PubMed Health⌕ Search

Biomedical subjects

A Butkus

Publications and source records attributed to A Butkus.

At least 19 recordsLinked to original sources
PubMed1993

Studies on stanniocalcin: characterization of bioactive and antigenic domains of the hormone.

Stanniocalcin (STC) decreases branchial Ca(2+)-uptake in fish. In order to determine its bioactive domain, synthetic fragments (U amino acids (aa) 1-20; V aa 103-136; W aa 202-231) of eel STC were tested for their effect on Ca2+ uptake in tilapia (Oreochromis mossambicus). Ca2+ uptake was inhibited by an N-terminal fragment but not by a midfragment nor a C-terminal fragment of the mature hormone. We provide theoretical and experimental evidence that a midportion of STC, which is included in the synthetic fragment V, is the most antigenic site of the molecule. Polyclonal antibodies against stanniocalcin are directed against this midportion although this region of STC appears not to be essential for signal transduction. These results suggest that the currently available antibodies will recognize inactive STC fragments in the circulation. We conclude that the bioactive portion of STC does not correspond with the major antigenic portion of the hormone. The results imply that studies on plasma STC levels employing a polyclonal antiserum against STC should be interpreted with care.

Animals↗
PubMed1990

The mechanism of the quinone reductase reaction of pig heart lipoamide dehydrogenase.

The relationship between the NADH:lipoamide reductase and NADH:quinone reductase reactions of pig heart lipoamide dehydrogenase (EC 1.6.4.3) was investigated. At pH 7.0 the catalytic constant of the quinone reductase reaction (kcat.) is 70 s-1 and the rate constant of the active-centre reduction by NADH (kcat./Km) is 9.2 x 10(5) M-1.s-1. These constants are almost an order lower than those for the lipoamide reductase reaction. The maximal quinone reductase activity is observed at pH 6.0-5.5. The use of [4(S)-2H]NADH as substrate decreases kcat./Km for the lipoamide reductase reaction and both kcat. and kcat./Km for the quinone reductase reaction. The kcat./Km values for quinones in this case are decreased 1.85-3.0-fold. NAD+ is a more effective inhibitor in the quinone reductase reaction than in the lipoamide reductase reaction. The pattern of inhibition reflects the shift of the reaction equilibrium. Various forms of the four-electron-reduced enzyme are believed to reduce quinones. Simple and 'hybrid ping-pong' mechanisms of this reaction are discussed. The logarithms of kcat./Km for quinones are hyperbolically dependent on their single-electron reduction potentials (E1(7]. A three-step mechanism for a mixed one-electron and two-electron reduction of quinones by lipoamide dehydrogenase is proposed.

Animals↗
PubMed1990

Effects of synthetic peptide fragments of teleocalcin (hypocalcin) on calcium uptake in juvenile rainbow trout (Salmo gairdneri).

A rainbow trout fry bioassay based on 45Ca uptake was used to compare the effects of pure coho salmon teleocalcin (TC) and several synthetic peptide fragments of TC. Calcium uptake in the fry exhibited a cycle, with an amplitude variation of 3.3 to 48.8 mumol.kg-1.hr-1 and a periodicity of 8 to 21 days. The N-terminal 1-20 amino acid peptides of both eel and salmon TC significantly inhibited 45Ca uptake at the high point of the calcium uptake cycle (up to 75%), although the effective doses of the peptides on a molar basis were 20 to 200 times that of the intact molecule. In contrast, the C-terminal fragment of eel TC (amino acids 202-231) did not have an inhibitory effect on calcium uptake. Instead, it significantly enhanced 45Ca uptake in trout fry (up to sixfold) at the low point of the calcium uptake cycle.

Amino Acid Sequence↗
PubMed1990

Immunoreactive erythropoietin concentration and haemoglobin type in the perinatal period in sheep of various haemoglobin genotypes.

