Studies of the factors modulating antidiuretic hormone excretion in man in response to the osmolar stimulus: effects of oestrogen and angiotensin II

1983 ◽  
Vol 104 (3) ◽  
pp. 295-302 ◽  
Author(s):  
Michel B. Vallotton ◽  
Ulrich Merkelbach ◽  
Rolf C. Gaillard
Keyword(s):  
Angiotensin Ii ◽  
Antidiuretic Hormone ◽  
Hypertonic Saline ◽  
Plasma Renin ◽  
Electrolyte Balance ◽  
Renin Substrate ◽  
Oestrogen Treatment ◽  
Significant Difference ◽  
The Mean ◽  
Ethinyl Oestradiol

Abstract. The aim of this study was to assess the influence of hormones known to regulate fluid and electrolyte balance on the release of antidiuretic hormone induced by raising serum osmolality. The stimulus provoked by the infusion of a 2.5% NaCl solution induces an increase of urinary [arginine-8]vasopressin from 1.12 to 2.64 ng/h in men and from 1.65 to 7.27 ng/h in women as has been previously reported. These results were compared to those obtained in males infused with angiotensin II (All) before and during a hypertonic sodium load and in males infused with hypertonic saline on the fourth day of administration of ethinyl-oestradiol. During the combined infusion of All and then hypertonic saline, the mean hourly urinary excretion of AVP increased from 2.8 to 5.67 ng/h. Within each group the increase of urinary AVP was highly significant. The rise of urinary AVP during All infusion was significantly different from the rise observed both in untreated males and untreated females, lying in between. The mean hourly excretion rate of AVP increased before and after hypertonic saline loading from 2.65 to 5.3 ng/h in males pre-treated with ethinyl-oestradiol. The significant difference observed between males and females is reduced when males treated with oestrogen were compared to female subjects. In each group plasma renin activity decreased to low values during the salt-loading test. During oestrogen treatment PRA and plasma renin substrate rose, while urinary aldosterone remained almost unchanged. We conclude that All stimulates the release of AVP in males and potentiates the response of AVP to the osmolar stimulus, and that oestrogen potentiates in man the release of AVP in response to the osmolar stimulus. This oestrogenic effect may account for the observed sex difference.

Angiotensin II (AII) and adrenal gland AII receptors in rats with congenital hypothyroidism

1993 ◽  
Vol 137 (2) ◽  
pp. 231-238 ◽  
Author(s):  
M. J. Matilla ◽  
M. Montiel ◽  
E. Jiménez
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Congenital Hypothyroidism ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hormone Deficiency ◽  
Electrolyte Balance ◽  
Renin Substrate ◽  
Receptor Isoforms ◽  
Ace Activity

ABSTRACT Plasma angiotensin II (AII) concentration, plasma renin concentration (PRC), lung angiotensin-converting enzyme (ACE) activity and adrenal gland AII receptor isoforms have been evaluated in the postnatal development of the rat, in order to determine the alterations of the renin-angiotensin system (RAS) which occur in congenital hypothyroidism. The developmental AII profiles observed in control and hypothyroid rats were quite similar. Thus, AII was elevated at birth and declined at week 5 of life to reach adult values. However, AII levels were lower in hypothyroid than in euthyroid animals before their stabilization. On the other hand, PRC in newborn hypothyroid and euthyroid animals was higher than in adulthood, being significantly increased immediately after birth in hypothyroid rats. Pulmonary ACE activity in both experimental groups was low at birth and increased with age. This increase was greater in euthyroid rats than in congenitally hypothyroid animals from day 28 of life. These results confirm that plasma AII levels in rats are predominantly controlled by plasma renin activity, although other factors, such as renin substrate availability, may be responsible for the reduced plasma AII concentration in congenital hypothyroidism during the first weeks of life. The developmental profile of the adrenal gland AII receptor showed four isoforms, with pI values of 6·8, 6·7, 6·5 and 6·3. AII receptor-complex expression increased with age but, in congenitally hypothyroid rats, a higher induction of AII receptor isoforms migrating to pI 6·8, 6·5 and 6·3 was observed. These findings show that thyroid hormone deficiency in early life can have an important role in the postnatal induction of the RAS components, which may be essential for the regulation of blood pressure, and for fluid and electrolyte balance in developing rats. Journal of Endocrinology (1993) 137, 231–238

TO COMPARE THE EFFECTIVENESS OF NEBULISATION WITH ADRENALINE, 3% HYPERTONIC SALINE AND NORMAL SALINE IN BRONCHIOLITIS IN CHILDREN OF 2 TO 24 MONTHS OF AGE BASED ON CLINICAL SEVERITY SCORE AND NEBULISATION FREQUENCY.

