RESUMO
In the crystal structure of the title compound, C(9)H(14)N(2)O(3), the molecules are linked by N-H.O=C bonds into chains parallel to [001]. Large crystals are readily obtained, presumably because of the hydrogen bonds and an energetically stable conformation of the molecule.
RESUMO
Angiotensin II (Ang II) and potassium (K+) increase aldosterone (Aldo) production in vitro via Ca2+-dependent mechanisms. To determine the effects of Ca2+ antagonism in vivo, we examined the influence of nifedipine on the Aldo response to Na+ depletion and K+ loading in 11 healthy subjects. On the fifth day of a low-Na+/high-K+ diet (10 mmol Na+/100 mmol K+) the subjects were randomly given either nifedipine 30 mg po or placebo, and on the sixth day they received the alternative drug. KCl in 5% glucose was infused on days 5 and 6 from 10:00 to 12:00 AM (0.6 mmol/kg over 2 hours). Dexamethasone was given to suppress adrenal corticotrophic hormone. Plasma renin activity (PRA) and plasma Aldo were determined every 20 minutes. Nifedipine induced a rise in heart rate at 60 minutes but did not change blood pressure. During KCl/glucose infusions, plasma glucose increased significantly, but plasma K+ remained stable. PRA, but not baseline plasma Aldo, was stimulated by nifedipine. KCl provoked a significant and similar Aldo rise (P less than .01) under placebo and nifedipine. Baseline Aldo/PRA ratio was reduced under nifedipine when compared to placebo (P less than .01), whereas during KCl infusions this ratio was similarly elevated under placebo and nifedipine. We conclude that acute inhibition of slow Ca2+ channels does not interfere with K+-induced Aldo secretion in man, suggesting that adaptive mechanisms operate in vivo.
Assuntos
Aldosterona/biossíntese , Dieta Hipossódica , Nifedipino/farmacologia , Cloreto de Potássio/administração & dosagem , Adulto , Aldosterona/urina , Pressão Sanguínea/efeitos dos fármacos , Humanos , Masculino , Potássio/sangue , Potássio/urina , Renina/sangue , Sódio/urinaRESUMO
Multiple hypothalamic factors seem to influence ACTH release. In vitro and/or in vivo animal models have shown that angiotensin II, vasopressin and some of its analogs are ACTH secretagogues capable of potentiating the corticotropin releasing activity of CRF41. Since these effects are controversial in man, we investigated in 3 groups of volunteers the corticotropin releasing activity of a 2h-infusion of angiotensin II (7 ng/kg/min), vasopressin (1 ng/kg/min) and desmopressin (1 ng/kg/min) given alone or in combination with a bolus injection of 100 micrograms CRF41 by measuring plasma concentrations of ACTH, cortisol, dehydroepiandrosterone and delta 4-androstenedione. Given alone angiotensin II and desmopressin had no significant effect in contrast to vasopressin which increased significantly the ACTH and steroid levels. Angiotensin II and vasopressin were both able to potentiate the corticotropin releasing activity of CRF41, whereas desmopressin was unable to produce such a potentiation. These results suggest that in man vasopressin and angiotensin II may well regulate the responsiveness of the pituitary-adrenal axis in various physiological or pathophysiological situations.
Assuntos
Angiotensina II/farmacologia , Hormônio Liberador da Corticotropina/farmacologia , Desamino Arginina Vasopressina/farmacologia , Vasopressinas/farmacologia , Hormônio Adrenocorticotrópico/sangue , Adulto , Androstenodiona/sangue , Angiotensina II/efeitos adversos , Hormônio Liberador da Corticotropina/efeitos adversos , Desamino Arginina Vasopressina/efeitos adversos , Desidroepiandrosterona/sangue , Sinergismo Farmacológico , Humanos , Hidrocortisona/sangue , Cinética , Masculino , Vasopressinas/efeitos adversosRESUMO
To test the hypothesis that the trophic action of angiotensin II on the adrenal zona glomerulosa may allow a sustained stimulation of aldosterone by ACTH by preventing the morphological changes of the zona glomerulosa cells into zona fasciculata-like elements we investigated the effects in rats of a 6-day treatment with ACTH (100 micrograms/kg/day) alone or combined with angiotensin II (300 ng/kg/day) on corticosterone and aldosterone production and adrenal morphology. The responsiveness of both steroids to an acute ACTH dose was also studied on the last day of long-term treatment. Morphologic data showed that prolonged ACTH treatment stimulated the growth of zona glomerulosa cells, though it transformed the tubulo-lamellar cristae of mitochondria into a homogeneous population of vesicles. Angiotensin II furthered the trophic effects of ACTH but prevented the mitochondrial transformation. Despite its ability to conserve the well differentiated aspect of the zona glomerulosa cells, the administration of angiotensin II was unable to prevent the fall in the secretion of aldosterone caused by chronic ACTH treatment and its subsequent unresponsiveness to ACTH stimulation.
