- Email: [email protected]
9A 1. Adrenal function—I 302. The role of aldosterone in renal hypertension
Abstracts
total suspension. Then the stimulation test with ACTH was performed. With the decrease of cortisone from 36 to 0 mg the level of 17-KS did not undergo important changes, 17-OHCS decreased from 4 to 0 mg, I7-KGS decreased from 22 to 6 mg. Pregnanediol did not show any important change and E3 decreased from 42 to 24mg. With the administration of 25, 50 and 75 U.I. of ACTH, 17-KS did not show any alteration, 17-OHCS increased from 4.6 to 8mg I7-KGS from 8.7 to 22mg. Pregnanediol increased from 21 to 31 mg and E, from 70 to 120mg. In conclusion, there is an increase in the different steroid metabolites by the administration of ACTH. We would emphasize that Berg and Carmody commented on the benefit of ACTH in the maintenance of pregnancy, when a deficiency of steroid hormones exists. Furthermore, the decrease of estradiol observed when the maintenance dose of corticoid was suspended. is comparable to the decrease of the two corticoids studied, which implies that these last may also serve as parameters of fetal distress. 299. Cortisol in amniotic fluid and human parturition JOLIVET, A., Department of Obstetrics and Gynaecology. C.H.I.C. 94010 Creteil, France In order to determine whether corticosteroids influence human parturition as they do in other species, cortisol has been studied during late pregnancy. Measurements in maternal blood did not show any variations during the last weeks of pregnancy, before confinement, but a two fold increase occurred during labour, the maximum being at delivery. For a better estimate of fetal adrenal activity, free cortisol in amniotic fluid was measured during the last weeks of normal pregnancies. Amniotic fluid was collected by abdominal amniocentesis and frozen (- 20’ C) until the assay. Cortisol was estimated by a radiocompetitive protein binding assay using human CBG. Competitive steroids were removed by petroleum ether and carbon tetrachloride, and samples were then extracted with methylene chloride. A progressive increase of cortisol is related to gestational age but a sharp increase is seen during the last days before term parturition, as in premature deliveries. The mean values of cortisol in amniotic fluid were 2.30 k 0.53 pg/lOO ml in the 10 to 30 days period before birth and 3.32 _+ 0.74pg/ 100 ml in the 1 to 5 days period @ < 0.01) and 4.43 k 1.38 pg/ 100 ml on the day of parturition for term deliveries; cortisol values were respectively 1.83 _+ 0.51 pg/lOO ml and 3.08 + 0.83 pg/lOO ml @ < 0.05) and 3.56 + 0.79 pg/lOO ml in cases of premature delivery. Cortisol levels in amniotic fluid were two-fold higher in patients submitted to ethinyl oestradiol treatment, but variations were similar. Whether the increase of cortisol in amniotic fluid during late pregnancy is related to fetal influence on the onset of labour will be discussed. 300. Adrenocortical hyperfunction in the pregnant golden hamster BRINCE-JOHNSEN, T. and KILHAM, L., Pathology and
361
Microbiology, N.H., U.S.A.
Dartmouth
Medical
School,
Hanover,
Plasma cortisol in the hamster, assayed by the Porter-Silber technique and radioimmunoassay, rose during pregnancy from about 0.5 gg”/, to 30 pg% on the 15th day and fell to 0.5pgy; one day after parturition. In pregnancy, ACTH stimulation increases cortisol further, and adrenalectomy effectively reduces plasma cortisol, excluding the placenta as the site of cortisol production. Endotoxin stimulation increases cortisol levels markedly during pregnancy from 0.5 to 5 pg”& at the time of mating, from 2 to 9 pg”/, in the 7 days pregnant, from 4 to 25pg?< in the 9 days pregnant and from 30 to 120 pg3, in the 15 days pregnant animal. Treatment with estrogens and progesterone did not, but prolonged stimulation with Human Chorionic Gonadotropin in the non pregnant hamster increased both cortisol levels and the adrenocortical responsiveness to endotoxin. Fetal death induced by H-l virus, leaving the placenta intact, did not reduce the high cortisol levels. The marked adrenocortical hyperfunction demonstrated in the pregnant hamster, is probably not caused by increased transcortin levels induced by estrogens, but appears to be caused by placental factors stimulating the maternal adrenal cortex. (USPHS Grants CA 06010 and HD 07775). 