PubMed Health⌕ Search

Biomedical subjects

C Sernia

Publications and source records attributed to C Sernia.

At least 37 records · Page 2Linked to original sources
PubMed1996

Short-term growth hormone (GH) treatment of GH-deficient adults increases body sodium and extracellular water, but not blood pressure.

Initiation of GH treatment in adults is frequently complicated by the development of symptomatic fluid retention. To investigate the mechanism and extent of fluid retention that occurs with dosages of GH used in the treatment of GH-deficient adults, we conducted a double blind study in which seven GH-deficient patients (aged 24-74 yr) each received in random order daily sc injections of placebo, a physiological dose of GH (0.04 U/kg, low dose), and a supraphysiological dose of GH (0.08 U/kg, high dose) for 7 days, separated by 21-day washout periods. On the seventh day, measurements were made of serum insulin-like growth factor I, body weight, exchangeable sodium, plasma volume, angiotensinogen, PRA, aldosterone, atrial natriuretic peptide (ANP), and mean 24-h ambulatory heart rate and blood pressure. GH significantly increased mean insulin-like growth factor I levels from 105 +/- 11 to 304 +/- 45 micrograms/L during low dose treatment (P = 0.006) and 400 +/- 76 micrograms/L during high dose treatment (P = 0.004). High dose GH caused a 1.2 +/- 0.3 kg increase in body weight (P = 0.01) and a 193 +/- 65 mmol increase in exchangeable sodium (P = 0.008). Low dose GH had a lesser effect, with no significant increase in body weight, but an increase in exchangeable sodium of 113 +/- 37 mmol (P = 0.02). Plasma volume was not significantly affected by GH treatment. Mean supine angiotensinogen levels were significantly higher during both GH treatments compared to placebo (low dose, P = 0.017; high dose, P = 0.028) as were mean supine PRA levels (low dose, P = 0.0002; high dose, P = 0.0025). Supine angiotensin II, aldosterone, and ANP levels were not significantly affected by GH treatment. There was no significant change from placebo in any of the sodium-regulating hormones in the erect posture. The mean 24-h heart rate was significantly higher during low dose (82 +/- 2 beats/min; P = 0.0001) and high dose (88 +/- 3 beats/min; P = 0.0001) GH treatment than during placebo (67 +/- 3 beats/min). However, no significant change in mean 24-h systolic or diastolic blood pressure was observed. In summary, acute GH administration using doses currently employed in treating adults causes a dose-related increase in body weight and body sodium, but no associated increase in blood pressure. We conclude that 1) sodium retention is a physiological effect of GH, but does not cause an acute rise in blood pressure; and 2) the mechanism of sodium and fluid retention is not primarily due to enhanced aldosterone secretion or inhibition of ANP release, but more likely to a direct renal tubular effect.

Adult↗
PubMed1996

Effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal polypeptide on cyclic AMP accumulation in sheep pituitary cells in vitro.

Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) are known to stimulate adenylate cyclase activity in rat pituitary cells but no direct effects have been reported on sheep pituitary cells. In this study we determined whether either peptide could stimulate intracellular cAMP accumulation in dispersed sheep pituitary cells in primary culture. Time course studies with PACAP showed that tachyphylaxis developed rapidly and so a short incubation time (5 min) was used to define the dose-response relationship. PACAP dose-dependently stimulated intracellular cAMP levels with a half-maximum response at 2.9 +/- 0.2 nmol/l (n = 4). In contrast, VIP only caused a small increase in intracellular cAMP levels at the highest dose tested (1 mumol/l). The VIP antagonist [4Cl-D-Phe6,Leu17]VIP had no effect on the cAMP response to either PACAP or VIP while the peptide PACAP(6-38), a putative PACAP antagonist, blocked the cAMP response to PACAP. The desensitisation to PACAP was further investigated by pretreating cells with PACAP for 30 min. After a further 15 min in culture medium alone, these cells showed no cAMP response to subsequent treatment with PACAP but could respond to forskolin. When a longer incubation period of 240 min was used between the first and second treatment with PACAP, a partial return in responsiveness to PACAP was observed. In summary, these results show that PACAP activates adenylate cyclase in sheep pituitary cells but that there is rapid development of tachyphylaxis. Experiments with the antagonists suggest that the response to PACAP is via the PACAP type I receptor. In contrast, physiological doses of VIP do not stimulate cAMP accumulation in sheep pituitary cells.