Assuntos
Glândulas Suprarrenais/efeitos dos fármacos , Hormônio Adrenocorticotrópico/farmacologia , Aldosterona/biossíntese , Angiotensina II/farmacologia , Corticosterona/biossíntese , Glândulas Suprarrenais/metabolismo , Glândulas Suprarrenais/ultraestrutura , Animais , Masculino , Mitocôndrias/ultraestrutura , Ratos , Ratos Endogâmicos , Fatores de TempoRESUMO
To appreciate the aldosterone secretion status in panhypopituitarism, the steroid response to stimulation was studied in a homogeneous group of 20 female patients presenting with global hypopituitarism. Specific effects of glucocorticoid and thyroid hormone deficiencies were also assessed by studying the same patients before and after cortisol (F) and cortisol plus thyroid hormone (F + T) substitution. The patients were submitted to two stimulation tests before and after each treatment: the orthostasis test (O-T) and the furosemide test (Furo-T). The results obtained in the 3 situations were compared, each patient serving as her own control. Comparison was also established with the results obtained in healthy women serving as control group. Basal plasma aldosterone levels in the untreated patients were not significantly different from those of the control group (5.43 +/- 0.51 vs 7.16 +/- 0.80 ng/100 ml, mean +/- SEM). They were significantly lower after F (3.91 +/- 0.42) and F + T substitution (3.31 +/- 0.23) than those of untreated patients and controls. Response to both stimulations was blunted in the untreated patients (O-T: 14.10 +/- 2.81; Furo-T: 9.78 +/- 1.35) as compared to the control group (O-T: 26.46 +/- 4.67; Furo-T: 23.96 +/- 3.30). F treatment did not improve the response to either tests, (O-T: 11.42 +/- 2.55; Furo-T: 10.32 +/- 1.23). F + T treatment normalized the orthostasis response (20.83 +/- 3.59) and increased the response to furosemide which remained, however, lower (15.28 +/- 1.83) than in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
Assuntos
Aldosterona/metabolismo , Hipopituitarismo/fisiopatologia , Adulto , Quimioterapia Combinada , Eletrólitos/sangue , Feminino , Furosemida , Humanos , Hidrocortisona/uso terapêutico , Hipopituitarismo/tratamento farmacológico , Masculino , Postura , Tiroxina/uso terapêuticoRESUMO
Plasma cortisol levels and the response of the adrenal gland to 0.25 mg ACTH administration were measured in 12 patients receiving 15 mg or more of a short-acting steroid (fluocortolone or prednisone) on three out of four days, in 10 patients on daily steroid treatment (15 mg prednisone or more per day), and in 9 normal subjects. The basal plasma cortisol level of the first group was between that of patients on daily prednisone treatment and that of normal subjects. The adrenal function in patients on the three out of four day treatment schedule appeared to be slightly diminished, yet still within the accepted limits for adrenals capable of responding adequately to stress. The adrenal function proved insufficient in all patients on daily steroids. The three out of four day steroid regimen thus offers a solution with many advantages over continuous steroid treatment for patients refractory to the alternate-day schedule.
Assuntos
Hormônio Adrenocorticotrópico , Síndrome de Cushing/induzido quimicamente , Fluocortolona/efeitos adversos , Hidrocortisona/sangue , Lúpus Eritematoso Sistêmico/tratamento farmacológico , Prednisona/efeitos adversos , Adolescente , Adulto , Idoso , Síndrome de Cushing/sangue , Esquema de Medicação , Feminino , Fluocortolona/uso terapêutico , Humanos , Lúpus Eritematoso Sistêmico/sangue , Masculino , Prednisona/uso terapêuticoRESUMO
Renin activity, renin substrate and aldosterone were measured in plasma of 17 children aged 12 to 28 months and suffering from severe malnutrition (marasmic kwashiorkor). Plasma renin activity was very high (median 29.0 ng/ml/hr) at admission, decreased after equilibration with a normal sodium diet (9.9 ng/ml/hr) and was negatively correlated with urinary sodium excretion. Plasma renin substrate and aldosterone concentrations were in the normal range; plasma aldosterone correlated positively with serum potassium. The hyperactivity of the renin-angiotensin system may be of relevance to the renal function in severe malnutrition.
