Increase in plasma concentrations of atrial natriuretic peptide during infusion of hypertonic saline in conscious newborn calves.

Plasma concentrations of atrial natriuretic peptide (ANP), plasma renin activity (PRA), plasma concentrations of aldosterone, urine flow rate and sodium and potassium excretion were studied in two groups of four conscious 3-day-old male calves, infused with hypertonic saline or vehicle. Hypertonic saline infusion (20 mmol NaCl/kg body weight) was accompanied by a progressive rise in plasma concentrations of ANP (from 16.5 +/- 0.2 pmol/l at time 0 to 29.3 +/- 3.0 pmol/l at 30 min; P less than 0.05) and by a gradual decrease in PRA (from 1.61 +/- 0.23 nmol angiotensin I/l per h at time 0 to 0.54 +/- 15 nmol angiotensin I/l per h at 90 min; P less than 0.05); there was no change in the plasma concentration of aldosterone. Within the first 2 h of the 24-h urine collection period there was a marked rise in urine flow rate and sodium excretion in treated calves when compared with control animals (66.0 +/- 8.3 vs 15.9 +/- 1.2 ml/kg body weight per 2 h (P less than 0.05) and 6.7 +/- 1.3 vs 0.4 +/- 0.02 mmol/kg body weight per 2 h (P less than 0.01) respectively). During the following 22 h, urinary water and sodium excretion remained at significantly high levels. Thus, in the conscious newborn calf, changes in plasma ANP levels and urinary water and sodium excretion during hypertonic saline infusion are compatible with the hypothesis that endogenous ANP participates, at least in part, in the immediate diuretic and natriuretic renal response induced by the sodium overload.

Effect of a hypertonic saline load on plasma concentrations of atrial natriuretic peptide in fetal calves and their dams.

Plasma concentrations of atrial natriuretic peptide (ANP) were studied in eight adult non-pregnant cows and in two groups of six chronically catheterized bovine fetuses and their mothers in the eighth month of pregnancy. The first group of fetuses was used for studying the effect of an acute i.v. sodium load (240 mmol NaCl/fetus) on fetal ANP; the second group acted as controls. The mean basal ANP levels in the third-trimester bovine fetus were three to four times higher than maternal values (39.5 +/- 5.5 and 9.4 +/- 0.6 pmol/l respectively; P less than 0.01). Basal maternal plasma ANP levels were twice as high in pregnant cows in the third trimester of pregnancy than in non-pregnant cows (9.4 +/- 0.6 and 4.3 +/- 0.7 pmol/l respectively; P less than 0.05). In response to an i.v. hypertonic saline injection, fetal plasma ANP levels increased significantly (P less than 0.01) to a maximum of 86.7 +/- 17.6 pmol/l 10 min after the injection, and returned to baseline within 60 min after the treatment; during the 20 min following the i.v. sodium load, fetal plasma ANP correlated significantly with fetal plasma sodium concentrations (r = 0.96; n = 12) and with fetal plasma osmolality (r = 0.94; n = 12). No significant changes in maternal ANP values were observed in the two groups of animals. These results suggest that ANP secretion is stimulated during pregnancy in cows, and that, in the bovine fetus, a hypertonic sodium load appears to be a potent stimulus for ANP release.

Perinatal changes in plasma and adrenal corticosterone and aldosterone concentrations in the mouse.

The concentrations of corticosterone and aldosterone in the plasma and adrenal glands of foetal, newborn and mother mice were estimated during the last 4 days of pregnancy and throughout the perinatal period. The level of corticosterone in the maternal and foetal plasma fell from day 17 of gestation until birth, and then remained stable. Whereas the corticosterone content of the maternal adrenal glands did not change significantly, that of the foetal adrenal glands reached a peak on day 19 of gestation. At every stage of gestation, the level of corticosterone in the maternal plasma was higher than that in the foetus. Changes in the concentration of aldosterone in the foetal plasma and adrenal glands were similar and characterized by peak values at birth. In the mother during the last 4 days of pregnancy, the level of aldosterone in the plasma was higher than in non-pregnant mice, but lower than that in the foetus.

