The renal circulation of conscious rabbits

1. The renal circulatory instability that some believe is inherent in rabbits was studied. 2. In five, conscious rabbits, glomerular filtration rate (GFR) averaged 4.2 +/- 0.6 ml/min/kg body wt after 1 hr, but changed to an overall average of 3.5 +/- 1.5 ml/min/kg wt after 3 hr. 3. Between-measurement coefficient of variation for GFR was more than 30% for three rabbits and 10% or less for two. 4. Renal blood flow (RBF) was even more variable. 5. The renal circulatory instability may be associated with differences in sympathetic activity by mechanisms not existing in other mammals.     

A comparison of chloride, bromide, and sucrose dilution volumes in neonatal pigs

Use of 36Cl, 82Br, and [3H]sucrose to estimate extracellular water volume was evaluated in 14 piglets (7-14 days old). 36Cl and 82Br were distributed in approximately the same volume, but a period of 5-6 hr after injection was required to reach equilibrium in the neonatal pig. Dilution volumes calculated before equilibration (2-5 hr) for 36Cl (326 +/- 11 ml/kg) and 82Br (328 +/- 13 ml/kg) were different from equilibration (6-8 hr) phase volumes (356 +/- 13 ml/kg and 355 +/- 13 ml/kg, respectively; P less than 0.001). A 3-hr sample estimated the same volume distribution calculated by extrapolation of the 6- to 8-hr period because of the relationship between the two slopes of the plasma clearance curves. After the 82Br and 36Cl had achieved equilibration, each was distributed in a volume equivalent to total body chloride space (362 +/- 29 ml/kg) measured by neutron activation; no statistical differences were found (P = 0.6). The early equilibration phase measured a 10% smaller, faster exchangeable fraction of total body Cl. Sucrose dilution volume (332 +/- 19 ml/kg) required multiple plasma samples for extrapolation and measured a dilution volume 7% smaller (P less than 0.05) than total body chloride space.     

Glutamine supplementation promotes anaplerosis but not oxidative energy delivery in human skeletal muscle

The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine alpha-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at approximately 70% maximal O2) uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L-(+)-ornithine alpha-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L-glutamine dissolved in 5 ml/kg body wt solution (GLN). Vastus lateralis muscle was biopsied 1 h postsupplement and after 10 min of exercise. The sum of four measured TCAI (SigmaTCAI; citrate, malate, fumarate, and succinate, approximately 85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, SigmaTCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 +/- 0.61) than in the CON condition (3.74 +/- 0.38, P < 0.05) and the OKG condition (3.85 +/- 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced (P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of alpha-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.     

Kinetic compartmental analysis of carnitine metabolism in the dog

This study was undertaken to quantitate the dynamic parameters of carnitine metabolism in the dog. Six mongrel dogs were given intravenous injections of L-[methyl-3H]carnitine and the specific radioactivity of carnitine was followed in plasma and urine for 19-28 days. The data were analyzed by kinetic compartmental analysis. A three-compartment, open-system model [(a) extracellular fluid, (b) cardiac and skeletal muscle, (c) other tissues, particularly liver and kidney] was adopted and kinetic parameters (carnitine flux, pool sizes, kinetic constants) were derived. In four of six dogs the size of the muscle carnitine pool obtained by kinetic compartmental analysis agreed (+/- 5%) with estimates based on measurement of carnitine concentrations in different muscles. In three of six dogs carnitine excretion rates derived from kinetic compartmental analysis agreed (+/- 9%) with experimentally measured values, but in three dogs the rates by kinetic compartmental analysis were significantly higher than the corresponding rates measured directly. Appropriate chromatographic analyses revealed no radioactive metabolites in muscle or urine of any of the dogs. Turnover times for carnitine were (mean +/- SEM): 0.44 +/- 0.05 h for extracellular fluid, 232 +/- 22 h for muscle, and 7.9 +/- 1.1 h for other tissues. The estimated flux of carnitine in muscle was 210 pmol/min/g of tissue. Whole-body turnover time for carnitine was 62.9 +/- 5.6 days (mean +/- SEM). Estimated carnitine biosynthesis ranged from 2.9 to 28 mumol/kg body wt/day. Results of this study indicate that kinetic compartmental analysis may be applicable to study of human carnitine metabolism.     