Assuntos
Kwashiorkor/sangue , Sistema Renina-Angiotensina , Aldosterona/sangue , Angiotensinogênio/sangue , Pré-Escolar , Humanos , Hidrocortisona/sangue , Lactente , Rim/metabolismo , Kwashiorkor/metabolismo , Masculino , Sódio/urina , Equilíbrio HidroeletrolíticoRESUMO
RU 486 [17 beta-hydroxy-11 beta-(4-dimethylaminophenyl)17 alpha-(prop-1-ynyl)estra-4,9-dien-3-one] is a synthetic steroid receptor antagonist. To evaluate the peripheral antiglucocorticoid action of this compound, we investigated its ability to antagonize cutaneous steroid-induced vasoconstriction. This phenomenon, produced by three different topical steroids in six normal men, was consistently and significantly attenuated or abolished by oral administration of 6 mg/kg RU 486. This demonstration of a peripheral action of RU 486 is important in relation to the potential therapeutic use of this well tolerated drug in states of hypercortisolism. It also indicates that the cutaneous vasoconstrictor effects of topical steroids are mediated by occupancy of glucocorticoid receptors.
Assuntos
Anti-Inflamatórios/antagonistas & inibidores , Estrenos/farmacologia , Vasoconstrição/efeitos dos fármacos , Administração Tópica , Adulto , Anti-Inflamatórios/farmacologia , Betametasona/análogos & derivados , Betametasona/antagonistas & inibidores , Clobetasol/análogos & derivados , Clobetasol/antagonistas & inibidores , Método Duplo-Cego , Humanos , Hidrocortisona/sangue , Masculino , Mifepristona , Distribuição Aleatória , Receptores de Glucocorticoides/fisiologia , Pele/irrigação sanguíneaRESUMO
To assess the relationship between pressor and depressor factors in essential hypertension, the urinary excretion rates of prostaglandins E2 and F2 alpha, kallikrein, vasopressin and aldosterone were compared between 53 untreated hypertensive patients and 53 age- and sex-matched normotensive controls. Mean basal levels of plasma renin activity and of urinary prostaglandins, vasopressin and aldosterone were similar in both groups, but urinary kallikrein was significantly lower in the hypertensive patients. A weak relationship was found in the hypertensives between diastolic blood pressure, and vasopressin or aldosterone, and between vasopressin and prostaglandin E2, and in the normotensives between vasopressin and prostaglandin F2 alpha. In conclusion, these results do not provide evidence for an important imbalance between pressor and depressor factors in essential hypertension, as reflected by the urinary excretion of the major humoral factors and hormones involved in the regulation of blood pressure.
Assuntos
Aldosterona/urina , Hipertensão/urina , Calicreínas/urina , Prostaglandinas E/urina , Prostaglandinas F/urina , Vasopressinas/urina , Adulto , Pressão Sanguínea , Dinoprosta , Dinoprostona , Feminino , Humanos , Hipertensão/fisiopatologia , Rim/fisiopatologia , Masculino , Pessoa de Meia-Idade , Valores de ReferênciaRESUMO
RU 486 is a synthetic steroid hormone antagonist which acts at the receptor level. It has both intrinsic anti-progesterone and antiglucocorticosteroid properties in animals. We investigated the antiglucocorticosteroid activity in humans by evaluating the pituitary-adrenal response to RU 486 in men and in pregnant and nonpregnant women. In non-pregnant women, RU 486 (approximately equal to 1 mg/kg of body weight per day) produced an interruption of the luteal phase without affecting the pituitary-adrenal axis, thereby indicating a more potent anti-progesterone than antiglucorticosteroid effect. In the course of pregnancy interruption by RU 486 (approximately equal to 4 mg/kg per day), there was a significant increase in plasma corticotropin, beta-lipotropin, and cortisol concentrations. In normal men, RU 486 administration led to a dose-dependent stimulation of plasma corticotropin, beta-endorphin, and cortisol. This disinhibition of the pituitary-adrenal axis was only observed during the morning hours of the circadian rhythm. When administered concomitantly with 1 mg of dexamethasone at midnight, 6 mg of RU 486 per kg completely suppressed the dexamethasone inhibitory effect on the pituitary-adrenal axis. These results indicate that RU 486 is an antiglucocorticosteroid that disrupts the negative pituitary feedback of both the morning cortisol rise and administered dexamethasone. Furthermore, they demonstrate the possibility of optimizing the anti-progestational effect of the compound and its potential use for human fertility control by modifying the dose and the time of administration of the drug and thereby minimizing the antiglucocorticosteroid effect.
