Changes in activity of the renin-angiotensin system of the rat by induction of acute inflammation

Angiotensinogen is the precursor of biologically active peptide angiotensin II and its hepatic synthesis is increased by the induction of acute inflammation. Studies were carried out to know whether the rise in plasma angiotensinogen is actually involved in the activity of the renin-angiotensin system during acute inflammation. The plasma level of angiotensinogen in rats was increased to 2.5 times the normal level 16 h after the induction of acute inflammation by administration of lipopolysaccharide (LPS). The plasma renin concentration (PRC) was decreased to about 40% of the normal level concomitantly with a reduction of plasma renin activity (PRA) at 4 h after LPS administration. In contrast, 16 h after LPS injection, when plasma angiotensinogen showed a high level and PRC had recovered to the normal range, PRA was increased to 1.7 times the normal level. These results indicate that acute inflammation induced by LPS causes a biphasic change in the generation of angiotensin I, i.e., an early decrease depending upon the reduction of PRC and later increase depending upon elevation of the angiotensinogen concentration.     

Changes of plasma renin and renal renin concentration in HgCl2 induced acute renal failure in rats.

Acute renal failure (ARF) was produced by the single intraperitoneal injection of 3 mg/kg mercuric chloride (HgCl2) in male Wistar rats. Immediately after, and in the 1st, 3rd, 6th, 24th and 48th hour after HgCl2 administration the following variables were monitored: plasma renin concentration (PRC), renal renin concentration (RRC) blood-urea nitrogen (BUN), plasma sodium (PNa), plasma creatinine (PCr) concentrations and haematocrit (Ht). Haematocrit and PNa increased during the first hour and returned to the control value in the 3rd hour. Thereafter, their level remained unchanged. Plasma renin concentration increased threefold during the first six hours after the HgCl2 injection, however, by the 48th hour it returned to the control value. In the first 24 hours of ARF, RRC remained unchanged. However, by the 48th hour its level increased four times the control value. After mercury injection BUN and PCr increased progressively. We were not able to establish any significant correlation between the changes of PRC and BUN. A gradual increase of RRC was observed in the course of ARF.     

C-reactive protein in rat: in development, pregnancy and effect of sex hormones

1. In Wistar strain rats, the serum concentration of C-reactive protein (CRP) was 3.6 +/- 0.8 micrograms/ml at the birth and no apparent change was observed during 15 days after delivery. 2. Thereafter it increased about 30 times rapidly until day 30 and then rather gradually reaching the adult level of 0.4-0.8 mg/ml. 3. Before delivery, there were two peaks in the CRP level, on day 0 and day 15 of gestation. The concentrations were 0.70 +/- 0.06 and 0.77 +/- 0.10 mg/ml, respectively. 4. The CRP level decreased to 0.42 +/- 0.05 mg/ml at the delivery and increased to 0.54 +/- 0.05 mg/ml within 2 days after delivery. 5. The treatment with estradiol-17 beta resulted in the decrease of CRP (52%) in both ovariectomized and non-treated female rats. 6. The treatment with testosterone resulted in the increase of CRP in male but not in female rats. 7. However, in ovariectomized rats, testosterone elevated the serum CRP. 8. In neither ovariectomized nor intact female rats, progesterone and corticosterone showed any remarkable effect.     