This study examines the hypotheses that (i) erythropoietin (the hormone responsible for red blood cell production) is higher in the fetus (at low PO2) than in the neonate (at high PO2); and (ii) that the level of erythropoietin in the neonate is influenced by the presence of high oxygen affinity haemoglobin. Haematocrit (PCV), PO2 and plasma immunoreactive erythropoietin were measured in 4 chronically cannulated fetal sheep (120 days to birth, n = 22) and in 7 neonatal lambs until 233 days post-conception (75-85 days after birth, n = 83). The percentage of globin chains (alpha, gamma, beta A, beta B, beta C) was quantitated by gel electrophoresis. Plasma erythropoietin values, in 4 fetuses were 9.8 +/- 1.3 mU/ml at 120-132 days of gestation, declined significantly (P less than 0.01) to 5.2 +/- 0.4 at 133 days until birth, then increased significantly (P less than 0.001) to 24.2 +/- 5.5(5), 26.3 +/- 7.3 (6), and 24.8 +/- 8.5 (6), respectively in weeks 1, 2 and 3 of postnatal life. By weeks 5-8 the erythropoietin was 13 +/- 0.6 (4) mU/ml. PO2 was 17.4 +/- 0.9 mmHg before birth and 88.0 +/- 10.7 in the first week after birth. PCV was constant until three weeks after birth and then declined. Fetal haemoglobin had virtually disappeared from the circulation by 166 days (3 weeks after birth); in the 4 heterozygotes (beta A beta B) beta C was expressed transiently, with a maximum value of 4%, whilst in the homozygote lamb (beta A beta A) the maximum beta C was 12%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Effect of hormone-induced premature parturition on hemoglobin switching in sheep.

This study examines the effect of premature delivery on the switch from fetal (alpha 2 tau 2) to adult (alpha 2 beta 2) Hb, in lambs in which premature parturition was induced by the intrafetal infusion of ACTH or corticotropin releasing hormone. Of 10 chronically cannulated ovine fetuses given ACTH at the rate of 79 ng/min for a 15 min period every 2 h starting at days 125 (n = 9) or 126 (n = 1) of gestation, three died in utero at days 131, 131, and 130, respectively. The remaining seven were born alive at 133 +/- 1.6 days. Five control fetuses, treated with vehicle (0.9% NaCl, wt/vol) only were delivered at 149 +/- 2.7 days of gestation, which is not significantly different from the duration of pregnancy in other chronically cannulated lambs in this flock. Hb switching, as measured by the globin synthesis ratio, beta/alpha, was complete at term in the control lambs. The beta/alpha globin synthesis ratio of the prematurely delivered lambs was not accelerated by birth, and was similar to that of control fetuses of the same gestational age still in utero. The four lambs surviving premature birth more than 70 days did not complete the switch to normal adult Hb until after 220 days postconception.

Adrenocorticotropic Hormone↗
PubMed1988

The effect of potassium loading on sodium status and pressor responsiveness in the sheep.

The effect of increased potassium (K) intake (800 mmol/day) was investigated in conscious sheep to elucidate the mechanism of the anti-hypertensive effect of K loading. Mean arterial pressure rose (4mm Hg, n = 13, p less than 0.001). Cardiac output (n = 5) increased from 4.4 +/- 0.1 to 6.1 +/- 0.2 1/min (p less than 0.001). Calculated total peripheral resistance fell from 17 +/- 1 to 12 +/- 1 mmHg.min/1 (p less than 0.001). There was no change in plasma volume (n = 5), but extracellular fluid volume (n = 5) increased from 221 +/- 26 to 271 +/- 27 ml/kg (p less than 0.05). Glomerular filtration rate and effective renal plasma flow (n = 5) were unchanged. Plasma K concentration, fluid intake and urine volume increased. Urinary Na excretion increased from 106 +/- 11 to a maximum of 217 +/- 28 mmol/day on day 2 (p less than 0.001), and was decreased on day 7, 44 +/- 13 mmol/day (p less than 0.05). Calculated Na deficit was -268 mmol by day 10, but there was no change in responsiveness to infused angiotensin II, noradrenaline, vasopressin or tyramine. These changes differ from those seen with Na depletion alone in sheep, and are not compatible with the hypothesis that K loading exerts its effects solely by increasing Na excretion.