2021 ◽  
Vol 5 (2) ◽  
Author(s):  
Priyanka Jain ◽  
Rakesh Jain
Keyword(s):  
Hypertonic Saline ◽  
Normal Saline ◽  
Mean Difference ◽  
Clinical Severity ◽  
Research Centre ◽  
P Value ◽  
College Hospital ◽  
Mean Values ◽  
Significant Difference ◽  
The Mean

Background & Method: We conducted a double blinded study at Index Medical College Hospital & Research Centre, Indore. The sample size was determined to be minimum of 120 cases as based upon previous years admission due to acute bronchiolitis. Initially, 146 cases were included in the study out of which 23 cases dropped out of the study after giving consent by guardian for participation in the study as they left against medical advice from the hospital. Result: The mean difference of CSS between 0 minutes to 60 minutes of nebulisation between groups in all cases was 0.4 ± 0.6, between 60 minutes and 4 hours was 0.8 ± 0.6, between 4 to 8 hours was 0.7 ± 0.6, between 8-12 hours was 0.6 ± 0.4, between 12-24 hours was 1.6 ± 0.9 and between 24-48 hours was 1.9 ± 0.9.The mean values and resultant p-value of ANOVA of various nebulising agents used for improvement in CSS shows significant association between various nebulising agents used along with improvement in CSS at the end of assessment at 48 hours of treatment. Conclusion: This study was conducted to establish the efficacy of each nebulisation agent (i.e.  adrenaline, 3% hypertonic saline and normal saline) currently used and compare the outcomes as there is not enough evidence amongst Indian population on level of efficacy of each drug in causing improvement in symptoms and signs in various severities of bronchiolitis in early childhood. Comparison of significant improvement in mean difference in CSS at various intervals in all cases compared between groups by post hoc test revealed non-significant difference (p-value 0.700) between 3% hypertonic saline and normal saline. Keywords: nebulisation, adrenaline, bronchiolitis & clinical.

Does heparin inhibit renin activity?

1991 ◽  
Vol 69 (9) ◽  
pp. 1360-1363 ◽  
Author(s):  
Masato Matsunaga ◽  
Yoko Yamanaka ◽  
Noriko Nagano ◽  
Yuki Iwasaki ◽  
Yumi Saito ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Substrate ◽  
Significant Difference ◽  
Inactive Renin

Although heparin was reported in the 1960s to inhibit renin activity, this has not always been confirmed by other investigators. Hence, we re-examined whether heparin really inhibits renin or not. Renin activities were determined by radioimmunoassay of angiotensin I generated at pH 7.4. (i) No significant difference was found between the two kinds of plasma samples obtained with heparin and with EDTA as anticoagulant, in ARC (renin activity with addition of sheep renin substrate), TRC (ARC after activation of inactive renin by trypsin), or PRA (plasma renin activity without additional substrate), (ii) Even in higher concentrations of heparin up to 500 U/mL, neither PRA, ARC, nor TRC of plasma was affected significantly. (iii) Heparin, in concentrations up to 500 U/mL, exerted no significant effect on TRC of the media of human vascular smooth muscle cell culture. In conclusion, heparin does not exert any significant inhibitory effect on human renin nor does it affect activation of inactive renin by trypsin in the range of concentration of practical use, under the conditions employed in this study.Key words: plasma renin, tissue renin, inactive renin, vascular smooth muscle cell, trypsin.

Intrarenal renin inhibition increases renal function by an angiotensin II-dependent mechanism

1988 ◽  
Vol 255 (4) ◽  
pp. F749-F754 ◽  
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Competitive Inhibitor ◽  
Urinary Flow ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Renin Inhibition

ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +/- 1.4 to 15.1 +/- 5.1 and 19.9 +/- 3.2 mu eq/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +/- 2.5 to 35.6 +/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis.