Perinatal development of hepatic cholesterol synthesis in the rat

Rates of cholesterol synthesis and HMG CoA reductase activity in rat liver, have been reported to be high before and low after birth. The timing of the decline in perinatal rates of cholesterol synthesis, however, is uncertain. These studies, therefore, determined in vivo rates of cholesterol synthesis using [3H]water and hepatic reductase activity in vitro in perinatal rats. The lipid composition of the plasma, liver and its microsomal subfraction were also determined. Reductase activity increased during late gestation, remained high immediately after birth, then decreased with the commencement of suckling. Rates of cholesterol synthesis increased from gestation day 18 to 20, but in contrast to reductase activity, decreased on the day before birth. Plasma cholesterol and triacylglycerol levels increased to gestation day 19, then decreased to term. By the 6th h after birth, plasma and liver cholesterol and triacylglycerol levels had increased markedly. By 48 h after birth, the high hepatic cholesterol content was associated with an increase in the cholesteryl ester fraction. The microsomal cholesterol/phospholipid molar ratio decreased from gestation day 16 until 12 h after birth, then increased markedly from 36 to 48 h. There was an apparent inverse relationship between the change in microsomal cholesterol/phospholipid molar ratio and the fatty acid unsaturation index from gestation day 16 to 36 h after birth. The results suggest that in late gestation and before suckling, the low in vivo rate of hepatic cholesterol synthesis may not be due to low activity of HMG CoA reductase.     

Development of gluconeogenesis from different substrates in newborn rabbit hepatocytes

The rates of glucose production from various substrates entering gluconeogenesis at different steps were investigated in hepatocytes isolated from term-fetus and newborn rabbits fasted during the first 2 days of life. The data were compared to the rate of glucose production measured in hepatocytes from young rabbits (50-60 days) starved for 48 h. The net production of glucose from substrates (lactate, pyruvate, propionate, alanine) entering gluconeogenesis below phosphoenolpyruvate was very low at birth and increased during the first day of life, in relation with an increased cytosolic phosphoenolpyruvate carboxykinase activity. The net production of glucose from precursors entering gluconeogenesis at the level of triose phosphates (dihydroxyacetone, fructose) was low at birth but a maximal capacity for gluconeogenesis was reached within 6 h after birth. This enhanced gluconeogenic capacity was associated with a fall in hepatic fructose 2,6-bisphosphate concentration and a reduced glycolytic flux. In contrast, a high glucose production from galactose was already present at birth and did not rise at 24 or 48 h after delivery. These results suggest that the development of gluconeogenic capacity in hepatocytes isolated from newborn rabbit is dependent upon two factors, a decrease in the F2,6-P2 concentration which reduces the glycolytic flux and an increase in the activity of cytosolic phosphoenolpyruvate carboxykinase.     

Increased renin excretion is associated with augmented urinary angiotensin II levels in chronic angiotensin II-infused hypertensive rats

Renin expression in principal cells of collecting ducts (CD) is upregulated in angiotensin II (ANG II)-dependent hypertensive rats; however, it remains unclear whether increased CD-derived renin undergoes tubular secretion. Accordingly, urinary levels of renin (uRen), angiotensinogen (uAGT), and ANG II (uANG II) were measured in chronic ANG II-infused Sprague-Dawley rats (80 ng/min for 14 days, n = 10) and sham-operated rats (n = 10). Systolic blood pressure increased in the ANG II rats by day 5 and continued to increase throughout the study (day 13; ANG II: 175 ± 10 vs. sham: 116 ± 2 mmHg; P < 0.05). ANG II infusion increased renal cortical and medullary ANG II levels (cortical ANG II: 606 ± 72 vs. 247 ± 43 fmol/g; P < 0.05; medullary ANG II: 2,066 ± 116 vs. 646 ± 36 fmol/g; P < 0.05). Although plasma renin activity (PRA) was suppressed in the ANG II-infused rats (0.3 ± 0.2 vs. 5.5 ± 1.8 ng ANG I·ml(-1)·h(-1); P < 0.05), renin content in renal medulla was increased (12,605 ± 1,343 vs. 7,956 ± 765 ng ANG I·h(-1)·mg(-1); P < 0.05). Excretion of uAGT and uANG II increased in the ANG II rats [uAGT: 1,107 ± 106 vs. 60 ± 26 ng/day; P < 0.0001; uANG II: 3,813 ± 431 vs. 2,080 ± 361 fmol/day; P < 0.05]. By day 13, despite suppression of PRA, urinary prorenin content increased in ANG II rats [15.7 ± 3 vs. 2.6 ± 1 × 10(-3) enzyme units excreted (EUE)/day, P < 0.01] as was the excretion rate of renin (8.6 ± 2 × 10(-6) EUE/day) compared with sham (2.8 ± 1 × 10(-6) EUE/day; P < 0.05). Urinary renin and prorenin protein levels examined by Western blot were augmented ～10-fold in the ANG II-infused rats. Concomitant AT(1) receptor blockade with candesartan prevented the increase. Thus, in ANG II-dependent hypertensive rats with marked PRA suppression, increased urinary levels of renin and prorenin reflect their augmented secretion by CD cells into the luminal fluid. The greater availability of renin and AGT in the urine reflects the capability for intratubular ANG II formation which stimulates sodium reabsorption in distal nephron segments.     