Animals↗
PubMed1987

Purification and cloning of a corpuscles of Stannius protein from Anguilla australis.

The kidneys of teleost fish are associated with tissues containing secretory granules--the corpuscles of Stannius (CS). Electron microscopy indicates that the granules are of a proteinaceous nature and may represent hormones or enzymes of unrecognized physiological and biochemical function. In the present study, two-dimensional gel electrophoresis and electroelution was used to purify the major protein to homogeneity; it is approximately 32,000 Da in the reduced form and glycosylated. From the partial NH2-terminal sequence, a 75-mer oligonucleotide probe was synthesized and used to isolate a cDNA clone from which the complete amino acid sequence of the major CS protein was deduced. Polyclonal antibodies raised against CS homogenates were specific for the CS proteins (confirmed by immunohistochemistry). Hybridization histochemistry was used to confirm the location of the mRNA encoding the isolated protein. Incubation of CS homogenate with eel plasma or ovine renin substrate did not result in any angiotensin-like peptides whereas kidney homogenate did.

Amino Acid Sequence↗
PubMed1986

Distribution of glomerular peripolar cells in different mammalian species.

Peripolar cells are granulated glomerular epithelial cells that form a cuff around the vascular pole of the glomerulus. Quantitation of these cells in 17 species of mammals (including man, several laboratory animals and a variety of other species) indicated that they were detectable by light microscopy in all but one of the mammals that were examined (the Australian hopping mouse). In adult mammals with detectable peripolar cells, the "peripolar cell index" (the percentage of randomly sectioned glomeruli that displayed peripolar cells in histological sections of kidney) ranged from 0.15 (for echidna) to 11.86 (for sheep). Newborn lambs and rats showed strikingly high values (23.30 and 10.76, respectively) compared with their adult counterparts. Using electron microscopy, peripolar cells were observed in all species that were examined, including the Australian hopping mouse. Morphologically, peripolar cells were similar in all species although their size and granule population varied. They showed a predominantly outer cortical glomerular distribution and a close anatomical relationship with the renin-containing myo-epithelioid cells. These findings indicate that peripolar cells are present in a wide variety of species and support the view that such cells may play a significant role in the regulation of normal renal function.

Aging↗
PubMed1986

Depression, immunocompetence, and prostaglandins of the E series.

Plasma prostaglandin E1 and E2, and quantitative and qualitative measures of immune function, were determined in depressed patients and healthy controls. Prostaglandin E2 was significantly elevated in the depressed group, and prostaglandin E1 showed a trend in the same direction. Lymphocyte stimulation responses, as measured by phytohemagglutinin, concanavalin A, and pokeweed mitogen, were significantly lower in the depressed group. Helper and suppressor T cell percentages did not significantly differ in the two populations. In the depressed group, prostaglandin E1 showed a significant inverse correlation with concanavalin A, and prostaglandin E2 showed a similar trend. These preliminary data suggest prostaglandins of the E series may be related to abnormalities of cellular immunity previously documented in depression.

Alprostadil↗
PubMed1985

The effect of ACTH on the plasma concentrations of the "hypertensinogenic" steroids, 17 alpha-hydroxyprogesterone and 17 alpha,20 alpha-dihydroxy-4-pregnen-3-one in sheep.

The plasma concentrations of 17 alpha-hydroxyprogesterone (17 alpha OHP) and 17 a'20 alpha-dihydroxy-4-pregnen-3-one (17 alpha 20 alpha OHP) have been measured in sheep during 5 days of ACTH administration at 20 micrograms/kg/day a rate of infusion known to produce hypertension. Five days of ACTH administration produced a progressive increase in plasma 17OHP from 0.45 +/- 0.12 to 128.9 +/- 28.4 nmol/l and in 17 alpha 20 alpha OHP from 0.54 +/- 0.15 to 73.1 +/- 7.2 nmol/l. Calculation of the blood production rate of both steroids during ACTH treatment confirms that the rates of infusion of 17OHP (3.0 mumol/h) and 17 alpha 20 alpha OHP (1.5 mumol/h) used to produce hypertension, when infused together with the other major ovine adrenocortical steroids, produced plasma concentrations in the range as found following administration at a rate to increase blood pressure.