Adenylyl Cyclases↗
PubMed1996

Identification and characterization of angiotensinIV binding sites in rat neurone and astrocyte cell cultures.

This study demonstrates the existence of the putative receptor for the hexapeptide (3-8) fragment of angiotensin II (AngIV) on rat astrocytes and neurons grown in cell culture. Binding of 125I-AngIV was saturable and distinct from that of the AngII receptor subtypes. Equilibrium binding was attained in 15 min in astrocytes and 75 min in neurons at 22 degrees C. The bound peptide was confirmed by HPLC to be intact AngIV while the bound peptide was substantially degraded, even in the presence of peptidase inhibitors. Scatchard analysis of equilibrium binding was consistent with a two binding site model, revealing a high affinity and a low affinity binding site in both cell types. In neurons, the respective association constants (Ka) were 2.72 +/- 0.23 nM-1 and 727 +/- 354 nM-1, with associated receptor densities of 109.30 +/- 58.87 and 1723 +/- 1167 fmol/mg protein. Similar analyses in astrocytes gave Kas of 5.71 +/- 2.85 nM-1 and 277 +/- 205 nM-1, and respective densities of 191.1 +/- 90.1 and 1425 +/- 1250 fmol/mg protein. However, the quantitative reliability of these binding isotherms may be influenced by the degration of unbound peptide. Competitive binding analysis was used to determine the specificity of the receptor site, with the relative order of affinities being AngIV > AngIII > AngII(4-8), and no displacement by AngII, Iosartan and PD123319 in either neurons or astrocytes. Autoradiography with 125I-AngIV performed on neuronal cultures demonstrated that binding was confined to a subpopulation of the total cells. These data support the existence of a specific binding site for AngIV in both neurons and astrocytes, consistent with the properties of binding reported previously in the brain, and distinguish this site from the AngII receptor subtypes.

Angiotensin II↗
PubMed1995

Effect of changing from a short-day to long-day photoperiod on the breeding season of the brushtail possum (Trichosurus vulpecula).

In Queensland, possums (Trichosurus vulpecula) in the wild and in captivity first give birth during March and April and continue to give birth throughout the year until November. The possum has a gestation length of 17.5 days, gives birth to one young, and lactation continues for approximately 180 days. If the newborn possum is removed during the breeding season, the possum will ovulate approximately 9 days later and give birth approximately 26 days after removal of the pouch young (RPY). Repeated RPY may be used to determine the duration of the breeding season. In this study, the effect on the breeding season of a marked change in photoperiod From a short-day to a long-day was examined by comparing three groups of possums in different photoperiods for 13 months. One group of five female and two mail possums (group A) was housed in a natural photoperiod and a second group (B) was housed in a short-day photoperiod (10 h light: 14 h dark) throughout the study. The third group (C) was housed in a short-day photoperiod until each possum gave birth, the pouch young was removed, and the possum transferred to a long-day photoperiod room (14 h light: 10 h dark) for the remainder of the study. The possums held in a natural photoperiod, group A, gave birth to a total of 27 births in the one breeding season from March to October.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Molecular forms of rat angiotensinogen in plasma and brain: identification by isoelectric focusing and immunoblot analysis.