Magnesium and blood pressure. I. Animal studies.

The relationship between experimental magnesium deficiency and blood pressure is complex and still the subject of much debate. The effect of Mg deficiency and blood pressure in Wistar rats receiving a Mg deficient diet (0.080 g/kg) for 40 weeks was examined. Deficient rats, when compared to controls, showed an initial transitory phase of hypotension, followed by normalization of blood pressure and then hypertension beginning after 15 weeks on the deficient diet. During the whole experimental period, heart rate was significantly increased in deficient rats as compared to controls. The fact that hypotension resulting from Mg deficiency of short duration can be inhibited by antihistamines and by indomethacin suggests that various mediators seen during the inflammatory period of Mg deficiency could be involved. Mg deficiency of long duration was accompanied by hypertension. When Mg-deficient rats received the control diet for a period of 3 weeks, Mg supplementation only partially corrected the hypertension. The hypertension was not a consequence of stimulation of the renin-angiotensin system since the plasma renin activity was not modified and ACE activity was reduced. These deficient rats showed a significantly lower vasopressor response to noradrenaline than control rats. Several factors such as increase in collagen, changes in elastin and arterial elasticity, total lipid content, and calcifications may account for the hyporesponsiveness to contractile agonists.(ABSTRACT TRUNCATED AT 250 WORDS)

[Secretion, metabolism and transport of aldosterone during the neonatal period of the guinea pig]. / Sécrétion, métabolisme et transport de l'aldostérone dans la période néonatale chez le cobaye.

Aldosterone-binding to plasma proteins was determined in the guinea-pig by equilibrium dialysis, and the metabolic clearance rate (MCR) of aldosterone was calculated from experiments in which the labelled hormone was infused at a constant rate into the circulation during the neonatal period; no specific aldosterone-binding protein was found in the plasma. The hormone was weakly bound to the albumine. The MCR of aldosterone (1/day/100 g body weight) was unchanged from birth to day 8, and its values were similar to those found in adults. Since there was no modification in aldosterone-binding to plasma proteins and no change in the MCR from birth to day 3, the high plasma aldosterone concentrations in the guinea-pig were probably related to intense adrenal activity.

Changes in the concentrations of aldosterone in the plasma and adrenal glands of the foetus, the newborn and the pregnant guinea-pig during the perinatal period.

Plasma and adrenal aldosterone concentrations have been estimated by radioimmunoassay and by gas phase chromatography in the foetus, the newborn and the mother between day 62 of pregnancy and day 8 of post-natal life. The pre-natal period is characterized by a gradual increase in plasma and adrenal aldosterone levels from day 62 up to 67. Birth greatly stimulates the synthesis and the release of aldosterone. In the neonatal period there are two peaks of maximum intensity in the plasma aldosterone concentration, one at 12 h together with a high adrenal aldosterone level, the other on day 5. In the mother the plasma aldosterone concentration is always higher than that of the foetus during the pre-natal period and increases from day 64 of gestation until parturition and remains high during the first 24 h after parturition.

[Plasma concentration and metabolic clearance rate of aldosterone at weaning, at puberty, and in adult guinea pigs]. / Concentration plasmatique et taux de clairance métabolique de l'aldostérone chez le cobaye au sevrage, à la puberté et à l'âge adulte.

Plasma aldosterone concentrations were measured by radioimmunoassay and metabolic clearance rates (M.C.R.) were determined by a continuous infusion of H3-aldosterone on day 20 and 50 and at 3, 6 and 24 months in the male and the female guinea-pig. Plasma aldosterone concentration rose gradually from day 20 up to 24 months. At every stage the values were always higher in the female than in the male. M.C.R. (1/24 h/100 g) decreased from day 20 to 24 months and appeared to be sex-dependent in the guinea-pig.

Diuretic, natriuretic and hypotensive effects of synthetic atrial natriuretic factor in conscious newborn calves.