17-alpha-Hydroxyprogesterone↗
PubMed1983

Structural and functional studies of the adrenal zona glomerulosa in sodium-depleted and sodium-loaded sheep.

The effects of alterations in sodium status upon the morphology of the adrenal zona glomerulosa in sheep have been examined qualitatively and quantitatively, using light- and electron microscopy, and correlated with functionally related biochemical data. With severe sodium depletion induced by parotid-cannula drainage, there was mitotic activity throughout the zona glomerulosa, and glandular cells showed striking ultrastructural changes. These changes particularly affected mitochondria, which were enlarged, rounded and showed replacement of their normal lamelliform cristae by thin elongated cristal elements and bundles of tubular "rod-like" structures. Quantitative morphometric studies showed an increase in the volumes of zona glomerulosa cells, nuclei, mitochondria, smooth and granular endoplasmic reticulum, and Golgi profiles. In contrast, with dietary sodium loading, zona glomerulosa cells appeared shrunken and showed cytoplasmic lipid accumulation; mitochondria and other organelles were not significantly altered. The correlation of the ultrastructural cytological alterations in zona glomerulosa cells in sodium-depleted sheep with raised blood aldosterone levels suggests that such morphologic changes reflect a heightened capacity of these cells for aldosterone biosynthesis and secretion. These changes may also account for the increased sensitivity of the zona glomerulosa to aldosterone-producing stimuli during sodium deficiency.

Adrenal Cortex↗
PubMed1983

Blood pressure and metabolic effects of ACTH in normotensive and hypertensive man.

ACTH administration (0.5 mg Synacthen Depot I/M 12 hourly for 5 days) significantly increased systolic blood pressure in normotensive subjects (n=6) and mild essential hypertensives (n=6) but not in 2 Addisonian women, indicating that the pressure rise was adrenally dependent. ACTH administration was associated with urinary sodium retention, hypokalaemia, elevation of fasting blood glucose, lymphopaenia and eosinopaenia. Body weight was increased only in the normotensive subjects. Plasma renin concentration fell and renin substrate rose. Inactive renin fell in the hypertensive subjects only. Plasma cortisol, 11-deoxycortisol, corticosterone, deoxycorticosterone, 17 alpha-hydroxyprogesterone and 17-hydroxy, 20-dihydroprogesterone were all increased by ACTH treatment. Plasma aldosterone rose initially in the normotensives but then fell. ACTH administration in man produces metabolic and hormonal changes similar to those produced by ACTH in sheep but the rise in blood pressure is systolic only in man. The steroid(s) responsible for the blood pressure rise with ACTH in man have not been defined.

Addison Disease↗
PubMed1982

Thromboxane biosynthesis in platelets of diabetic and coronary artery diseased patients.

We have shown that platelets of diabetic patients (D) with coronary artery disease (CAD) produce more thromboxane A2 (TXA2) compared to normal subjects (N), when induced to aggregate with arachidonic acid. The purpose of this investigation was to determine: 1) whether TXA2 biosynthesis in platelets of D without exogenous substrate is increased, 2) whether platelets of D without CAD produce more TXA2 than N and 3) to compare platelet TXA2 biosynthesis in D with those angiographically diagnosed as having CAD but without D. TXB2 (stable metabolite of TXA2) was measured by RIA in platelets of 100 volunteer subjects: 24 D without other clinical complications, 10 D with retinopathy or nephropathy, 7 D with CAD, 30 CAD without D and 11 had D and hypertension. Eighteen subjects had no D, CAD or hypertension. TXA2 synthesis in platelets, stimulated to aggregate with both endogenous and exogenous substrate was higher in all patient classes studied as compared to normal subjects. Plasma triglyceride concentration was higher in diabetics as compared to controls while total cholesterol as well as platelet phospholipid fatty acid distributions were similar in all groups of subjects indicating a similar substrate concentration for TXA2 biosynthesis. It is concluded that platelets of D and CAD with or without D have greater sensitivity to aggregation which might be due to the increased thromboxane synthetase system at one or more sites.