PIP: RU 486, a synthetic steroid hormone antagonist which acts at the receptor level, has both intrinsic antiprogesterone and antiglucocorticosteroid properties in animals The antiglucocorticosteroid activity in humans was investigated by evaluating the pituitary-adrenal response to RU 486 in men and in pregnant and nonpregnant women. In nonpregnant women, RU 486 (approximately 1 mg/kg of body weight/day) produced an interrpution of the luteal phase without affecting the pituitary-adrenal axis, thereby indicating a more potent antiprogesterone than antiglucocorticosteroid effect. In the course of pregnancy interruption by RU 486 (approximately 4 mg/kg/day), there was s significant increase in plasma corticotropin, beta-lipotropin, and cortisol concentrations. In normal men, RU 486 administration led to a dose-dependent stimulation of plasma corticotropin, beta-endorphin, and cortisol. This disinhibition of the pituitary-adrenal axis was only observed during the morning hours of the circadian rhythm. When administered concomitantly with 1 mg dexamethasone at midnight, 6 mg of RU 486/kg completely suppressed the dexamethasone inhibitory effect on the pituitary-adrenal axis. These results indicated that RU 486 is an antiglucocorticosteroid that disrupts the negative pituitary feedback of both the morning cortisol rise and administered dexamethasone. Furthermore, they demonstrate the possibility of optimizing the antiprogestational effect of the compound and its potential use for human fertility control by modifying the dose and time of administration of the drug and thereby minimizing the antiglucocorticosteroid effect.
Assuntos
Ritmo Circadiano , Dexametasona/antagonistas & inibidores , Estrenos/farmacologia , Sistema Hipófise-Suprarrenal/efeitos dos fármacos , Abortivos Esteroides , Hormônio Adrenocorticotrópico/sangue , Endorfinas/sangue , Feminino , Humanos , Hidrocortisona/sangue , Masculino , Menstruação/efeitos dos fármacos , MifepristonaRESUMO
Spironolactone (S), known to act as a mineralocorticoid antagonist, has been shown in some circumstances to inhibit steroid biosynthesis. To investigate these two actions in vivo in the rat, animals fed a normal or low Na+ diet were treated with S for 7 days. In animals fed a normal Na+ diet, urinary and faecal electrolytes, aldosterone and corticosterone excretion were measured daily, plasma renin, aldosterone, corticosterone, ACTH, progesterone, DOC and 18-OH-DOC were determined after 4 and 7 days of treatment. In animals fed a low Na+ diet, urinary electrolytes were measured daily and plasma and urinary aldosterone and corticosterone were determined at intervals during the introduction of the diet and in the course of treatment. On a normal Na+ diet, S induced a slight non significant rise in the urinary Na+/K+ ratio on the first day of treatment, no change in faecal electrolyte excretion, and a sustained increase in aldosterone but not in corticosterone excretion. It produced a 6-fold elevation in plasma aldosterone levels, a less marked rise in renin and progesterone, a delayed increase in DOC and no change in ACTH, 18-OH-DOC or corticosterone concentration. On a low Na+ diet, treatment induced a rise in the urinary Na+/K+ ratio, and in urine and plasma aldosterone levels and no change in corticosterone values. Our results confirm, in the intact rat, the antimineralocorticoid action of S characterized by an increase in Na+ excretion but no change in K+ elimination. No inhibitory effect of spironolactone on aldosterone, corticosterone or 18-OH-DOC biosynthesis could be demonstrated in our experimental model.