Conformational changes expected in endogenous opioid peptides upon their interaction with acidic lipids

The amino terminal amino acid sequence of purified human angiotensinogen has been determined. The first 25 residues with the exception of number 14 were identified. The sequence of the first ten amino acids is that of angiotensin I. The sequence surrounding the renin cleavage site in this protein is Leu-¹⁰Val-¹¹Ile-¹²His-¹³. Thus, human renin must cleave a Leu-Val peptide bond in human angiotensinogen to release angiotensin I, rather than a Leu-Leu bond as reported for other species. The differences between the sequence of human angiotensinogen and that previously reported for a tetradecapeptide derived from equine and porcine angiotensinogen may be responsible for the known species specificity of renin.     

Correlation of 24-hour fluctuations in renin granules of juxtaglomerular cells and in renin and angiotensinogen in blood plasma of the rat

Summary Subcellular structures of juxtaglomerular (JG) cells in the rat kidney were morphometrically examined at six evenly spaced times over 24 h. Plasma renin activities and angiotensinogen concentrations were also measured at these times. The cell volumes were larger at 20.00 h and 04.00 h than at 00.00 h, whereas the nuclear volumes peaked at 20.00 h and 08.00 h, decreasing at 00.00 h and 16.00 h. The volume and surface densities of renin granules and their individual volumes and surface areas peaked at 16.00 h and 00.00 h, decreasing at 20.00 h and 08.00 h, whereas their numerical densities peaked at 20.00 h, decreasing at 12.00 h. The surface densities of the rough endoplasmic reticulum (rER) peaked at 20.00 h, decreasing at other times, except at 08.00 h, when rER volume and surface density were relatively high. The plasma renin activity was maximal at 20.00 h, whereas it was minimal at 08.00 h. The variation in plasma angiotensinogen concentrations was inversely correlated with that in plasma renin activities. These results suggest that JG cells actively synthesize and release renin during the dark period, especially at 20.00 h, whereas during the light period they gradually synthesize renin and produce the granules, most of which may be stored in the cells during this period.     

Myocardial renin is neither necessary nor sufficient to initiate or maintain ventricular hypertrophy

We tested the hypothesis that the myocardial renin-angiotensin system (RAS) is both necessary and sufficient to initiate and maintain all classes of ventricular hypertrophy. Myocardial and plasma renin and angiotensinogen were measured in rats during initiation and maintenance of ventricular hypertrophy associated with DOCA implants and 1% NaCl drinking water, with and without the AT(1) ANG II receptor blocker losartan. Additional groups of rats were given a low-sodium diet (0.04%) for 3 wk. Ventricular hypertrophy was initiated within 7 days and maintained for 35 days in DOCA-treated rats despite significantly low myocardial and plasma renin, normal or low myocardial and plasma angiotensinogen, or the presence of losartan. Furthermore, there was no ventricular hypertrophy in low-salt diet-fed animals despite increased myocardial and plasma renin levels and normal angiotensinogen levels. Therefore, the myocardial RAS is not necessary to initiate or maintain cardiac hypertrophy in DOCA-treated rats and is not sufficient to initiate cardiac hypertrophy in low-salt diet-fed rats. Additionally, myocardial renin and angiotensinogen were significantly correlated with corresponding plasma levels.     