Blood Platelets↗
PubMed1981

[Asp1, Val5] angiotensin-(1-8)octapeptide does not stimulate aldosterone secretion in sodium-depleted sheep.

1. To test the hypothesis that [Asp1,Val5]-angiotensin-(1-8)octapeptide ([Asp1,Val5]ANG II) is a more potent agonist to aldosterone secretion in the sodium-depleted animal than is [Asn1,Val5]angiotensin-(1-8)octapeptide ([Asn1,Val5]ANG II), local adrenal arterial infusion of the two peptides has been carried out in sheep with cervical adrenal autotransplants. 2. Neither [Asp1,Val5]ANG II nor [Asn1,Val5]-ANG II further stimulated the increased level of aldosterone secretion in conscious moderately sodium-depleted sheep. Greater sodium deficiency further increased aldosterone secretion. 3. The conclusion of Campbell, Schmitz & Itskovitz [Clinical Science (1979), 56, 325-333] that the free acid form of angiotensin II was a more potent agonist of aldosterone secretion than was the amide form under conditions of reduced sodium status is not supported by studies in sodium-depleted sheep.

Aldosterone↗
PubMed1981

Blood pressure, renal and metabolic effects of ACTH in normotensive man.

1. The blood pressure, renal and metabolic effects of adrenocorticotropic hormone (ACTH) have been studied in six normotensive subjects and two patients with Addison's disease on maintenance steroid therapy. 2. In normotensive subjects, 5 days ACTH treatment (0.5 mg 12 hourly) was associated with a rise in systolic blood pressure and mean arterial pressure. There was a small rise in diastolic pressure but no consistent change in heart rate. Plasma sodium increased and plasma potassium fell. Serum creatinine and urea concentrations were unchanged. Fluid intake increased and urine output was unchanged but ACTH withdrawal was associated with a diuresis. There was an initial reduction in urinary sodium excretion and a natriuresis after ACTH withdrawal. Plasma volume and body weight rose. 3. ACTH produced increases in plasma cortisol, 11-deoxycortisol, corticosterone, deoxycorticosterone, aldosterone, 17 alpha-hydroxyprogesterone and 17 alpha,20 alpha-dihydroxyprogesterone. Plasma renin concentration fell. 4. Patients with Addison's disease showed no change in blood pressure or in any other metabolic variable studied. 5. The effects of ACTH in man resembled those found in sheep.

Adolescent↗
PubMed1981

Dopaminergic modulation of aldosterone secretion?

Metoclopramide (10 mg i.v. injection followed by 10 mg/h i.v. for 2 h) caused a transient rise in blood concentrations of aldosterone in sodium-replete and sodium-depleted sheep. Infusion of metoclopramide into the adrenal artery of sheep with an autotransplanted adrenal gland, at a rate to give a similar concentration of metoclopramide at the adrenal cell level (calculated from rate of infusion and adrenal blood flow), resulted in no alteration in aldosterone secretion rate in either sodium-replete or sodium-deplete animals, even though intravenous metoclopramide caused transient stimulation of aldosterone secretion in the same sheep when sodium replete. Dopamine administered either into the adrenal arterial blood supply or intravenously had no significant effect on aldosterone secretion and did not reverse the stimulatory effects of angiotensin II on aldosterone secretion in the adrenal transplant. The data do not support the suggestion that direct dopaminergic elements play a tonic inhibitory role in aldosterone secretion. It is possible that the agonist effect of metoclopramide on aldosterone secretion may occur by some non-dopaminergic mechanism and it is tempting to speculate that the effect is centrally mediated.

Adrenal Glands↗