Angiotensinogen (Ao) is the glycoprotein precursor of the vasoactive peptide angiotensin II. While Ao is synthesized as multiple molecular forms, the biochemical characteristics of this protein in blood and other tissues have not been defined. In this study, the charge heterogeneity of Ao in rat plasma, cerebrospinal fluid and that secreted by astrocyte and neuronal cultures was examined using analytical isoelectric focusing in combination with immunoblotting and quantitative image analysis. Normal rat male plasma Ao separated into 9 isoforms in the pI range 4.34-4.92 (1, 4.34; 2, 4.41; 3, 4.48; 4, 4.58; 5, 4.61; 6, 4.66; 7, 4.68; 8, 4.81; 9, 4.92); the percentage contribution of each to total plasma Ao was 13, 20, 23, 18, 2, 7, 10, 5, and < 1, respectively. A similar isoelectric focusing pattern was observed in female rat plasma with the exception that the relative contribution of isoform 6 was reduced to 2% of total Ao. Cerebrospinal fluid Ao displayed a more diverse charge heterogeneity than plasma Ao, focusing over a broader pI range of 4.42-5.24. Astrocytes and neurons secreted Ao isoforms in the pI range 4.44-5.29 and 4.42-4.95, respectively, with the astrocyte cultures showing additional bands towards the cathode. It was concluded that rat Ao is secreted as multiple charged forms that are regulated in a sex- and cell-specific manner. These differences between plasma and brain Ao suggest a functional diversity, a view which is supported by recent evidence linking Ao variants to hypertension.

Angiotensinogen↗
PubMed1995

Specific binding sites for (3-8)angiotensin in C6 glioma cells.

A novel putative receptor for (3-8)angiotensin (AngIV) has recently been found in various tissues, including the brain. However, the localization of AngIV binding sites to specific types of brain cells has yet to be established. In this study tissue culture was used to determine the presence and characteristics of AngIV binding in a glioma cell line (C6) and in rat primary glial cells. Using [125I]AngIV as a radioligand, C6 glioma cells were found by radioreceptor assay to bind with a high affinity and in a saturable, reversible manner. The best fit to the data was for a two-binding-site model; a higher-affinity site with a Ka of 2.49 +/- 0.46 nM-1 and a density of 33.71 +/- 7.8 fmol/mg protein, and a second low-affinity site with a Ka of 176 +/- 7 microM-1 and a density of 563 +/- 190 fmol/mg protein. The ligand specificity of the AngIV sites was determined from competitive displacement assays with AngIV, AngIII, (4-8)AngII, [Sar1,Ile8]-AngII, losartan (an angiotensin subtype 1 receptor ligand) and PD123319 (an angiotensin subtype 2 receptor ligand). The relative order of binding affinity was AngIV > AngIII >> (4-8)AngII, while losartan, PD123319 and Sar1,Ile8-AngII failed to compete for the AngIV sites, even at 1 microM. The radioreceptor assay data were confirmed by receptor autoradiography on cells grown on glass slides. Moreover, the bound radioligand was shown by HPLC to be [125I]AngIV and not a breakdown product. Preliminary experiments with primary astrocyte cultures showed the presence of AngIV binding sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1995

Location and secretion of brain angiotensinogen.

Angiotensinogen is a glycoprotein with intriguing structural similarities to the serine proteinase inhibitors but with only one known function: to act as a substrate in the enzymatic generation of angiotensin peptides. It is expressed as a constitutive protein by the liver and various other tissues, including the brain. It is in this tissue that the expression of angiotensinogen attains its most complex and controversial manifestations. In late gestation, an unfolding of cellular expression occurs, starting at an epicentre in the eppendymal and astroglia cells of the hypothalamus, which rapidly and sequentially spreads to sub-cortical and then cortical regions, concentrating at sites of electrolyte, fluid and pressure regulation. This initial burgeoning of astroglial angiotensinogen is trailed by a wave of neuronal expression in various limbic and sensorimotor regions of the brain. The predominance of AT2 receptors in these regions suggests that the RAS actions are mediated by AT2 receptors. The angiotensinogen found in the CSF and secreted by cultures of glia and neurones is similar to the two major molecular sizes found in plasma. However, by electrophoretic separation on the basis of charge imparted by differential glycosylation, it can be shown that glia and neurones secrete distinct forms. The expression of different forms is under hormonal regulation. If these structural forms are shown to affect function, then the resulting ramifications may extend to pathological conditions, such as hypertension. Primary cell cultures of astrocytes secrete angiotensinogen constitutively and in a region-specific manner related to the size of the sub-population of secretory cells. Neurone cultures secrete angiotensinogen at about 25% the rate of hypothalamic astrocytes. The use of RT-PCR shows that both cell types express angiotensinogen mRNA. There is still an unresolved mismatch between these data and in situ hybridization histochemistry which shows expression limited to astrocytes but it is suggested that changes to more appropriate techniques will resolve any outstanding discrepancies.