The rate of breakdown of methyl methanesulphonate, dimethyl sulphate and N-methyl-N-nitrosourea in the rat

1. The rates of decomposition of methyl methanesulphonate, dimethyl sulphate and N-methyl-N-nitrosourea in the rat were measured. 2. Dimethyl sulphate is no longer detectable in the blood of the rat 3min. after an intravenous dose (75mg./kg. body wt.). Methyl methanesulphonate is only just detectable in the blood 1(1/2)hr. after an intravenous dose (100mg./kg. body wt.). N-Methyl-N-nitrosourea is no longer detectable in the blood 15min. after an intravenous dose (100mg./kg. body wt.). 3. The exhalation of (14)CO(2) after an intragastric dose of N[(14)C]-methyl-N-nitrosourea (100mg./kg. body wt.) is appreciably slower than after an intravenous dose, from which it is estimated that the lifetime in the rat is 2-3hr.     

Kinetics of homovanillic acid and determination of its production rate in the rhesus monkey.

Homovanillic acid (HVA) labelled with two deuterium atoms (d₂-HVA) was used to label the peripheral body pool of endogenous HVA (d₀-HVA). D₂-HVA was rapidly injected intravenously into Rhesus monkeys and concentrations of both d₂- and d₀-HVA in sequential samples of blood serum and urine determined by gas chromatography-mass spectrometry. Parameters describing the distribution and elimination of HVA, as well as its pool size, turnover, and synthesis rate were then calculated. Results indicate that the decline of serum d₂-HVA concentration with time is multiexponential, with a biological half-life ranging from 35.9 to 102 min in the four monkeys studied. The apparent volume of distribution of d₂-HVA in the body was 0.813–1.17 1/kg. Serum clearance was 7.28–18.2 ml/kg/min. For most animals, only about 50% of the administered dose of d₂-HVA was recovered unchanged in the urine. Renal clearance ranged from 3.79 to 17.0 ml/kg/min, and d₀-HVA excretion rates ranged from 19.5 to 64.1 μg/hr. The size of the peripheral body pool of HVA, calculated from serum kinetic parameters, was 63.3–80.7 μg; HVA turnover was 5.43–13.9 μg/1/hr; and HVA production rate was calculated to be 36.6–84.3 (5.23–12.6 μg/kg/hr).     

Plasma volume expansion in humans after a single intense exercise protocol.

We used intense intermittent exercise to produce a 10% expansion of plasma volume (PV) within 24 h and tested the hypothesis that PV expansion is associated with an increase in plasma albumin content. The protocol consisted of eight 4-min bouts of exercise at 85% maximal O2 uptake with 5-min recovery periods between bouts. PV, plasma concentrations of albumin and total protein (TP), and plasma osmolality were measured before and during exercise and at 1, 2, and 24 h of recovery from exercise. During exercise, PV decreased by 15%, while plasma TP and albumin content remained at control levels. At 1 h of recovery, plasma albumin content was elevated by 0.17 +/- 0.04 g/kg body wt, accounting for the entire increase in plasma TP content. PV returned to control level at 1 h of recovery without fluid intake by the subjects, despite a 820 +/- 120-g reduction in body weight. At 2 h of recovery, plasma TP content remained significantly elevated, and plasma TP and albumin concentration were significantly elevated. At 24 h of recovery, PV was expanded by 4.5 +/- 0.7 ml/kg body wt (10 +/- 1%), estimated from hematocrit and hemoglobin changes, and by 3.8 +/- 1.3 ml/kg body wt (8 +/- 3%), measured by Evans blue dye dilution. Plasma albumin content was increased by 0.19 +/- 0.05 g/kg body wt at 24 h of recovery. If 1 g of albumin holds 18 ml of water, this increase in plasma albumin content can account for a 3.4-ml/kg body wt expansion of the PV. No significant changes in plasma osmolality occurred during recovery, but total plasma osmotic content increased in proportion to PV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of saline infusion during exercise on thermal and circulatory regulations