The effects of synthetic Atrial Natriuretic Factor (ANF) on urine flow rate, sodium excretion, potassium excretion and arterial blood pressure were studied in 10-12 days-old female calves. In four female calves fitted with a Foley catheter, an intravenous administration of ANF (Ile-ANF 26; 1.6 micrograms/kg body wt during 30 min) induced an increase (P less than 0.01) in urine flow rate (from 1.8 +/- 0.2 to 12.8 +/- 1.1 ml/min), sodium excretion (from 0.15 +/- 0.02 to 0.81 +/- 0.06 mmol/min) and free water clearance (from 0.13 +/- 0.9 to 5.16 +/- 0.5 ml/min). It had no significant effect on potassium excretion. In four calves chronically-instrumented with a carotid catheter, an intravenous administration of synthetic ANF alone (1.6 micrograms/kg body wt during 30 min) induced a gradual decrease (P less than 0.01) in systolic, diastolic and mean arterial blood pressure (from 112 +/- 4 to 72, from 72 +/- 2 to 61 +/- 1 and from 90 +/- 2 to 65 +/- 2 mmHg respectively, at the end of ANF infusion). An intravenous administration of angiotensin II (AII) (0.5 micrograms/kg body wt during 45 min) induced a significant increase in systolic, diastolic and mean arterial blood pressure which was antagonized by an i.v. bolus injection of ANF (0.125 micrograms/kg body wt). However, during a simultaneous administration of AII (0.3 micrograms/kg body wt during 30 min) and ANF (1.6 micrograms/kg body wt. during 30 min), the atrial peptide did not influence the pressure action of AII. These findings indicate that the conscious newborn calf is sensitive to diuretic, natriuretic and hypotensive effects of synthetic ANF.

Effects of synthetic atrial natriuretic factor (ANF) on renin-aldosterone axis in the conscious newborn calf.

The effects of synthetic atrial natriuretic factor (ANF) on the renin-aldosterone axis were studied in fifteen 4-7 day-old male milk-fed calves divided into 3 groups of 5 animals each. Synthetic ANF intravenous (i.v.) administration (1.6 micrograms/kg body wt over 30 min) induced a transient significant fall in plasma renin activity (from 2.5 +/- 0.3 to 1.7 +/- 0.3 ng angiotensin l/ml/h; P less than 0.05) but failed to reduce basal plasma aldosterone levels in the first group of animals. Administration (i.v.) of angiotensin II (AII) (0.8 micrograms/kg body wt for 75 min) was accompanied by a progressive fall in plasma renin activity (from 2.2 +/- 0.3 to 0.8 +/- 0.1 ng angiotensin l/ml/h; P less than 0.01) and by an increase in plasma aldosterone levels (from 55 +/- 3 to 86 +/- 5 pg/ml; P less than 0.01) both in the second and the third groups; addition of ANF to AII infusion (AII: 0.5 mu/kg body wt for 45 min; AII: 0.3 micrograms/kg body wt and ANF 1.6 micrograms/kg body wt during 30 min) in the third group did not modify plasma renin activity or AII-stimulated plasma aldosterone levels when compared to the AII-treated group. These findings show that in the newborn calf ANF is able to reduce plasma renin activity but fails to affect basal and AII-stimulated plasma aldosterone levels, suggesting that the zona glomerulosa of the newborn adrenal cortex is insensitive to a diuretic, natriuretic and hypotensive dose of the atrial peptide.

Control of aldosterone secretion in domestic mammals during the perinatal period.