Aging↗
PubMed1995

In situ hybridization and immunohistochemistry of renal angiotensinogen in neonatal and adult rat kidneys.

Recent evidence suggests that a local renin-angiotensin system is operational in the kidney and that it mediates some of the actions of angiotensin II on renal tubules. In this study the ontogeny and renal distribution of the unique precursor to angiotensin II formation, angiotensinogen, was investigated in rats by use of immunohistochemistry, immuno-electron microscopy and non-isotopic hybridization histochemistry. At the light-microscopic level, intense staining for angiotensinogen was found in the proximal convoluted tubules of the cortex, with lighter staining in the straight proximal tubules of the outer stripe. The strongest immunostaining was found in the kidneys of neonatal rats, where glomerular mesangial cells and medullary vascular bundles were also immunopositive. The angiotensinogen content of the kidneys in late gestation embryos and neonates showed the presence of angiotensinogen by day E18 and a peak content in the neonate. Non-isotopic hybridization histochemistry with biotinylated oligodeoxynucleotide probes confirmed the presence of angiotensinogen mRNA expression in the proximal convoluted tubules of the renal cortex. Electron-microscopic immunohistochemistry showed staining of relatively few electron-dense structures close to the apical membrane of proximal convoluted tubule cells in the adult kidney. In the neonatal rat kidney, angiotensinogen immunostaining at the electron-microscopic level was found throughout the proximal tubule cells and was markedly stronger than that seen in adult kidney. The presence of angiotensinogen, from embryonic day 18, in the proximal tubules, mesangial cells and vasculature of the kidney suggests multiple potential sites of intrarenal angiotensin II generation with an ontogeny in late gestation.

Aging↗
PubMed1995

Immunocytochemical localization of angiotensinogen in the fetal and neonatal rat brain.

The aim of this study was to define the temporal appearance and regional distribution of angiotensinogen in the fetal and neonatal rat brain. This was done by immunocytochemical localization of angiotensinogen in brains from embryonic day 16 to postnatal day 12. Immunostaining was first observed on embryonic day 18, and persisted to postnatal day 2, in the choroid plexus and ependymal cells lining the third ventricle. This initial expression of angiotensinogen at embryonic day 18 was followed at postnatal day 20 by a rapid progression of angiotensinogen staining appearing in astrocytes in the paraventricular nucleus, medial preoptic area, ventromedial and arcuate hypothalamic nuclei; these areas showed the highest astrocyte staining intensity in the brain. This was followed sequentially by staining in areas of the thalamus, midbrain, forebrain and brainstem. In general, neuroglial staining was higher in regions proximal to the cerebral ventricles and cerebral aqueduct. Neuronal angiotensinogen was observed at day postnatal day 0 and later. The most consistent immunopositive areas were in the forebrain and thalamus; in particular, the hippocampus, anterior and posterior cingulate cortex, basal and lateral amygdala, the caudate-putamen, globus pallidus, lateral septum, medial habenular nuclei and lateral thalamic nuclei. Most of the immunopositive cells in the hypothalamus and brainstem were astrocytes, while those in the cortex were almost exclusively neurons. Staining in thalamic regions was both neuronal and neuroglial. From the intensity of staining and cell density, it was determined that a rapid increase in angiotensinogen occurs between embryonic day 20 and postnatal day 0, followed by further, smaller increases postnatally. In conclusion, this study has shown that angiotensinogen, the protein from which angiotensin II is generated, is present in the rat fetal brain. The timing of its appearance supports the establishment of a renin-angiotensin system by late gestation. Its predominance in fetal hypothalamic nuclei and in thalamic, cerebellar and cortical neurons suggests major roles in prenatal fluid and electrolyte balance, in sensorimotor development and in brain maturation.