To quantify the effect of an acute increase in plasma volume (PV) on forearm blood flow (FBF), heart rate (HR), and esophageal temperature (Tes) during exercise, we studied six male volunteers who exercised on a cycle ergometer at 60% of maximal aerobic power for 50 min in a warm [(W), 30 degrees C, less than 30% relative humidity (rh)] or cool environment [(C), 22 degrees C, less than 30% rh] with isotonic saline infusion [Inf(+)] or without infusion [Inf(-)]. The infusion was performed at a constant rate of 0.29 ml.kg body wt-1.min-1 for 20-50 min of exercise to mimic fluid intake during exercise. PV decreased by approximately 5 ml/kg body wt within the first 10 min of exercise in all protocols. Therefore, PV in Inf(-) was maintained at the same reduced level by 50 min of exercise in both ambient temperatures, whereas PV in Inf(+) increased toward the preexercise level and recovered approximately 4.5 ml/kg body wt by 50 min in both temperatures. The restoration of PV during exercise suppressed the HR increase by 6 beats/min at 50 min of exercise in W; however, infusion had no effect on HR in C. In W, FBF in Inf(+) continued to increase linearly as Tes rose to 38.1 degrees C by the end of exercise, whereas FBF in Inf(-) plateaued when Tes reached approximately 37.7 degrees C. The infusion in C had only a minor effect on FBF.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Hypoglycemic effect of methanol extract of Phyllanthus amarus Schum & Thonn on alloxan induced diabetes mellitus in rats and its relation with antioxidant potential

Methanolic extract of P. amarus was found to have potential anti-oxidant activity as it could inhibit lipid peroxidation, and scavenge hydroxyl and superoxide radicals in vitro. The amount required for 50% inhibition of lipid peroxide formation was 104 microg/ml and the concentrations needed to scavenge hydroxyl and superoxide radicals were 117 and 19 microg/ml respectively. The extract was found to reduce the blood sugar in alloxan diabetic rats at 4th hr by 6% at a dose level of 200 mg/kg body wt and 18.7% at a concentration of 1000 mg/kg body wt. Continued administration of the extract for 15 days produced significant (P < 0.001) reduction in blood sugar. On 18th day after alloxan administration values were almost similar to normal in the group taking 1000 mg/kg body wt.     

Effects of growth hormone-releasing factor and somatostatin on growth hormone secretion in hypophysial stalk-transected beef calves

The effects of growth hormone-releasing factor (GHRF) on growth hormone (GH) secretion were studied in beef calves after hypophysial stalk transection (HST). Peripheral GH concentration during surgery was elevated for 60 min after the initiation of anesthesia to 15 ng/ml, which was greater than plasma levels after HST and during the recovery period (0-30 hr mean, 3 ng/ml; P less than 0.05). Episodic GH secretion normally seen in sham-operated controls (SOC) was abolished after HST. Before HST, calves responded to 80% of the GHRF challenges, whereas after HST calves responded to every challenge of GHRF with an increase in plasma GH. A dose of 0.067 microgram human pancreatic (hp) hpGHRF(1-40)OH/kg body wt 3 days after HST increased plasma GH to 55 ng/ml from a control period mean of 5 ng/ml (P less than 0.04). On Day 8, HST calves received two injections of 0.067 microgram hpGHRF/kg body wt at 3-hr intervals, with feeding 70 min after the first injection. During two preinjection control periods, basal GH averaged less than 4 ng/ml and increased to 17 (P less than 0.02) and 9 (P less than 0.04) ng/ml immediately after the first and second injection of hpGHRF, but the response declined over the 8-day period after surgery. On Days 19 and 20, the HST calves were infused iv with 0.033 and 0.067 microgram somatostatin(SS)-14 (SRIH)/kg body wt, during which a pulse injection of 0.067 microgram hpGHRF/kg body wt was administered. GH increased to 9 and 5 ng/ml during the 0.033- and 0.067-microgram SRIH infusions after GHRF; no somatotropic rebound was observed after the SRIH was discontinued as was seen in the animals while the hypothalamic-hypophysial connections were intact. Five and six months after HST the responses to two analogs of rat hypothalamic GHRF were similar to those in SOC calves. These results indicate that HST calves responded to exogenous GHRF with an abrupt increase in plasma GH, but GH response to GHRF during SRIH infusion was greatly inhibited.     