Dissociation of hyperreninemia and renal prostaglandin synthesis in the adrenalectomized rat

The aim of this study was to determine whether hyperreninemia in the adrenalectomized (ADX) rat is dependent on renal prostaglandin synthesis, as has been suggested for two other hyperreninemic conditions, Bartter's syndrome and chronic liver disease. Plasma renin concentration (PRC) in anesthetized, ADX rats was significantly increased (delta +480%; p less than 0.001) compared to sham-operated controls. In vivo, indomethacin (10 mg/kg i.v.) significantly reduced PRC of anesthetized, ADX rats after both 45 min (delta -34%; p less than 0.05) and 90 min (delta -47%; p less than 0.05). In vitro renin release from renal cortical slices of ADX rats was also significantly greater (delta +130%; p less than 0.05) than from sham-operated control cortical slices. Renin release from cortical slices of ADX rats given dexamethasone (10 micrograms/kg/day) for 4 days prior to sacrifice did not differ from sham-operated control values. Prostaglandin E2 (PGE2) release from cortical slices of ADX rats did not differ significantly from controls. However, PGE2 synthesis in glomeruli microdissected from ADX rats was significantly increased (delta +110%; p less than 0.001) compared to controls. PGE2 synthesis in glomeruli of dexamethasone-treated ADX rats remained significantly elevated compared to controls. Ibuprofen (10(-6) M) decreased PGE2 synthesis in cortical slices by 80%. However, prostaglandin synthesis inhibition had no effect on renin release from either ADX or control renal cortical slices. These results suggest that despite increased glomerular synthesis, prostaglandins do not directly influence renin release in the ADX rat.     

Effect of vaginal distension on blood flow and hypoxia of urogenital organs of the female rat.

Vaginal delivery of children causes traumatic injury to tissues of the pelvic floor and is correlated with stress urinary incontinence; however, the exact mechanism of organ and tissue injury leading to incontinence development is unknown. The purpose of this project was to test the hypothesis that vaginal distension results in decreased blood flow to, and hypoxia of, the urogenital organs responsible for continence, which would suggest an ischemic and/or reperfusion mechanism of injury. Thirteen female rats underwent vaginal distension for 1 h. Thirteen age-matched rats were sham-distended controls. Blood flow to the bladder, urethra, and vagina were determined using a microsphere technique. Hypoxia of these organs was determined by immunohistochemistry. Blood flow to all three organs was significantly decreased just before release of vaginal distension. Bladder blood flow decreased further immediately after release of vaginal distension and continued to be significantly decreased 15 min after the release. Blood flow to both the urethra and vagina tripled immediately after release, inducing a rapid return to normal values. Vaginal distension resulted in extensive smooth muscle hypoxia of the bladder, as well as extensive hypoxia of the vaginal epithelium and urethral hypoxia. Bladders from sham-distended rats demonstrated urothelial hypoxia as well as focal hypoxic areas of the detrusor muscle. We have clearly demonstrated that vaginal distension results in decreased blood flow to, and hypoxia of, the bladder, urethra, and vagina, supportive of hypoxic injury as a possible mechanism of injury leading to stress urinary incontinence.     