Oestrogen treatment of adolescent tall girls; short term side effects

1986 ◽  
Vol 113 (4_Suppl) ◽  
pp. S170-S173 ◽  
Author(s):  
OLAV TRYGSTAD
Keyword(s):  
Side Effects ◽  
Idiopathic Scoliosis ◽  
Final Height ◽  
Psychosocial Problems ◽  
Short Term ◽  
Oestrogen Treatment ◽  
Duration Of Therapy ◽  
Tall Girls ◽  
The Mean ◽  
Ethinyl Oestradiol

Abstract In 1980-1985 680 preadolescent tall girls were treated with pharmacological doses of oestrogen to reduce final height. Indications for the therapy were predicted final height >+2.5 SD (180.75 cm), idiopathic scoliosis, and psychosocial problems. Until 1976 141 girls were given diethyl stilboestrol 5 mg daily. By advice of Prader this was then replaced by ethinyl oestradiol and a progestin was given on days 5-10 each month. The mean duration of therapy was close to 2 years. The observed short-term unwanted effects were due to the pharmacological actions of the drugs, (11 girls had galactorrhoea at the end of therapy; no pituitary prolactionoma was observed) or events happening by chance.

Renin, Angiotensin and Aldosterone in Human Pregnancy and the Menstrual Cycle

1971 ◽  
Vol 16 (3) ◽  
pp. 183-196 ◽  
Author(s):  
J. I. S. Robertson ◽  
R. J. Weir ◽  
G. O. Düsterdieck ◽  
R. Fraser ◽  
M. Tree
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin ◽  
Normal Pregnancy ◽  
Maternal Plasma ◽  
Plasma Aldosterone ◽  
Sodium Depletion ◽  
Aldosterone Secretion ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
In Pregnancy

Aldosterone secretion is frequently, although not invariably, increased above the normal non-pregnant range in normal pregnancy. Substantial increases in plasma aldosterone concentration have also been demonstrated as early as the sixteenth week. In pregnancy, aldosterone secretion rate responds in the usual way to changes in sodium intake. Plasma renin concentration is frequently, but not invariably, raised above the normal non-pregnant range. Plasma renin-substrate is consistently raised in pregnancy. Plasma angiotensin II has also been shown usually to be raised in a series of pregnant women. A significant positive correlation has been shown between the maternal plasma aldosterone concentration and the product of the concurrent plasma renin and renin-substrate concentrations. This suggests that the increased plasma aldosterone in pregnancy is the consequence of an increase in circulating angiotensin II, which in turn is related to the level of both renin and its substrate in maternal blood. For these reasons, estimations of renin activity in pregnancy are of dubious value. The increased renin, angiotensin and aldosterone concentrations may represent a tendency to maternal sodium depletion, probably mainly a consequence of the increased glomerular filtration rate. It is possible that the nausea and other symptoms of early pregnancy may be a consequence of this tendency to sodium depletion, with its attendant hormonal changes. In ‘pre-eclampsia’, renin and aldosterone values are generally slightly lower than in normal pregnancy. Human chorion can apparently synthesize renin independently of the kidney. The physiological significance of this remains at present obscure, but it seems unlikely that this source contributes much, if at all, to the often elevated maternal plasma renin. Plasma renin, renin-activity and angiotensin II concentrations, and aldosterone secretion are increased in the luteal phase of the menstrual cycle.