Angiotensinogen↗
PubMed1995

Regulation of neurohypophysial hormone secretion in an Australian marsupial.

The brushtail possum secretes the typically reptilian mesotocin (MT) and arginine vasopressin (AVP) as its neurohypophysial hormones. In this study we have looked at the regulation of MT and AVP secretion in conscious possums by studying the effects of surgical stress and handling of animals, hypertonic saline infusion, hemorrhage, and angiotensin II (ANG II) infusion on the plasma concentrations of MT and AVP. Surgical insertion of a jugular catheter and handling stress increased MT secretion for 3 days after surgery without affecting plasma AVP concentrations. Hypertonic saline infusion induced a gradual increase in plasma osmolarity and Na+ concentration throughout the infusion, which steadily increased plasma AVP without affecting plasma K+ or hematocrit. The relationship between plasma osmolarity and AVP was exponential. Plasma MT was stimulated only by supraphysiological plasma osmolarities. ANG II increased plasma MT and AVP concentrations equipotently throughout the infusion. Hemorrhage was a relatively specific stimulus for AVP secretion, but MT secretion was highly stimulated during severe hypovolemia. It was concluded that MT and AVP secretion is differentially regulated in the possum.

Angiotensin II↗
PubMed1995

Antisense inhibition of hypertension in the spontaneously hypertensive rat.

Phosphorothioated antisense oligodeoxynucleotide (ASODN) targeted to angiotensinogen mRNA was administered intracerebroventricularly in spontaneously hypertensive rats to test whether angiotensinogen reduction would lower their hypertensive blood pressures. The ASODN lowers hypertensive blood pressures to normotensive levels in spontaneously hypertensive rats; sense oligodeoxynucleotide had no effect. Administration of phosphorothioated ASODN produced a prolonged duration of lowered blood pressure. Injections of ASODN at the same dose that decreased hypertension when administered centrally did not result in blood pressure decreases when administered intra-arterially. Furthermore, angiotensinogen production was decreased in the brain stem and significantly decreased in the hypothalamus of the ASODN-treated rats (P < .05), supporting the concept of centrally mediated regulation of hypertension by an overactive brain angiotensin system. To determine the distribution of centrally administered oligodeoxynucleotides, fluorescein isothiocyanate-conjugated oligodeoxynucleotides were injected directly into the lateral ventricles. One hour later, oligodeoxynucleotides were distributed throughout the lateral and third ventricles, with tissue and cellular uptake observed in discrete cells at the injection site. This indicates that the oligodeoxynucleotides are taken up rapidly by brain cells and that they permeate the areas surrounding brain nuclei involved in central blood pressure regulation and volume homeostasis. The results confirm and extend our previous study with phosphodiester ASODN and show that phosphorothioation modification increases the duration of the response and is taken up in vivo. We conclude that with modification, ASODN inhibition of angiotensinogen mRNA translation can be used for a prolonged, profound decrease in mean arterial pressure in the spontaneously hypertensive rat through a central mechanism.

Angiotensinogen↗
PubMed1995

Characterization of vasopressin and oxytocin receptors in an Australian marsupial.