Aldosterone in ovine fetal circulation is mainly of fetal origin. Three of the renin-angiotensin system (RAS) parameters (renin, renin substrate and angiotensin II) originate in the fetus. The fetal RAS responds to stimulation (furosemide administration, hemorrhage, hypoxemia) or inhibition (phenylephrine or angiotensin II infusion) in a manner similar to that of the adult. The response of the fetal adrenal gland to angiotensin II is age-dependent and the near-term adrenal gland is not fully sensitive to angiotensin II and relatively insensitive to potassium (K+) as well as to adrenocorticotrophin hormone (ACTH) stimuli. In the newborn, the RAS is fully operative since it responds to diuretic stimulation in the lamb and the calf or to inhibition by angiotensin II administration in the lamb. Angiotensin II infusion, or angiotensin-converting enzyme blockade in the newborn lamb is followed by changes in plasma renin activity (PRA) or plasma aldosterone concentration (PAC) that suggest that angiotensin II regulates aldosterone secretion and that there is a negative feed back loop between angiotensin II and renin release. The newborn lamb adrenal gland is sensitive to potassium ions while in the newborn calf, ACTH stimulates cortisol secretion but fails to induce any change in PAC, suggesting that, in this species, the zona glomerulosa of the adrenal cortex is insensitive to ACTH.

Plasma renin activity and aldosterone concentration in sodium-depleted cattle following ACTH or metoclopramide injection.

Adrenocorticotropic hormone (ACTH) treatment (7 micrograms X kg-1 body weight) induced an increase in plasma aldosterone concentration in both Na-deficient heifers (following saliva loss after right parotid duct cannulation) and Na-replete heifers, but had no significant effect on plasma renin activity in either of these groups. The dopamine antagonist, metoclopramide, injected i.v. (1 mg X kg-1 body weight) did not modify plasma renin activity, aldosterone or cortisol concentrations in either group. These results indicate that dopamine did not play a major role in the regulation of aldosterone secretion in Na-replete or Na-depleted heifers.

Cardiovascular and arginine vasopressin (AVP) responses to haemorrhage and nitroprusside infusion in conscious newborn calves.

The effects of normotensive and hypotensive hypovolaemia (haemorrhage) as well as isovolaemic hypotension (nitroprusside administration) on diastolic, systolic and mean arterial blood pressure, heart rate and plasma concentrations of arginine vasopressin were studied in two sets of experiments on 8-10 days old conscious newborn calves bearing an indwelling aortic catheter for continuous recording of arterial blood pressure. Removal of 20% of the estimated blood volume resulted in an average maximum decrease of systolic, diastolic and mean arterial blood pressure from 132 +/- 2 to 118 +/- 8 mm Hg (P less than 0.05), from 72 +/- 2 to 67 +/- 2 mmHg (P less than 0.05) and from 92 +/- 3 to 82 +/- 6 mmHg (P less than 0.05) respectively. In the same time heart rate increased from 124 +/- 3 to 143 +/- 5 beats.min-1. Plasma concentrations of arginine vasopressin increased before blood loss had induced any change in arterial blood pressure (from 5.7 +/- 0.7 pg/ml-1 at time 0 to 25.2 +/- 3 pg/ml-1 at time 20 min; P less than 0.01). The significant fall in blood pressure was accompanied by a further prompt increase in plasma concentration of arginine vasopressin which reached maximum values (90.1 +/- 9.7 pg/ml-1) at completion of haemorrhage. The conscious newborn calf responded to i.v. nitroprusside infusion (10 micrograms/kg-1/min-1 for 10 min) with a prompt fall in diastolic (-71%, P less than 0.01), systolic (-70%, P less than 0.01) and mean (-56%, P less than 0.01) arterial blood pressure within 3 min of the infusion. Time course changes in heart rate were opposite to those in arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of changes in plasma hepatic-portal and systemic osmolality on plasma concentrations of arginine vasopressin in conscious newborn calves.