Longitudinal study of platelet angiotensin II binding in human pregnancy

1992 ◽  
Vol 82 (4) ◽  
pp. 377-381 ◽  
Author(s):  
Philip N. Baker ◽  
Fiona Broughton Pipkin ◽  
E. Malcolm Symonds
Keyword(s):  
Longitudinal Study ◽  
Angiotensin Ii ◽  
Post Partum ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Significant Rise ◽  
Renin Substrate ◽  
Plasma Renin Concentration ◽  
Plasma Angiotensin ◽  
In Pregnancy

1. Platelet angiotensin II binding, circulating angiotensin II levels, plasma renin substrate and plasma renin concentration were measured in a longitudinal study of 30 women during pregnancy and the puerperium. 2. There was a significant fall in platelet angiotensin II binding from 11 weeks gestation to 18 weeks gestation (P < 0.01). There were no further significant changes in platelet angiotensin II binding until after delivery, a significant rise in platelet angiotensin II binding being found at 6 weeks post partum as compared with at 36 weeks gestation (P < 0.01). There was no further significant change from 6 to 12 weeks post partum, and platelet angiotensin II binding at 6 and 12 weeks post partum in the pregnant cohort approximated to that in non-pregnant women. These changes parallel those known to occur in pressor responsiveness to angiotensin II in pregnancy. 3. Plasma angiotensin II concentration, plasma renin substrate and plasma renin concentration were all significantly higher during pregnancy than in the puerperium (P < 0.001). There were no significant changes during pregnancy in plasma angiotensin II concentration or plasma renin concentration, although plasma renin substrate rose throughout. 4. Significant inverse correlations between platelet angiotensin II binding and plasma angiotensin II concentration (P < 0.01), plasma renin substrate (P < 0.01) and plasma renin concentration (P 0>001) were found during pregnancy. These data suggest that down-regulation of platelet angiotensin II binding by the components of the renin-angiotensin system pertains in pregnancy. 5. We are currently investigating parallelism between platelet and vascular angiotensin-binding sites. If such is confirmed, studies of platelet angiotensin II binding in pregnancy may be of both basic physiological and clinical interest in relation to the hypertensive diseases of pregnancy.

ACTH Stimulates Plasma Renin and Angiotensin II in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 273s-275s ◽  
Author(s):  
W. Oelkers ◽  
A. Köhler ◽  
L. Belkien ◽  
R. Fuchs-Hammoser ◽  
M. Maiga ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Normal Male ◽  
Renin Substrate ◽  
Trophic Effect ◽  
Physiological Regulator ◽  
Lag Period ◽  
Male Subjects

1. Adrenocorticotropic hormone (ACTH; 10 i.u./day) was infused for 34 h into normal male subjects. Some subjects were additionally treated with propranolol or indomethacin. Others received sham infusions or hydrocortisone infusions instead of ACTH. 2. ACTH, but not sham or hydrocortisone infusions, led to a significant increase in plasma renin activity and angiotensin II concentration with a lag period of 7–10 h and a maximum response after 24 h. ACTH may be a physiological regulator of renin secretion, perhaps through a ‘trophic’ effect on the juxtaglomerular apparatus. 3. The effect of ACTH on renin is not mediated by a rise in plasma renin substrate, probably not by renal β-adrenoreceptors, but perhaps by prostaglandins. 4. A dissociation between plasma cortisol and aldosterone during ACTH infusion suggests that ACTH, in this dosage, stimulates aldosterone on the second day through renin and angiotensin II, before its secretion is finally suppressed during more prolonged infusion.

MEASUREMENT OF PLASMA RENIN-SUBSTRATE IN MAN

1973 ◽  
Vol 56 (2) ◽  
pp. 159A-171 ◽  
Author(s):  
MALCOLM TREE
Keyword(s):  
Angiotensin Ii ◽  
Substrate Concentration ◽  
Plasma Renin ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Potential Sources ◽  
Sources Of Variation ◽  
Method Of Measurement ◽  
Inhibitor Solution

SUMMARY Values of plasma renin-substrate concentration in man vary widely according to the method of measurement used. Potential sources of variation have been tested and, as far as possible, excluded in the method described here. Blood was diluted rapidly in an angiotensinase-inhibitor solution containing EDTA and phenanthroline; plasma was separated by centrifugation and the renin-substrate in the specimen was hydrolysed by renin to angiotensin I which was identified as such by chromatography and radioimmunoassay. Angiotensin I was used as a standard to determine the amount of angiotensin formed on incubation. Use of angiotensin II for a standard, as in other methods, led to falsely low values of plasma renin-substrate concentration. Recovery of added substrate was 94%. Changes of plasma renin-substrate concentration in some physiological and pathological states are reported briefly.

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