301. The role of cortisol in human parturition and lung maturation PEARXIN MURPHY, BCVERLIY E.. Departments of Experimental Medicine and Obstetrics and Gynaecology. McGill University. Montreal, Canada Studies in animals suggest that serum cortisol levels rise a few days prior to parturition and this is a factor in the initiation of labour. Since cortisol in these animals is known to promote lung maturation it seems likely that these two processes are related, the final surge of cortisol ensuring that the fetus is ready for air-breathing as well as triggering its birth. To determine if such a relationship holds in man, serum cortisol levels were studied in mixed umbilical cord blood at delivery in normal, term, and premature infants after spontaneous labour, induced labour, Caesarean section with and without labour, both in normal subjects and in those where the infant developed the idiopathic respiratory distress syndrome (RDS), an indication of lung immaturity. The mean value for all spontaneous labours (58.7 k 1 I.7 ng/ml SE) exceeded (p < 0.01) that of cases without spontaneous labour (26.9 + 4.9 ng/ml). The mean level in infants who developed RDS (23.1 k 3.5 ng/ml) was low (p < 0.01) and similar to that of normal term infants who had not undergone spontaneous labour, while that of babies without RDS (68.5 + 14.0 ng/ml) was similar to that of normal infants born after spontaneous labour. Since most of the RDS infants were born after spontaneous labour, these data suggest that in the RDS group labour is triggered by a mechanism not involving the prepartum cortisol surge which occurs in most normal infants.
9. Clinical aspects 9A 1. Adrenal function-I 302. The role of aldosterone in renal hypertension KOLPAKOV, M. G., MARKEL, A. M. and PROTSENKO, M. I., Laboratory of Endocrinology, Institute
of Cytology
and Genetics,
Novosibirsk,
U.S.S.R.
The dynamics of the development of arterial hypertension provoked by the constriction of the renal arteries have been studied during 1 month. It was found that, in the pathogenesis of hypertension, in the first week a vascular factor predominated and towards the end of the experi-
36X
Abstracts
mental period there was predomination of a cardiac component. The concentration of aldosterone in peripheral blood doubled by the end of the month. The increase in aldosterone level in peripheral blood correlated positively with the increase of arterial blood pressure and also with some indices of cardiac dynamics (cardiac output and the rate of blood leaving the left ventricle). No significant correlation between hormone concentration in blood and general vascular resistance has been found. The mass of the circulating blood did not rise. The results suggest the existence of a cardiotonic effect of aldosterone. which is one of the main causes of the hyperkinetic stage of renal hypertCllhiol1.
30.1.
Adrenocortical activity in different types of renal hypertension DIETZ. R.. MAST. G. J.. VECSEI. P.. GLESS. K. H.. MOHRINC;. J.. OSTER. P. and Gross. F.. Department of Pharmacology. University of Heidelberg. West Germanv
In rats. stenosis of one renal artery in the presence of an intact contralateral kidney induces acute malignant hypertension, when blood pressure exceeds a “critical” level of 180 mmHg and sodium loss occurs. Signs of malignant hypertension are also observed after ligation of the aorta between the origins of the renal arteries. In both types of malignant hypertension, the plasma concentrations of angiotensin II are markedly elevated. After stenosis of either both renal arteries or the remaining one after unilateral nephrectomy. no sodium loss or other signs of acute malignant hypertension appear, although the blood pressure exceeds the “critical” level. In these forms of renal hypertension. plasma angiotensin II concentrations are in the normal range or only slightly elevated. Aldosterone was assayed by two methods first. by direct radioimmunoassay of the plasma concentration and second, by the jr1 viro radioimmunoassay. which indicates the free aldosterone in the “inner pool”. All rats with malignant hypertension had high endogenous aldosterone production (in viva RIA) and an elevated plasma aldosterone concentration. Plasma corticosterone concentration was also increased. but less than that of aldosterone. In rats with a benign type of renal hypertension aldosterone production and plasma concentration were in the normal range. It is concluded that acute malignant hypertension develops in the presence of an intact contralateral kidney, which is exposed to the high blood pressure. By negative sodium and fluid balance the reninangiotensin-system is further stimulated and aldosterone production is increased. 