Systemic plasma concentrations of arginine vasopressin (AVP) were studied in three groups of 10-15 day-old conscious newborn calves. Animals in the first group (control group) and in the second group (systemic-hypertonic-injected group) received respectively isotonic and hypertonic (8 mmol NaCl/kg body weight) saline injection into the right jugular vein. Animals in the third group were fitted with chronic mesenteric and hepatic-portal catheters and received a 1 h-hypertonic saline infusion (2 mmol NaCl/kg body weight) into the main mesenteric vein. In animals in the second group there were parallel increases in systemic plasma concentration of Na+ (from 148.0 +/- 2.6 to 177 +/- 8 mmol/l; P less than 0.01), osmolality (from 289 +/- 2 to 319 +/- 4 mOsmol/kg H2O; P less than 0.01) and systemic plasma concentrations of AVP (from 4.2 +/- 0.4 to 11.1 +/- 0.6 pmol/l; P less than 0.01) 10 min after the injection. There were no significant changes in control animals. Hypertonic saline infusion into the main mesenteric vein in the third group induced an increase in concentration of Na+ (from 147.3 +/- 2.0 to 165.0 +/- 5.0 mmol/l; P less than 0.01) and osmolality (from 288 +/- 5 to 315 +/- 10 mOsmol/kg H2O; P less than 0.01) in hepatic-portal vein plasma but did not alter systemic plasma osmolality or concentrations of Na+ and AVP. This study demonstrates that the relationship between plasma concentrations of AVP and systemic osmolality is operative in the newborn calf but does not support the hypothesis that hepatic portal osmo-receptors sensitive to hyperosmolality influence AVP release.

Aldosterone metabolism in pregnant ewes and fetal and newborn lambs.

Twenty primiparous Limousine ewes whose fetuses had been chronically catheterized in utero on day 120 of gestation were used. Plasma aldosterone levels were measured by radioimmunoassay during the last 15 days of gestation both in dams and fetuses, and during the first neonatal week in lambs. Aldosterone metabolic clearance rates in dams, fetuses and newborns were determined by continuous infusion of [1, 2, 6, 7-3H]-aldosterone. The highest plasma aldosterone levels were observed in dams on days 130 and 142 of gestation, and in fetuses on days 135 and 140. No correlation was observed between plasma aldosterone and electrolyte levels in the mother, fetus or newborn. Aldosterone metabolic clearance rate decreased between days 142 and 145 in dams and at birth in fetuses of both sexes. No aldosterone transfer could be demonstrated either from dam to fetus or vice-versa.

Renin-aldosterone system and arginine vasopressin in diarrhoeic calves.

Plasma renin activity, plasma aldosterone and arginine-vasopressin concentrations were determined in five diarrhoeic and five healthy newborn calves. In animals suffering from diarrhoea these three parameters were 10-15 times higher than those observed in controls. These results suggest that the hormonal systems that control fluid and electrolyte homeostasis are highly stimulated by dehydration and salt depletion induced by faecal losses of water and sodium in calves affected with diarrhoea.

Effects of angiotensin II, arginine-vasopressin, endothelin and catecholamines on plasma atrial natriuretic peptide concentrations in the conscious newborn calf.

The effects of epinephrine (E), norepinephrine (NE), angiotensin II (AII), arginine-vasopressin (AVP) and endothelin on plasma ANP levels were studied according to a latin square design in six 12-21 days-old conscious Jersey calves weighing 30 +/- 4 kg. The animals chronically-instrumented with a carotid catheter for blood pressure recording, received at 11.00 a.m. an i.v. right jugular continuous infusion for 30 min of two different sub-pressor or pressor dose-levels of each substance; E: 0.6 and 5.5 nmol/min per kg body wt; NE: 0.6 and 6 nmol/min per kg body wt; AII: 9.6 and 96 pmol/min per kg body wt; AVP: 0.6 and 69 pmol/min per kg body wt; and endothelin: 1.2 and 12 pmol/min per kg body wt). Control animals received, in the same way, the same volume (2 ml/kg body wt) of NaCl 0.9%. In Jersey calves, basal plasma atrial naturetic peptide (ANP) levels were around 5 pmol/l. Marked increases in this parameter were produced by all substances when given at the highest dose-level. The maximal rise of 600% was observed with AII; however on a molar basis, endothelin appeared more potent than AII and at the same dose-level, E appeared more effective than NE to increase circulating ANP (17.8 +/- 0.3 vs 9.5 +/- 0.1 respectively at time 70 min; P less than 0.01). The time-course of plasma ANP levels was positively correlated (P less than 0.01) by linear regression with the increase in blood pressure when pressor agents were given at the highest dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Diurnal change in plasma natriuretic factor and arginine vasopressin in young jersey calves.