A synthetic surfactant based on a poly-Leu SP-C analog and phospholipids: effects on tidal volumes and lung gas volumes in ventilated immature newborn rabbits.

Available surfactants for treatment of respiratory distress syndrome in newborn infants are derived from animal lungs, which limits supply and poses a danger of propagating infectious material. Poly-Val-->poly-Leu analogs of surfactant protein (SP)-C can be synthesized in large quantities and exhibit surface activity similar to SP-C. Here, activity of synthetic surfactants containing a poly-Leu SP-C analog (SP-C33) was evaluated in ventilated premature newborn rabbits. Treatment with 2.5 ml/kg body wt of 2% (wt/wt) SP-C33 in 1,2-dipalmitoyl-sn-3-glycero phosphoryl choline (DPPC)-1-palmitoyl-2-oleoyl-sn-3-glycero phosphoryl choline (POPC)-1-palmitoyl-2-oleoyl-sn-3-glycero phosphoryl glycerol (POPG), 68:0:31, 68:11:20, or 68:16:15 (wt/wt/wt) suspended at 80 mg/ml gave tidal volumes (Vt) of 20-25 ml/kg body wt, with an insufflation pressure of 25 cmH2O and no positive end-expiratory pressure (PEEP), comparable to the Vt for animals treated with the porcine surfactant Curosurf. Nontreated littermates had a Vt of approximately 2 ml/kg body wt. The Vt for SP-C33 in DPPC-egg phosphatidylglycerol-palmitic acid [68:22:9 (wt/wt/wt)], DPPC-POPG-palmitic acid [68:22:9 (wt/wt/wt)], and DPPC-POPC-POPG [6:2:2 (wt/wt/wt)] was 15-20 ml/kg body wt. Histological examination of lungs from animals treated with SP-C33-based surfactants showed incomplete, usually patchy air expansion of alveolar spaces associated with only mild airway epithelial damage. Lung gas volume after 30 min of mechanical ventilation were more than threefold larger in animals treated with Curosurf than in those receiving SP-C33 in DPPC-POPC-POPG, 68:11:20. This difference could be largely counterbalanced by ventilation with PEEP (3-4 cmH2O). An artificial surfactant based on SP-C33 improves Vt in immature newborn animals ventilated with standardized peak pressure but requires PEEP to build up adequate lung gas volumes.     

Effect of thiopental sodium and barbitone sodium on the total acetylcholine content and acetylcholinesterase activity in the brain tissue of Arvicanthis niloticus

The total ACh content and AChE activity were determined 1 hr after the i.p. injection of different doses of thiopental sodium (5, 10 and 20 mg/ml/100 g body wt) and barbitone sodium (20, 40 and 80 mg/ml/100 g body wt). The effect of different time intervals (1 min, 10 min, 30 min, 1 hr, 2.5 hr, 5 hr, 8 hr, 12 hr, 24 hr and 48 hr) on the total ACh content and AChE activity was investigated after i.p. injection of 10 mg thiopental sodium and 40 mg barbitone sodium/ml/100 g body wt. Both thiopental sodium and barbitone sodium increased the total ACh content in the brain tissue of Arvicanthis niloticus. Both drugs inhibited the brain AChE activity. It is thought that the increase in the total ACh content in the brain tissue of Arvicanthis niloticus may be due to a decrease in the release of ACh from the neuronal tissue and a decrease in AChE activity.     

Growth hormone-releasing factor on growth hormone secretion in prepubertal calves

The effects of iv administration of growth hormone-releasing factor (GRF) on growth hormone (GH) release and on nitrogen metabolism were measured in prepubertal calves. Crossbred beef heifers (111 kg) were used in a Latin square design to test the effects of 0, 0.01, 0.033, 0.067, and 0.1 microgram human pancreatic (hp) GRF [hpGRF (1,40)OH]/kg body wt on plasma GH concentrations. When they were given doses of 0.067 and 0.1 microgram hpGRF/kg body wt, plasma GH increased (P less than 0.05) within 5-15 min, compared with injections of control buffer, and then returned to preinjection concentrations. The response to 0.067 microgram hpGRF/kg body wt every 3 hr for 42 hr was studied in five heifers (137 kg body wt). The animals responded to 50% of the GRF injections with an increase in plasma GH during every 6-hr period measured. Nitrogen retention, hormone concentrations, and weight gain were measured in five bull calves (90 kg body wt) administered 0 or 0.067 microgram Nle rat hypothalamic GRF (1,29)NH2/kg body wt every 4 hr for 10 days. Metabolic parameters were interpreted to indicate an anabolic response to GRF even though increases of 16% in nitrogen retention, 23% in plasma somatomedin C concentrations, and 36% in weight gain with pulsatile GRF treatment were variable and statistically similar to those of controls. These results indicate that GRF induces peak GH secretion within 15 min in prepubertal calves and that calves can respond to multiple injections of GRF with an increase in plasma GH.     