304. Evidence for a derangement in corticosteroid metabolism in essential hypertension : Its possible relationship to the etiological mechanism KORNHL. L.. Steroid Unit. Rush-Presbyterian-St. Luke’s Medical Center. Chicago. Illinois. U.S.A. The results of our previous studies on corticosteroid metabolism in normotensive subjects (N) and patients with essential hypertension (H) revealed a deranged metabolism ofadrenal steroids in H (Research on Steroids 5:413, 1973). These lindings have now been confirmed in a large number of patients. Following i.v. administration of tracer [4-iJC] cortisol, plasma and urinary metabolites of cortisol (F) were determined in 70 N and 21 H. by methods previously pubhshed (Steroidologia 1:225, 1970; ibid 2: 197. 1971). In addition, a.m. and p.m. plasma levels of F (CPB method)
were also determined in these subjects. The followmg significant differences 0, < 0.01) between N and H were revealed (mean f S.D.): (1 ) Urintrr!~ eucrctim (‘I,, ol’ total metabolites):THF+THE(Sr.+S[j). N 42.8 & 4.8. H 26.9 & 3.9; 70(r+b)-dihydro-F, N 4.6 & 1.6. H X.4 ) 2.1: 20. dihydro-6-OH-F(all4 isomers), N 13.1 ) 3.4. H 27.2 F 4.9; (2)pla.snza/evels(“,,total metabolites): THF+THE(Scr+S/j). N 36.4 & 3.8. H 26.3 f 4.9; 20(r+/&dihydro-F, N 2.7 i 1.0. H 6.4 + 2.3: 20-dihvdro-6-OH-F (all 4 isomers). N 8.9 ? 1.4, H 13.5 t 3.1. so significant difference between N and H was found in plasma F. These results provide evidence for a decreased activity of cortisol I’-hydrogenase. and increased activities of cortisol 30-reductase and h-hydroxylase in H. while plasma levels of F remain normal. Recently, Genest et al. reported tindings (Ann. Int. Med. 79: 411, 1973) pointing to an analogous derangement in the metabolism of aldosterone (Aldo) in H. However, plasma levels of Aldo were found to be significantly higher in H than in N. The correlation of our findings with those of Genest et al. permits the deduction that. as a result of an overall decrease in the activity of hepatic corticosteroid d”-hydrogenase in H. there is a compensatory increase in the production rates of certain steroid metabolites noreduced in ring A (incl. .4ldo itself). The role of these steroids in the mechanism of hypertension remains to bc elucidated. (Supported in part by NIH Grant HE-l 1651). 305. Preoperative identification of aldosterone producing adenoma (APA) SCHAMBELAN. M., HOGAN, M. and BIGLIERI, E. G., Univ. Calif. Med. Serv. San Francisco General Hospital, San Francisco, Ca., U.S.A. Superior surgical results necessitate pre-operative distinction of patients with APA from other types of possible primary aldosteronism. Studies were performed in 4 groups of patients with subnormal plasma renin concentration (PRC). Urinary aldosterone excretion was elevated in 25 patients with surgically proven APA(35.4 F 2.9 /(g/24 h, N 4-l 7) and 6 with bilateral hyperplasia (IHA) (25.3 + 4.8); slightly elevated in 5 with so-called indeterminate hyperaldosteronism (IndHA) (20.0 i 1.7): and normal in 8 with low renin essential hypertension (LRH) (9.0 k I .3).Administration of deoxycorticosterone acetate (DOCA) failed to suppress elevated aldosterone excretion in APA(35.3 k 3,4lrg, 24 h) and IHA(20.9 + 9.7). but suppression occurred in IndHA(9.7 _+ 1.5). Surgery has been deferred in the latter group. Overnight recumbent X am plasma aldosterone CPAC) was clearly elevated in APA(35.5 k 2~6ng/lOOml. N 4-10) in contrast to borderline levels in IHA(14.0 + 2.1) and IndHA(13.6 + 1.X) and normal levels in LRH(8.X i 0.4). The expected upright noon rise in PAC was seen in IHA and IndHA; a paradoxical fall was unique to APA (19/25). Localization of APA was accomplished by iodocholesterol scanning and/or adrenal vein catheterization in IO consecutive patients. This systematic approach permits pre-operative separation of patients with APA from other types of possible mineralocortical excess. 306. Influence of dietary sodium and potassium on the response of the glomerolosa cell to acute stimulation WILLIAMS, G. H.. DLUHY, R. G. and HOLLENBERG, N. K., Endocrine-Metabolic Unit and Department of Radiology, Peter Bent Brigham Hospital and Harvard Medical School. Boston. Ma.. U.S.A. The