Diurnal changes in plasma ANF and AVP levels were investigated in four calves under standardized conditions. Both levels in plasma were measured at hourly intervals for 24 h along with arterial blood pressure, blood haematocrit, plasma cGMP, sodium, potassium, osmolality, proteins and albumin. Plasma ANF exhibited a first peak at mid-day while plasma AVP was low and a second peak at evening while plasma AVP was high. Changes in plasma cGMP correlated with variations in plasma ANF. feeding and/or plasma volume elevation probably accounted for both peaks in plasma ANF and the low mid-day level of plasma AVP, but the rise in plasma AVP at evening may represent a diurnal rhythm.

Hormonal, fluid, and electrolyte changes during a 72-h recovery from a 24-h endurance run.

To examine body fluid regulation over 72 h of recovery from a 24-h endurance race, changes in plasma volume (delta PV) and plasma aldosterone (A), cortisol (CO), antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP) were studied in nine male runners before (C) and after (1-2 h = D0; 24 h = D1; 48 h = D2; 72 h = D3) the race, 24-h urine collections were made 1 week before (C), during the 24-h race/U0), and during the 3 days following the end of the race (U1, U2, and U3). On D0 delta PV decreased (2%). A, CO and ADH increased (380%, 200%, and 133%, respectively, from C values) and ANP decreased (68%). No significant changes were found in sodium, potassium, osmolality in plasma, in 24-h urine volume (UV), and natriuresis (Na+). Urinary potassium excretion (K+) increased (256% from C value). During the 3 days of recovery delta PV rose markedly with a peak on D2 (24%) and remained elevated on D3 (15%). CO, ADH, and ANP returned to baseline on D1 and A on D3. Significant inverse effects were observed on ADH (P less than 0.001) and ANP (P less than 0.01): from C values, ADH decreased (21% and 29%) and ANP increased (41% and 58%) on D2 and D3, respectively. UV and Na+ were depressed on D1 and D2. This study shows that the hormonal responses observed immediately after the 24-h run favored a relative fluid conservation. The hypervolemia that occurred during the 3-day recovery was related to renal responses on D1 and D2 and appeared to be the primary factor in the hormonal responses on D2 and D3.

Renin-aldosterone axis and arginine-vasopressin responses to sodium depletion in camels.

Urinary output, urinary sodium and potassium excretion, plasma electrolyte concentrations and osmolality, plasma renin activity (PRA), and plasma aldosterone and arginine-vasopressin (AVP) concentrations were determined in eight camels in Tadla (Morocco). After administration of furosemide (2 mg.kg-1 body wt) urinary water, sodium and potassium excretions increased, inducing hypovolemia (as reflected by 14.6% increase in hematocrit), hyponatremia (142 +/- 1.0 vs 150 +/- 2.1 mmol.liter-1 in controls; P < 0.05), plasma hypo-osmolality (287.5 +/- 11.5 vs 307 +/- 1.4 mOsm.kg-1 H2O in controls; P < 0.05), and hypokalemia (3.7 +/- 0.2 vs 4.6 +/- 0.1 mmol.liter-1 in controls; P < 0.05). Such body fluid volume and composition changes were associated with parallel increases in PRA and plasma aldosterone concentrations (5.9 +/- 0.6 vs 0.9 +/- 0.2 ng AI.ml-1.hr-1 and 132.4 +/- 35.5 vs 25.1 +/- 6.5 pg.ml-1 in controls, respectively; P < 0.05). They were also associated with a fourfold increase in plasma arginine-vasopressin concentrations (0.8 +/- 0.2 vs 0.2 +/- 0.1 pg.ml-1; P < 0.05). In furosemide-treated animals, plasma aldosterone concentrations correlated positively with PRA (r = 0.85; n = 64; P < 0.01) and negatively with plasma sodium concentrations (r = -0.80; n = 64; P < 0.01), suggesting that in sodium-depleted camels the nexus between the renin-angiotensin system and aldosterone was restored.