Oxygen free radicals in rat limbic structures after kainate-induced seizures

Several indices of free radical generation were determined in limbic structures after kainate (KA)-induced seizure activity in adult and postnatal day (PND) 12 and 17 rats. Superoxide dismutase, catalase, and glutathione peroxidase activities were measured in piriform cortex and hippocampal subfields at 8, 16, 48 h, and 5 days after KA injection in adults and pups, and also at 3 weeks postinjection in adults. KA-induced seizure activity had no significant effect on enzyme activities in PND 12 and 17 rats. In adults, superoxide dismutase and catalase activities were significantly increased at 5 days after KA administration, and returned to preinjection levels by 3 weeks. Glutathione peroxidase activity was also increased significantly at 5 days postinjection, but remained elevated at 3 weeks. Lipid peroxidation, as indicated by malondialdehyde (MDA) concentration, exhibited an early significant increase at 8 and 16 h, followed at 48 h and 5 days by a significant decrease. At 3 weeks postinjection, MDA levels were still significantly decreased in CA3 and dentate gyrus. KA administration in PND 12 and 17 rats had no significant effect on MDA content. KA-induced seizure activity in adults also resulted in a large and sustained increase in protein oxidation in piriform cortex and hippocampus. The early increase in MDA and protein oxidation in adult rats strongly suggests the involvement of oxygen free radicals in the initial phases of KA-induced pathology, whereas the changes in scavenging enzyme activities and MDA content at 5 days and 3 weeks post KA injection possibly reflect glial proliferation subsequent to neuronal death.     

Effect of maternal nutrient restriction in early to mid gestation and thyrotrophin-releasing hormone on lamb survival following Caesarean section delivery near to term

We investigated the influence of restricted maternal nutrition between 28 and 77 days gestation on survival and thermoregulatory adaptation following Caesarean section delivery near to term. This study was designed to examine the hypothesis that adaptation after birth would be compromised in those lambs born to nutrient restricted ewes. We further hypothesised that this would be due in part to inadequate hypothalamic-pituitary-thyroidal function. Lambs born to nutrient restricted ewes were untreated (RU) or treated with thyrotrophin-releasing hormone (TRH; RT) immediately prior to umbilical cord clamping. Single bearing ewes consumed either 6.60 MJ x day(-1) (controls, n = 4) or 3.00 MJ x day(-1) (nutrient restricted, n = 15) from 28-77 days gestation, after which all ewes consumed 7.20 MJ x day(-1). All lambs born to control ewes commenced continuous breathing and began to shiver following Caesarean section delivery and survived to 6 h after birth. Only 4 out of 9 RU lambs established continuous breathing and survived to 6 h after birth compared with all RT lambs. Six hours after birth, RT lambs possessed perirenal brown adipose tissue with a higher thermogenic activity than 6 h old RU or control lambs. Lamb birth weight was similar in all groups. In conclusion, near-term lambs born to ewes nutrient restricted in early to mid gestation are at increased risk of death following Caesarean section delivery. Survival after birth can be significantly enhanced if TRH is administered to the lambs immediately before delivery.     

Blockade of first ovulation in pubertal rats by delta-9-tetrahydrocannabinol: requirement for advanced treatment due to early initiation of the critical period

Successful blockade of ovulation in pubertal rats by delta-9-tetrahydrocannabinol (THC) required earlier treatment during proestrus than was required in adults under the same conditions. Only 1 of 8 adult rats ovulated after treatment with THC (10 mg/kg body weight, i.p.) at 1400 h proestrus, whereas 77% of pubertal rats released full sets of ova following similar treatment during proestrus of the first or second vaginal cycle. When treatment of pubertal rats was advanced to 1300 h, only 2 of 10 THC-treated rats exhibited full ovulation, an incidence significantly lower than the 80% ovulation rate observed in vehicle-treated animals (p less than 0.05). To determine whether the requirement for earlier THC treatment in pubertal rats was related specifically to THC or reflected possible age-associated differences in timing of the critical period, the ovulation-blocking efficacy of atropine sulfate (ATR) was tested in pubertal rats for comparison with that of THC. The serum concentrations of luteinizing hormone (LH) during the first proestrus (1200-1900 h) were determined in pubertal rats that remained untreated. The incidence of ovulation in rats treated with ATR (350 mg/kg, s.c.) at 1400 h proestrus was not significantly reduced from that in vehicle-treated rats; however, after ATR treatment at 1300 h, only 2 of 11 animals released full sets of ova whereas all vehicle-treated rats ovulated (p less than 0.025). The mean serum LH concentration in untreated pubertal rats was not significantly increased over baseline at 1300 h proestrus, but was markedly elevated by 1400 h (1009 +/- 375 ng/ml; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in free fatty acids and diglycerides in mouse brain at birth and during anoxia