response
of aldosterone
tsldo)
secretion
to acute
total suspension. Then the stimulation test with ACTH was performed. With the decrease of cortisone from 36 to 0 mg the level of 17-KS did not undergo important changes, 17-OHCS decreased from 4 to 0 mg, I7-KGS decreased from 22 to 6 mg. Pregnanediol did not show any important change and E3 decreased from 42 to 24mg. With the administration of 25, 50 and 75 U.I. of ACTH, 17-KS did not show any alteration, 17-OHCS increased from 4.6 to 8mg I7-KGS from 8.7 to 22mg. Pregnanediol increased from 21 to 31 mg and E, from 70 to 120mg. In conclusion, there is an increase in the different steroid metabolites by the administration of ACTH. We would emphasize that Berg and Carmody commented on the benefit of ACTH in the maintenance of pregnancy, when a deficiency of steroid hormones exists. Furthermore, the decrease of estradiol observed when the maintenance dose of corticoid was suspended. is comparable to the decrease of the two corticoids studied, which implies that these last may also serve as parameters of fetal distress. 299. Cortisol in amniotic fluid and human parturition JOLIVET, A., Department of Obstetrics and Gynaecology. C.H.I.C. 94010 Creteil, France In order to determine whether corticosteroids influence human parturition as they do in other species, cortisol has been studied during late pregnancy. Measurements in maternal blood did not show any variations during the last weeks of pregnancy, before confinement, but a two fold increase occurred during labour, the maximum being at delivery. For a better estimate of fetal adrenal activity, free cortisol in amniotic fluid was measured during the last weeks of normal pregnancies. Amniotic fluid was collected by abdominal amniocentesis and frozen (- 20’ C) until the assay. Cortisol was estimated by a radiocompetitive protein binding assay using human CBG. Competitive steroids were removed by petroleum ether and carbon tetrachloride, and samples were then extracted with methylene chloride. A progressive increase of cortisol is related to gestational age but a sharp increase is seen during the last days before term parturition, as in premature deliveries. The mean values of cortisol in amniotic fluid were 2.30 k 0.53 pg/lOO ml in the 10 to 30 days period before birth and 3.32 _+ 0.74pg/ 100 ml in the 1 to 5 days period @ < 0.01) and 4.43 k 1.38 pg/ 100 ml on the day of parturition for term deliveries; cortisol values were respectively 1.83 _+ 0.51 pg/lOO ml and 3.08 + 0.83 pg/lOO ml @ < 0.05) and 3.56 + 0.79 pg/lOO ml in cases of premature delivery. Cortisol levels in amniotic fluid were two-fold higher in patients submitted to ethinyl oestradiol treatment, but variations were similar. Whether the increase of cortisol in amniotic fluid during late pregnancy is related to fetal influence on the onset of labour will be discussed. 300. Adrenocortical hyperfunction in the pregnant golden hamster BRINCE-JOHNSEN, T. and KILHAM, L., Pathology and
361
Microbiology, N.H., U.S.A.
Dartmouth
Medical
School,
Hanover,
Plasma cortisol in the hamster, assayed by the Porter-Silber technique and radioimmunoassay, rose during pregnancy from about 0.5 gg”/, to 30 pg% on the 15th day and fell to 0.5pgy; one day after parturition. In pregnancy, ACTH stimulation increases cortisol further, and adrenalectomy effectively reduces plasma cortisol, excluding the placenta as the site of cortisol production. Endotoxin stimulation increases cortisol levels markedly during pregnancy from 0.5 to 5 pg”& at the time of mating, from 2 to 9 pg”/, in the 7 days pregnant, from 4 to 25pg?< in the 9 days pregnant and from 30 to 120 pg3, in the 15 days pregnant animal. Treatment with estrogens and progesterone did not, but prolonged stimulation with Human Chorionic Gonadotropin in the non pregnant hamster increased both cortisol levels and the adrenocortical responsiveness to endotoxin. Fetal death induced by H-l virus, leaving the placenta intact, did not reduce the high cortisol levels. The marked adrenocortical hyperfunction demonstrated in the pregnant hamster, is probably not caused by increased transcortin levels induced by estrogens, but appears to be caused by placental factors stimulating the maternal adrenal cortex. (USPHS Grants CA 06010 and HD 07775). 