In this study arginine vasopressin (AVP) and oxytocin (OT) receptors have been characterized in the brushtail possum. AVP receptors were characterized using [3H]AVP and the radioiodinated AVP V1a receptor antagonist 125I-labelled [C6H5-CH2CO)-O-methyl-D-Tyr-Phe-Gln-Asn-Arg-Pro-Arg-Tyr-NH2] while OT receptors were characterized using the radioiodinated OT receptor antagonist 125I-labelled d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr-NH2(9)]-vasotocin. The receptor affinities and densities have been compared with the rat AVP and OT receptors. Low densities of OT receptors were present in the possum ovary and kidney. High densities of AVP-binding sites were found in the possum adrenal, testis, mesenteric artery, ovary and renal medulla and lower densities in the possum liver. The AVP-binding sites showed marked differences in ligand-binding characteristics from the rat AVP V1a and V2 receptors. Receptor affinities were similar between tissues, except for a distinctly lower value in the renal medulla. It is concluded that the brushtail possum expresses AVP receptors with distinct ligand specificities from those of the rat AVP V1a and V2 receptors.

Adrenal Glands↗
PubMed1995

Comparative aspects of oxytocin-like hormones in marsupials.

Unlike eutherian mammals which secrete only oxytocin (OT), marsupials secrete the typically reptilian mesotocin (MT) and/or OT as their oxytocic peptides. Our laboratories have been conducting research on various aspects of the roles of OT-like peptides in three marsupials, the brushtail possum, the northern brown bandicoot and the tammar wallaby. By providing information on the functions of OT-like peptides in these species we hope to provide some clues as to the evolution of neurohypophysial hormones in marsupials. Brain and peripheral distributions of OT-like peptides have been studied in the possum and bandicoot. As in eutherian mammals, OT-like peptides are distributed throughout the brain and are present in the testis, corpus luteum, prostate and adrenal glands. Studied on the regulation of release of MT into plasma in the possum show that it is regulated by similar mechanisms to OT release in eutherian mammals. OT receptors have been characterized and localized in the possum and the tissue distributions and pharmacological characteristics of the receptor are similar to both the sheep and rat OT receptors. The marsupial OT receptor shows no pharmacological specificity for MT over OT which is reflected in the similar potency of these peptides in eliciting contractions of the uterus of the tammar wallaby in vitro. MT seems to play an important but not essential role in parturition in the tammar. MT concentrations are increased immediately after delivery in the tammar but infusion of an OT antagonist before expected birth delays but does not prevent parturition. The presence of OT receptors in the marsupial mammary gland and the sensitivity of the gland to exogenous OT and stimulation of mesotocinergic neurones demonstrates that these peptides are important for marsupial lactation. Our data suggest that the presence of MT with or without OT in marsupials is a result of a neutral mutation rather than functional evolution.

Animals↗
PubMed1994

Adrenoceptor-mediated cardiac and vascular responses in hypothyroid rats.

This study has investigated adrenoceptor-mediated responses and beta-adrenoceptors in neonatal-onset hypothyroidism in rats. Four groups of adult rats were studied: controls, neonatal-onset uncorrected hypothyroidism (continuous oral methimazole treatment) and after chronic triiodothyronine (T3) replacement of these rats at either 25 or 100 micrograms/kg/day for 8 weeks beginning at 12 weeks of age. Hypothyroid rats were 61% smaller with an 18% decrease in heart rate; food and water intake were reduced to 43% and 52%, respectively; O2 consumption was reduced to 20% and rectal temperature was 2.9 degrees lower. T3 administration increased body weight to 60-62% of controls; metabolic changes were reversed; but tachycardia and cardiac hypertrophy (60-120% increases) resulted. The positive inotropic responses to the selective alpha 1-adrenoceptor agonist, phenylephrine, in left ventricular papillary muscles were abolished; the beta 1-adrenoceptor agonist, noradrenaline, was significantly less potent as an inotropic compound in isolated cardiac tissues from hypothyroid rats. The potency of phenylephrine to contract thoracic aortic rings was reduced in hypothyroid rats. These changes in alpha- and beta-adrenoceptor mediated responses were reversed by T3 administration. Both beta 1- and beta 2-adrenoceptor densities were increased in the hypothyroid left ventricle; T3 administration further increased beta 1-adrenoceptor density. We conclude that neonatal hypothyroidism produces pronounced physiological responses, changes in adrenoceptor-mediated responses and an increased ventricular beta 1-adrenoceptor density. T3 replacement reversed the changes in cardiac responses and metabolic parameters, except body weight, but produced cardiac symptoms of hyperthyroidism (tachycardia, hypertrophy as well as an increased beta 1-adrenoceptor density).