Assuntos
Hormônio Adrenocorticotrópico/sangue , Potássio/metabolismo , Renina/sangue , Sódio/metabolismo , Espironolactona/farmacologia , Aldosterona/sangue , Aldosterona/urina , Animais , Corticosterona/urina , Dieta , Dieta Hipossódica , Fezes/análise , Masculino , Potássio/urina , Ratos , Ratos Endogâmicos , Sódio/urinaAssuntos
Hormônio Adrenocorticotrópico/farmacologia , Aldosterona/metabolismo , Sistema Renina-Angiotensina/efeitos dos fármacos , Glândulas Suprarrenais/efeitos dos fármacos , Adulto , Aldosterona/análogos & derivados , Angiotensina II/farmacologia , Dieta Hipossódica , Humanos , Hidrocortisona/sangue , Masculino , Renina/sangue , Sódio/urina , Espironolactona/farmacologia , Triantereno/farmacologiaRESUMO
1. The influence of four diuretics on renal prostaglandins was investigated in a study designed in two parts (A and B): A, 24 normal subjects on a constant sodium intake received frusemide (80 mg daily), or hydrochlorothiazide (100 mg), or triamterene (200 mg) or spironolactone (300 mg); B, the same subjects were pretreated for 3 days with indomethacin (150 mg daily), which was continued during the 3 day administration of the respective diuretics and during a 2 day post-diuretic period. 2. In study A, only triamterene provoked a rise in urinary prostaglandins E2 and F2 alpha (+ 474 +/- SEM 92%, P less than 0.01, and + 192 +/- 7%, P less than 0.01). In study B, prostaglandins were significantly inhibited in all subjects. After indomethacin, the natriuretic effect of frusemide and spironolactone was reduced by 80 +/- 12% (P less than 0.01) and 54 +/- 11% (P less than 0.001), whereas the natriuresis induced by hydrochlorothiazide and triamterene was unchanged. No correlation was found between urinary PGE2 and F2 alpha and natriuresis. 3. When triamterene was associated with indomethacin, two subjects developed reversible acute renal failure. 4. Plasma renin activity and urinary aldosterone were stimulated by the four diuretics in study A, but their response was blunted in study B. Urinary antidiuretic hormone was not modified by diuretics but was suppressed by indomethacin. 5. Diflunisal, a structurally unrelated nonsteroidal anti-inflammatory drug, given to 12 of the subjects provoked similar interactions with frusemide, hydrochlorothiazide and spironolactone. 6. The results suggest that prostaglandins contribute to the natriuretic effects of frusemide and spironolactone, but not to those of hydrochlorothiazide and triamterene.
Assuntos
Diuréticos/farmacologia , Indometacina/farmacologia , Adulto , Aldosterona/urina , Creatinina/urina , Interações Medicamentosas , Feminino , Furosemida/farmacologia , Humanos , Hidroclorotiazida/farmacologia , Masculino , Potássio/urina , Prostaglandinas E/urina , Prostaglandinas F/urina , Renina/urina , Sódio/urina , Espironolactona/farmacologia , Triantereno/farmacologia , Vasopressinas/urinaAssuntos
Abortivos Esteroides , Abortivos , Estrenos , Fenômenos Químicos , Química , Feminino , Humanos , Mifepristona , Gravidez , Progesterona/antagonistas & inibidoresRESUMO
PIP: The 19-nor steroid, RU-486, has an affinity for progestin receptors, and is also a progesterone as shown in animal studies. RU-486 was administered orally in a dose of 200 mg a day for 4 consecutive days to 11 women aged 18-34 seeking 1st trimester abortion. Bleeding occurred, in most cases, on the 1st day, followed by expulsion on the 3rd day in 2 cases, on the 4th day in 3 cases, on the 5th day in 3 cases, and on the 8th day in 1 case. 2 patients failed to abort. There were no complications, and only 1 patient required blood transfusion. Normal ovarian activity resumed in all cases. RU-486 can also be used to induce menstruation when administered in a dose of 50 mg a day for 4 days beginning on the 22nd day of a normal cycle. The use of RU-486 as an abortifacient agent seems to be more effective than the use of massive doses of estrogen or of prostaglandins, and to be certainly less traumatic than curettage or vacuum aspiration. Contraindications to its use and potential side effects, especially hepatic, have still to be established.^ieng
Assuntos
Abortivos Esteroides , Abortivos , Aborto Induzido , Primeiro Trimestre da Gravidez , Animais de Laboratório , Serviços de Planejamento Familiar , Gravidez , Reprodução , PesquisaRESUMO
RU-486 is a steroid which possesses a great affinity for the progesterone receptor, does not have a progesterone activity, but is indeed a strong antagonist of progesterone effects in animals. Oral administration induces the interruption of the luteal phase of the menstrual cycle and that of early pregnancy in women. Its mode of administration and its properties enable us to envisage a new methodology for menstrual cycle regulation and human birth control.