301. The role of cortisol in human parturition and lung maturation PEARXIN MURPHY, BCVERLIY E.. Departments of Experimental Medicine and Obstetrics and Gynaecology. McGill University. Montreal, Canada Studies in animals suggest that serum cortisol levels rise a few days prior to parturition and this is a factor in the initiation of labour. Since cortisol in these animals is known to promote lung maturation it seems likely that these two processes are related, the final surge of cortisol ensuring that the fetus is ready for air-breathing as well as triggering its birth. To determine if such a relationship holds in man, serum cortisol levels were studied in mixed umbilical cord blood at delivery in normal, term, and premature infants after spontaneous labour, induced labour, Caesarean section with and without labour, both in normal subjects and in those where the infant developed the idiopathic respiratory distress syndrome (RDS), an indication of lung immaturity. The mean value for all spontaneous labours (58.7 k 1 I.7 ng/ml SE) exceeded (p < 0.01) that of cases without spontaneous labour (26.9 + 4.9 ng/ml). The mean level in infants who developed RDS (23.1 k 3.5 ng/ml) was low (p < 0.01) and similar to that of normal term infants who had not undergone spontaneous labour, while that of babies without RDS (68.5 + 14.0 ng/ml) was similar to that of normal infants born after spontaneous labour. Since most of the RDS infants were born after spontaneous labour, these data suggest that in the RDS group labour is triggered by a mechanism not involving the prepartum cortisol surge which occurs in most normal infants.
9. Clinical aspects 9A 1. Adrenal function-I 302. The role of aldosterone in renal hypertension KOLPAKOV, M. G., MARKEL, A. M. and PROTSENKO, M. I., Laboratory of Endocrinology, Institute
of Cytology
and Genetics,
Novosibirsk,
U.S.S.R.
The dynamics of the development of arterial hypertension provoked by the constriction of the renal arteries have been studied during 1 month. It was found that, in the pathogenesis of hypertension, in the first week a vascular factor predominated and towards the end of the experi-
36X
Abstracts
mental period there was predomination of a cardiac component. The concentration of aldosterone in peripheral blood doubled by the end of the month. The increase in aldosterone level in peripheral blood correlated positively with the increase of arterial blood pressure and also with some indices of cardiac dynamics (cardiac output and the rate of blood leaving the left ventricle). No significant correlation between hormone concentration in blood and general vascular resistance has been found. The mass of the circulating blood did not rise. The results suggest the existence of a cardiotonic effect of aldosterone. which is one of the main causes of the hyperkinetic stage of renal hypertCllhiol1.
30.1.
Adrenocortical activity in different types of renal hypertension DIETZ. R.. MAST. G. J.. VECSEI. P.. GLESS. K. H.. MOHRINC;. J.. OSTER. P. and Gross. F.. Department of Pharmacology. University of Heidelberg. West Germanv
In rats. stenosis of one renal artery in the presence of an intact contralateral kidney induces acute malignant hypertension, when blood pressure exceeds a “critical” level of 180 mmHg and sodium loss occurs. Signs of malignant hypertension are also observed after ligation of the aorta between the origins of the renal arteries. In both types of malignant hypertension, the plasma concentrations of angiotensin II are markedly elevated. After stenosis of either both renal arteries or the remaining one after unilateral nephrectomy. no sodium loss or other signs of acute malignant hypertension appear, although the blood pressure exceeds the “critical” level. In these forms of renal hypertension. plasma angiotensin II concentrations are in the normal range or only slightly elevated. Aldosterone was assayed by two methods first. by direct radioimmunoassay of the plasma concentration and second, by the jr1 viro radioimmunoassay. which indicates the free aldosterone in the “inner pool”. All rats with malignant hypertension had high endogenous aldosterone production (in viva RIA) and an elevated plasma aldosterone concentration. Plasma corticosterone concentration was also increased. but less than that of aldosterone. In rats with a benign type of renal hypertension aldosterone production and plasma concentration were in the normal range. It is concluded that acute malignant hypertension develops in the presence of an intact contralateral kidney, which is exposed to the high blood pressure. By negative sodium and fluid balance the reninangiotensin-system is further stimulated and aldosterone production is increased. 