Abstract: Within the first few hours of life in the mouse, marked changes were seen in brain endogenous free fatty acids (FFA). A 21% decrease in the total FFA pool occurred during the 1st h of life, and a constant value was maintained thereafter to 10 h. Polyunsaturated fatty acids displayed a different pattern of change. There was 27% less free ararhidonic acid at birth (0 h) than 1 h later. Similar values were obtained for docosahexaenoic acid at birth and at 10 h, although palmitoleic and oleic acids decreased markedly after 1 h. The polyunsaturated fatty acyl chains of diglycerides (DG) showed a statistically significant increase as a function of time after birth, despite an unchanged total DG pool size. The brains of pups subjected to 40 min of N₂-anoxia immediately after delivery exhibited a decrease in FFA, especially the monoenoic components, but 60 min of anoxia yielded higher FFA levels. Anoxia induced at 10 h increased FFA and arachidonic acid was higher than when anoxia was induced at 0 h. FFA accumulation was further stimulated by raising the environmental temperature during anoxia. When anoxia was induced, DG exhibited a net increase in palmitate, oleate, and palmitoleate at 0 and 10 h. No arachidonoyl-DG accumulated at 0 h, even after 60 min of anoxia, and stearate was unchanged at 0 and 10 h. The lipid changes observed in the brain during the first hours of life suggest that the enzymatic reactions that promote accumulation of free arachidonic and docosahexaenoic acids and arachidonoyl-DG in the mature brain are present at low levels at the time of delivery. The sluggish modifications found in our study may be related to the longer resistance of newborns to oxygen deficiency.     

High Salt Intake Damages the Heart through Activation of Cardiac (Pro) Renin Receptors Even at an Early Stage of Hypertension

Objective

It has not yet been fully elucidated whether cardiac tissue levels of prorenin, renin and (P)RR are activated in hypertension with a high salt intake. We hypothesized that a high salt intake activates the cardiac tissue renin angiotensin system and prorenin-(pro)renin receptor system, and damages the heart at an early stage of hypertension.

Methods

Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) received regular (normal-salt diet, 0.9%) and high-salt (8.9%) chow for 6 weeks from 6 to 12 weeks of age. The systolic blood pressure, plasma renin activity (PRA) and plasma angiotensin II concentration were measured, and the protein expressions of prorenin, (pro)renin receptor, angiotensinogen, angiotensin II AT1 receptor, ERK1/2, TGF-β, p38MAPK and HSP27 in the myocardium were investigated. The cardiac function was assessed by echocardiography, and histological analysis of the myocardium was performed.

Results

The high-salt diet significantly increased the systolic blood pressure, and significantly reduced the PRA and plasma angiotensin II concentration both in the WKYs and SHRs. Cardiac expressions of prorenin, renin, (P)RR, angiotensinogen, angiotensin II AT1 receptor, phosphorylated (p)-ERK1/2, p-p38MAPK, TGF-β and p-HSP27 were significantly increased by the high salt diet both in the WKYs and SHRs. The high-salt diet significantly increased the interventricular septum thickness and cardiomyocyte size, and accelerated cardiac interstitial and perivascular fibrosis both in the WKYs and SHRs. On the other hand, dilatation of left ventricular end-diastolic dimension and impairment of left ventricular fractional shortening was shown only in salt loaded SHRs.

