg/min, packed cell volume increased and plasma volume decreased, but intravascular mass of albumin did not change. 4. Application of a hyperinsulinaemic, euglycaemic glucose clamp led to an increase in transcapillary escape rate of albumin and a decrease in intravascular mass of albumin. Packed cell volume remained constant, while plasma volume, measured by radiolabeled albumin, decreased. 5. We conclude that the previously reported changes in packed cell volume, plasma volume, intravascular mass of albumin and transcapillary escape rate of albumin during hypoglycaemia may be explained by the combined actions of adrenaline and insulin.

Pathogenesis of Arterial Hypertension after the Constriction of the Renal Artery Leaving the opposite Kidney Intact Both in the Anaesthetized and in the Conscious Dog

1972 ◽  
Vol 42 (6) ◽  
pp. 651-664 ◽  
Author(s):  
G. Bianchi ◽  
E. Baldoli ◽  
R. Lucca ◽  
P. Barbin
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Plasma Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Plasma Renin Concentration ◽  
Renal Artery Constriction

1. The renal artery was constricted leaving the opposite kidney intact in ten conscious and seven anaesthetized dogs. Intravenous infusion of exogenous renin was done in seven conscious dogs; in four of these the renal artery was constricted 15–17 days later. The following variables were measured in all animals before and after renal artery constriction: plasma renin concentration, blood pressure, cumulative sodium balance, plasma volume, extracellular fluid volume and plasma non-protein nitrogen. Before and after renal artery constriction in the conscious dogs cardiac output, stroke volume, total peripheral resistance and cardiac rate were also measured. In a few dogs angiotensin responsiveness and plasma concentration of renin substrate were also measured. 2. There was no significant difference between the regression of change in blood pressure on change in plasma renin concentration within 2 h from renal artery constriction in the conscious dogs and that observed during intravenous infusion of renin. Comparing the changes of these variables with the ones previously obtained with renal artery constriction to the lone remaining kidney, for a given increase of plasma renin concentration the rise of blood pressure was lower when the contralateral kidney was untouched. The changes of the other variables in the conscious dogs may be divided into three phases: a first phase lasting hours, in which, besides the changes described above, there was an increase of total peripheral resistance while the other variables remain unchanged: a second phase, 24 h after constriction, in which blood pressure, total peripheral resistance and plasma renin clearance decreased while plasma volume, cardiac output and extracellular fluid volume slightly increased; however, only the plasma volume change was statistically significant: and a third phase 6–7 days after constriction, when all the variables returned towards normal values, except that the blood pressure and total peripheral resistance remained significantly higher. Sodium balance remained at equilibrium throughout the study period. It is suggested that these results are compatible with the ‘autoregulation theory’ of renal hypertension. 3. Renal artery constriction in the anaesthetized animals caused a slight but significant sodium retention that very likely influenced the sequence of the events. On the second day after constriction, the plasma renin concentration was significantly increased, whereas the highest values of blood pressure, plasma volume and extracellular fluid volume occurred on the seventh day after constriction.

Changes in Blood Pressure, Body Fluids, Circulating Angiotensin II and Aldosterone, with Improved Diabetic Control

1982 ◽  
Vol 63 (s8) ◽  
pp. 415s-418s ◽  
Author(s):  
J. A. O'hare ◽  
J. B. Ferriss ◽  
B. M. Twomey ◽  
H. Gonggrijp ◽  
D. J. O'sullivan
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Metabolic Control ◽  
Plasma Volume ◽  
Diabetic Control ◽  
Escape Rate ◽  
Diabetic Patients ◽  
Exchangeable Sodium ◽  
Poor Metabolic Control ◽  
Transcapillary Escape Rate

1. We studied 12 normotensive non-ketotic diabetic patients during poor metabolic control, with sustained hyperglycaemia, and again, after an interval of 3 weeks, when metabolic control was improved. On each occasion we measured blood pressure, total exchangeable sodium, plasma volume, transcapillary escape rate of albumin, and plasma concentrations of angiotensin II and aldosterone. 2. With improved diabetic control there was a small but significant fall in arterial pressure. Total exchangeable sodium was normal when control was poor but rose significantly to above normal with improved control. 3. Plasma volume also rose significantly with improved control, and the transcapillary escape rate of albumin fell and the intravascular mass of albumin rose. 4. Plasma angiotensin II and aldosterone concentrations were significantly above normal during poor metabolic control, but fell to normal with improved control. 5. These findings indicate a resetting of the relationship between blood pressure and exchangeable sodium when diabetic control improves. The association between exchangeable sodium and concentrations of angiotensin II and aldosterone also appears altered in diabetic patients. These changes associated with varying metabolic control must be considered when studying cardiovascular disease in diabetic patients.

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