304. Evidence for a derangement in corticosteroid metabolism in essential hypertension : Its possible relationship to the etiological mechanism KORNHL. L.. Steroid Unit. Rush-Presbyterian-St. Luke’s Medical Center. Chicago. Illinois. U.S.A. The results of our previous studies on corticosteroid metabolism in normotensive subjects (N) and patients with essential hypertension (H) revealed a deranged metabolism ofadrenal steroids in H (Research on Steroids 5:413, 1973). These lindings have now been confirmed in a large number of patients. Following i.v. administration of tracer [4-iJC] cortisol, plasma and urinary metabolites of cortisol (F) were determined in 70 N and 21 H. by methods previously pubhshed (Steroidologia 1:225, 1970; ibid 2: 197. 1971). In addition, a.m. and p.m. plasma levels of F (CPB method)
were also determined in these subjects. The followmg significant differences 0, < 0.01) between N and H were revealed (mean f S.D.): (1 ) Urintrr!~ eucrctim (‘I,, ol’ total metabolites):THF+THE(Sr.+S[j). N 42.8 & 4.8. H 26.9 & 3.9; 70(r+b)-dihydro-F, N 4.6 & 1.6. H X.4 ) 2.1: 20. dihydro-6-OH-F(all4 isomers), N 13.1 ) 3.4. H 27.2 F 4.9; (2)pla.snza/evels(“,,total metabolites): THF+THE(Scr+S/j). N 36.4 & 3.8. H 26.3 f 4.9; 20(r+/&dihydro-F, N 2.7 i 1.0. H 6.4 + 2.3: 20-dihvdro-6-OH-F (all 4 isomers). N 8.9 ? 1.4, H 13.5 t 3.1. so significant difference between N and H was found in plasma F. These results provide evidence for a decreased activity of cortisol I’-hydrogenase. and increased activities of cortisol 30-reductase and h-hydroxylase in H. while plasma levels of F remain normal. Recently, Genest et al. reported tindings (Ann. Int. Med. 79: 411, 1973) pointing to an analogous derangement in the metabolism of aldosterone (Aldo) in H. However, plasma levels of Aldo were found to be significantly higher in H than in N. The correlation of our findings with those of Genest et al. permits the deduction that. as a result of an overall decrease in the activity of hepatic corticosteroid d”-hydrogenase in H. there is a compensatory increase in the production rates of certain steroid metabolites noreduced in ring A (incl. .4ldo itself). The role of these steroids in the mechanism of hypertension remains to bc elucidated. (Supported in part by NIH Grant HE-l 1651). 305. Preoperative identification of aldosterone producing adenoma (APA) SCHAMBELAN. M., HOGAN, M. and BIGLIERI, E. G., Univ. Calif. Med. Serv. San Francisco General Hospital, San Francisco, Ca., U.S.A. Superior surgical results necessitate pre-operative distinction of patients with APA from other types of possible primary aldosteronism. Studies were performed in 4 groups of patients with subnormal plasma renin concentration (PRC). Urinary aldosterone excretion was elevated in 25 patients with surgically proven APA(35.4 F 2.9 /(g/24 h, N 4-l 7) and 6 with bilateral hyperplasia (IHA) (25.3 + 4.8); slightly elevated in 5 with so-called indeterminate hyperaldosteronism (IndHA) (20.0 i 1.7): and normal in 8 with low renin essential hypertension (LRH) (9.0 k I .3).Administration of deoxycorticosterone acetate (DOCA) failed to suppress elevated aldosterone excretion in APA(35.3 k 3,4lrg, 24 h) and IHA(20.9 + 9.7). but suppression occurred in IndHA(9.7 _+ 1.5). Surgery has been deferred in the latter group. Overnight recumbent X am plasma aldosterone CPAC) was clearly elevated in APA(35.5 k 2~6ng/lOOml. N 4-10) in contrast to borderline levels in IHA(14.0 + 2.1) and IndHA(13.6 + 1.X) and normal levels in LRH(8.X i 0.4). The expected upright noon rise in PAC was seen in IHA and IndHA; a paradoxical fall was unique to APA (19/25). Localization of APA was accomplished by iodocholesterol scanning and/or adrenal vein catheterization in IO consecutive patients. This systematic approach permits pre-operative separation of patients with APA from other types of possible mineralocortical excess. 306. Influence of dietary sodium and potassium on the response of the glomerolosa cell to acute stimulation WILLIAMS, G. H.. DLUHY, R. G. and HOLLENBERG, N. K., Endocrine-Metabolic Unit and Department of Radiology, Peter Bent Brigham Hospital and Harvard Medical School. Boston. Ma.. U.S.A. The
response
of aldosterone
tsldo)
secretion
to acute