Assuntos
Abortivos Esteroides , Abortivos , Aborto Induzido , Estrenos , Menstruação/efeitos dos fármacos , Adolescente , Adulto , Animais , Gonadotropina Coriônica/sangue , Dexametasona/metabolismo , Estradiol/sangue , Estrenos/metabolismo , Estrenos/uso terapêutico , Feminino , Humanos , Mifepristona , Gravidez , Primeiro Trimestre da Gravidez/efeitos dos fármacos , Progesterona/antagonistas & inibidores , Progesterona/sangue , Receptores de ProgesteronaRESUMO
The role of renal prostaglandins (PGE2 and PGF2 alpha) and kallikrein in the renal escape from excess mineralocorticoid has been evaluated in 10 normal volunteers on a high sodium diet. Escape from 9-alpha-fluorohydrocortisone (9-alpha-FF) administered for 12 days (0.6 mg daily) occurred within 4-5 days when 345 +/- 50 mmol sodium had accumulated. Indomethacin, a cyclooxygenase inhibitor, was then administered for 3 days while maintaining 9-alpha-FF. This was followed by a further cumulative gain of 105 +/- 28 mmol sodium after which escape resumed. Potassium balance remained negative throughout the study. Both PGE2 and PGF2 alpha excretion increased significantly under 9-alpha-FF from respective control values of 220 +/- 50 and 818 +/- 86 ng/24 h. to 610 +/- 317 and 1213 +/- 132 ng/24 h at the time of escape. Concomitantly urinary kallikrein increased from 1.1 +/- 0.2 to 2.5 +/- 0.3 units/24 h. Creatinine clearance increased from a mean baseline value of 111 +/- 4 to 123 +/- 4 ml/min during the same period. Indomethacin produced an inhibition of prostaglandin excretion without significant alteration of kallikrein excretion. Overall these results and particularly the transient sodium retention induced by indomethacin at the time of mineralocorticoid escape, suggest that prostaglandins may contribute to the escape phenomenon, whereas the role of kallikrein does not appear to be determinant.
Assuntos
Rim/fisiologia , Mineralocorticoides/fisiologia , Prostaglandinas E/fisiologia , Prostaglandinas F/fisiologia , Sódio/metabolismo , Equilíbrio Hidroeletrolítico , Adulto , Aldosterona/urina , Dieta , Dinoprosta , Dinoprostona , Fludrocortisona/fisiologia , Humanos , Indometacina/farmacologia , Calicreínas/fisiologia , Masculino , Potássio/metabolismo , Renina/sangue , Cloreto de Sódio/administração & dosagem , Equilíbrio Hidroeletrolítico/efeitos dos fármacosRESUMO
Amongst the man physiological changes in human pregnancy are the sustained stimulation of the renin-angiotensin system and a decreases in plasma osmolality (Posm). In this study the effect osmolar and water loading on the renin-angiotensin system and arginine vasopressin (AVP) secretion has been tested in seven women during the third trimester and again 8-10 weeks after delivery. Pregnant women had markedly increased plasma renin substrate (PRS), plasma renin activity (PRA) and plasma renin concentration (PRC) values as well as aldosterone levels when compared to their post-partum values. Osmolar loading with intravenous infusion of hypertonic saline resulted in a decrease in PRA and aldosterone levels both during and after pregnancy but even at the end of the infusion the pregnant women still had values greater than the pre-infusion levels obtained post-partum. Surprisingly, oral water loading also significantly decreased PRA and aldosterone levels in pregnancy, possibly related to the redistribution of extracellular fluid centrally when the pregnant women were in left lateral recumbency. Despite the decreased basal Posm of pregnancy, urinary AVP increased and decreased appropriately during osmolar and water loading. Exact characterisation of the resetting of the threshold for AVP secretion in pregnancy awaits the development of a reliable radioimmunoassay for the determination of AVP in human pregnancy plasma.
Assuntos
Arginina Vasopressina/urina , Sistema Renina-Angiotensina , Solução Salina Hipertônica/farmacologia , Cloreto de Sódio/farmacologia , Água/administração & dosagem , Aldosterona/sangue , Feminino , Humanos , Período Pós-Parto , Gravidez , Terceiro Trimestre da Gravidez , Renina/sangue , Sistema Renina-Angiotensina/efeitos dos fármacos , Equilíbrio HidroeletrolíticoRESUMO
The influence of acute stimulation by ACTH, upright posture and angiotensin II on plasma aldosterone levels was assessed in human panhypopituitarism. While stimulation by ACTH in hypopituitary patients induced a plasma aldosterone increase similar to that observed in healthy controls, stimulation by upright posture or by infusion of angiotensin II resulted in a lower plasma aldosterone response than in controls in most of the patients. These results suggest that the presence of an anterior pituitary hormone, most likely ACTH, directly or indirectly exerts a permissive action on aldosterone secretion in man.