Contribution of the fluid phase endocytosis to bile flow in cholestasis and choleresis in rats

Using a single iv injection of 1 mg Evans blue dye/100 g body wt in rats, the contribution of the fluid phase endocytosis to bile flow was estimated. In control rats, this pathway contributed 2-4% of the bile flow or 10-20 microliter/hr/100 g body wt. This contribution was not affected by cholestasis induced by taurolithocholic acid or bile duct obstruction or by choleresis induced by dehydrocholic acid. It is concluded that fluid phase endocytosis does not significantly influence bile formation but, rather, may be implicated in the remodeling of liver cell plasma membranes.     

Oxygen consumption by portal vein-drained organs and by whole animal in conscious growing swine

A method was developed to measure simultaneously the O2 consumption (VO) by the whole animal and by the hepatic portal vein-drained organs (PVDO), including the gastrointestinal tract, spleen, and pancreas in conscious 3.5- to 4-month-old swine. The method was used to determine (i) the effect of feeding on hepatic portal vein blood flow rate (Qpv) and VO by PVDO and by the whole animal, and (ii) the significance of PVDO on the oxidative demand in the pig. Chronic cannulas were placed in the hepatic portal vein, carotid artery, and ileal vein. The Qpv was determined by an indicator dilution technique employing continuous constant infusion of 1% p-aminohippuric acid into the ileal vein. The VO2 by PVDO was estimated by multiplying Qpv by arterial-portal vein O2 difference measured with an arterial-venous O2 difference analyzer connected to the carotid artery and portal vein cannulas. Whole animal VO2 was measured with an open circuit indirect calorimeter. In seven pigs (3.5- to 4-month-old, 37.4 +/- 0.8 kg) trained to be fed once daily, feeding (1.2 kg of feed mixed with 1.2 liter of H2O) caused postprandial (6 hr) Qpv to increase more than 34 +/- 15% above the preprandial value of 34.5 +/- 4.2 ml.min-1.kg-1 body wt. The postprandial VO2 by PVDO was elevated more than 46 +/- 12% above the value of 1.52 +/- 0.20 ml.min-1.kg-1 body wt observed during the preprandial period. Whole animal VO2 increased 45 +/- 9 and 33 +/- 7% above the preprandial value of 6.23 +/- 0.57 ml.min-1.kg-1 body wt for the first 6 hr and the 7 to 12 hr after feeding, respectively. Although PVDO represent only 5% of body weight, they used 25% of whole body VO2. The study clearly illustrates the significance of PVDO on the whole animal oxidative demand in conscious growing swine.     

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.     

Hyperhydration with glycerol solutions

Glycerol was tested as an agent to promote hyperhydration of male and female subjects. Series I experiments involved ingesting 0.5, 1.0, or 1.5 g glycerol/kg body wt and within 40 min drinking 0.1% NaCl, 21.4 ml/kg. In series II, 1.0 g glycerol/kg body wt was ingested at time 0, and 25.7 ml/kg of 0.1% NaCl was ingested over a 3.5-h period. Experiments were of 4-h duration and included controls without glycerol as each subject served as his/her control. Blood samples were taken at 40- or 60-min intervals for hemoglobin (Hb), hematocrit (Hct), plasma osmolality, glycerol, and multiple blood chemistry analyses. Urine was collected at 60-min intervals. Glycerol ingestion increased plasma osmolality for 2 h and reduced the total 4-h urine volume. There were no significant changes in Hb or Hct as a result of the glycerol or excess fluid intake. This study demonstrates that glycerol plus excess fluid intake can produce hyperhydration for at least 4 h.