Conclusion

The high-salt diet markedly accelerated cardiac damage through the stimulation of cardiac (P)RR and angiotensin II AT1 receptor by increasing tissue prorenin, renin and angiotensinogen and the activation of ERK1/2, TGF-β, p38MAPK and HSP27 under higher blood pressure.     

Changes of nitric oxide,carbon monoxide and oxidative stress in term infants at birth

The higher risk of respiratory problem in infants delivered by elective caesarean section in comparison with vaginally born infants may be favoured by lower level of nitric oxide (NO) and carbon monoxide (CO) and higher oxidative stress in infants born by caesarean section. We studied healthy term infants born by vaginal delivery or by elective caesarean section. Nitric oxide, CO, guanosine 3–5 cyclic monophosphate, total hydroperoxide and advanced oxidation protein products (AOPP) were measured at birth and 48–72 h of life. Nitric oxide, CO and cGMP were lower at birth and at 48–72 h of life in infants born by elective caesarean delivery. Total hydroperoxide and AOPP levels were similar in the two groups and increased from birth to 48–72 h of life. In conclusion, nitric oxide and CO concentrations were higher in term infants vaginally born than in infants born by elective caesarean section and decreased from birth to 48–72 h of life. The mode of delivery did not affect the oxidative stress which increases from birth to 48–72 h of life.     

Glucose metabolism in the newborn rat. Hormonal effects in vivo

1. The concentrations of liver glycogen and plasma d-glucose were measured in caesarian-delivered newborn rats at time-intervals up to 3h after delivery after treatment of the neonatal rats with glucagon, dibutyryl cyclic AMP, cortisol or cortisol+dibutyryl cyclic AMP. Glycogenolysis was promoted by glucagon or dibutyryl cyclic AMP in the third hour after birth but not at earlier times. Cortisol and dibutyryl cyclic AMP together (but neither agent alone) promoted glycogenolysis in the second hour after birth, but no hormone combination was effective in the first postnatal hour. 2. The specific radioactivity of plasma d-glucose was measured as a function of time for up to 75 min after the intraperitoneal injection of d-[6-(14)C]glucose and d-[6-(3)H]glucose into newborn rats at delivery and after treatment with glucagon or actinomycin D. Glucagon-mediated hyperglycaemia at this time was due to an increased rate of glucose formation and a decreased rate of glucose utilization. Actinomycin D prevented glucose formation and accelerated the rate of postnatal hypoglycaemia. 3. The specific radioactivity of plasma l-lactate and the incorporation of (14)C into plasma d-glucose was measured as a function of time after the intraperitoneal injection of l-[U-(14)C]lactate into glucagon- or actinomycin D-treated rats immediately after delivery. The calculated rates of lactate formation were unchanged by either treatment, but lactate utilization was stimulated by glucagon administration. Glucagon stimulated and actinomycin D diminished (14)C incorporation into plasma d-glucose. 4. The factors involved in the initiation of glycogenolysis and gluconeogenesis in the rat immediately after birth are discussed.     

Changes of nitric oxide, carbon monoxide and oxidative stress in term infants at birth

The higher risk of respiratory problem in infants delivered by elective caesarean section in comparison with vaginally born infants may be favoured by lower level of nitric oxide (NO) and carbon monoxide (CO) and higher oxidative stress in infants born by caesarean section. We studied healthy term infants born by vaginal delivery or by elective caesarean section. Nitric oxide, CO, guanosine 3-5 cyclic monophosphate, total hydroperoxide and advanced oxidation protein products (AOPP) were measured at birth and 48-72 h of life. Nitric oxide, CO and cGMP were lower at birth and at 48-72 h of life in infants born by elective caesarean delivery. Total hydroperoxide and AOPP levels were similar in the two groups and increased from birth to 48-72 h of life. In conclusion, nitric oxide and CO concentrations were higher in term infants vaginally born than in infants born by elective caesarean section and decreased from birth to 48-72 h of life. The mode of delivery did not affect the oxidative stress which increases from birth to 48-72 h of life.