Animals↗
PubMed1994

Mesotocin and arginine-vasopressin in the corpus luteum of an Australian marsupial, the brushtail possum (Trichosurus vulpecula).

The neuropeptide hormones arginine-vasopressin (AVP) and oxytocin (OT) have been found in the ovarian follicles and corpora lutea (CL) of many eutherian mammals. In ruminants, there is persuasive evidence that luteal OT is involved in luteolysis via stimulation of uterine prostaglandins. However, based on scant evidence, the marsupial ovary has been viewed as being devoid of OT-like and AVP-like peptides. In this study, corpora lutea from the brushtail possum were examined for OT, AVP, and mesotocin (MT) by a combination of reverse phase HPLC, radioimmunoassay, and immunohistochemistry (IHC). Peptides extracted from each of five CL were separated by HPLC and each fraction was assayed for AVP, MT, and OT. Two immunoreactive peaks were found, corresponding to AVP and MT standards. The amount of each peptide was 8.7 +/- 2.22 pmol MT/g (mean +/- SEM) and 5.7 +/- 1.0 pmol AVP/g, respectively. The mean MT/AVP ratio was 1.55 compared to 0.26 for the pituitary. IHC (streptavidin-peroxidase method) of Bouin's-fixed CL showed staining for MT in the cytoplasm of luteal cells which was absent in stromal tissue and nonluteal ovarian tissue. Not all luteal cells were immunopositive and no topographical distribution of stained cells was observed. IHC localization of AVP was not attempted. It was concluded that the CL of the brushtail possum contains low quantities of MT and AVP, which in the case of MT is probably synthesized by the immunochemically staining cells of the CL.

Animals↗
PubMed1994

Cellular and ultrastructural location of angiotensinogen in rat and sheep kidney.

Recent evidence suggests the involvement of a local renin-angiotensin system in some renal actions of angiotensin II (Ang II). In this study the renal distribution of the precursor to angiotensin formation, angiotensinogen, was investigated in rats and sheep using immunohistochemistry, immunoelectron microscopy and non-isotopic hybridization histochemistry. Immunostaining for angiotensinogen was seen in proximal tubules (PCT) of both rat and sheep kidneys. In the rat the strongest immunostaining was found in the kidneys of neonatal (1 day old) rats. Staining declined after birth. Non-isotopic hybridization histochemistry using oligodeoxynucleotide probes labeled with biotin confirmed the presence of angiotensinogen mRNA expression in PCT of the rat renal cortex. Electron microscopic immunohistochemistry using antibodies raised against rat angiotensinogen showed weak staining in the adult of granule-like structures close to the apical membrane of PCT cells. In the neonatal rat kidney, angiotensinogen immunostaining was found throughout the PCT cells and was markedly stronger than that seen in adult rat kidney. In sheep, angiotensinogen immunostaining with an antibody raised against purified ovine angiotensinogen showed staining of PCT in fetal, newborn and adult sheep kidney. The strongest immunostaining seen was in fetal sheep kidney with a decline seen after birth. Reverse transcription polymerase chain reaction (RT-PCR) showed that angiotensinogen mRNA was expressed in the sheep kidney at all ages studied. Angiotensinogen expression was higher in fetal sheep kidneys (77 day and 141 day gestation) than in adult sheep kidney. In conclusion, angiotensinogen mRNA expression was detected in both rat and sheep kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensinogen↗