Effect of Long‐term Salbutamol Treatment on Renin‐aldosterone System in Twin Pregnancy

Abstract

Plasma renin activity (PRA), urinary aldosterone excretion (dU-Aldo), urinary electrolytes (dU-Na, dU-K) and plasma progesterone were studied weekly in 22 women with twin pregnancies for three weeks whilst on salbutamol therapy ( = 8 mg three times daily) in hospital. Fifteen patients in this group were treated with diuretics for on an average six weeks and the therapy continued. All the patients except three were treated also with depot-formed oxyprogesterone during the study. As an additional control group ten twin pregnant women without any drug therapies were studied.The mean level of PRA in twin pregnancy before betasympathomimetics was equal to that of the same phase (the 32nd week) of normal pregnancy. On the second day of the treatment the PRA levels was threefold (p<O.OOl) and later on twofold (p<O.O5) when compared with the level before the treatment.Before betasympathomimetics the mean level of dU-Aldo was in twin pregnancy already higher than in normal pregnancy (p<O.OI). During the treatment dU-Aldo increased within a week @<0.05-p<0.01) and a positive correlation between PRA and dU-Aldo was found (pCO.01). A decrease in dU-Na and an increase in dU-K were found (p < O.OS), corresponding to the increased effect of aldosterone. The increased levels of progesterone and aldosterone in twin pregnancy agree with earlier suggestions concerning the importance of progesterone in the secretion of aldoster-one during pregnancy. The stimulating effect of betasympathomimetics, however, leads to a renin-mediated secondary aldosteronism and therefore tend also to cause hypokalemia.Normal pregnancy is associated with a highly activated renin-angiotensin system, and with high aldosterone secretion (5). The basal level of PRA during pregnancy even exceeds the stimulatory reserves of the non-pregnant state, therefore, in addition to the kidney, an uteroplacental or chorionic site of renin production is suggested (4, 6). Twin pregnancy has more chorionic and placental tissue than a singleton pregnancy and pre-eclamptic toxemia with circulatory disorders is more frequent and severe (12). The high rate of preterm labors leads to frequent medical treatment during twin pregnancy: especially with tocolytics and diuretics.During pregnancy diuretic treatment leads to a strong compensatory activation of the renin-angiotensin system, to an increased PRA and to obvious secondary aldosteronism (7). Beta-sympathomimetic Table I. Presentation of the patients with twin pregnancy. Group A (10) Group B (12) Group C (10) Maternal age (years) (meankSEM) 25.92 1.7 Prepregnant weight (kg) 68.222.6 Weight gain (kg) l2.6k1.3 Week of hospitalization 32.2k0.3 Week of delivery 35.620.2 Weight of baby A (g) 2514t72 Weight of baby B (g) 2574k64 Weight of placenta (9) 816233 range 19-35 range 49 -77 range 6 -18 range 30-33 range 34-36 The figures within parenthesis denote number of patients. 28.1 kO.8 24-32 75.523.0 63 -95 12.3k1.9 0-19 31.8k0.3 30-33 36.320.5 35 -38 2670k 108 2680& 180 824249 26.222.0 69.0k3.2 11.4k1.6 32.2k0.3 36.8k0.4 2720298 2...

The pathophysiology of pulmonary oedema with the use of beta‐agonists

“…Animal studies 31,32 and human studies 33,34 have shown a rise in plasma arginine vasopressin levels during beta‐agonist therapy. Betamimetics have also been shown to activate the renin angiotensin system, which increases renal sodium resorption 30,32,34,36 . The resultant sodium and water retention has been noted in primates 37,38 and humans 30–33 , with significant decreases in maternal haemoglobin, haematocrit and serum albumin and, therefore, plasma colloid osmotic pressure 33,34,39 .…”

“…Betamimetics have also been shown to activate the renin angiotensin system, which increases renal sodium resorption 30,32,34,36 . The resultant sodium and water retention has been noted in primates 37,38 and humans 30–33 , with significant decreases in maternal haemoglobin, haematocrit and serum albumin and, therefore, plasma colloid osmotic pressure 33,34,39 . This positive fluid balance due to increased sodium retention 30,31,39 results in an increase in pulmonary capillary pressure 39,40,41 . latrogenic fluid overload: This may be due to the use of the wrong infusate or excessive administration of the appropriate infusate.…”

“…The resultant sodium and water retention has been noted in primates 37,38 and humans 30–33 , with significant decreases in maternal haemoglobin, haematocrit and serum albumin and, therefore, plasma colloid osmotic pressure 33,34,39 . This positive fluid balance due to increased sodium retention 30,31,39 results in an increase in pulmonary capillary pressure 39,40,41 .…”