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Biomedical subjects

A Butkus

Publications and source records attributed to A Butkus.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1980

Cushing's syndrome due to an ACTH-secreting adrenal medullary tumour.

A 35-year-old man with Cushing's syndrome due to ectopic ACTH production is described. The six-week history and severe proximal myopathy were highly suggestive of a malignant tumour, but a solitary phaeochromocytoma of the left adrenal gland was the source of ACTH production. The surgical outcome was successful and three months post-operatively the hypothalamic-pituitary-adrenal axis was normal. At 12 months follow-up he remains well with complete regression of the features of Cushing's syndrome.

Adrenal Gland Neoplasms↗
PubMed1980

Biosynthetic ad morphological evidence for inhibition of aldosterone production following administration of ACTH to sheep.

The effect of ACTH administration for 1-5 days on the morphology and steroidogenic capability of sheep adrenal tissue has been examined. During this period of treatment there was a gradual decline in the in vitro conversion of 3H-labelled precursors to products of solely zona glomerulosa origin (aldosterone and 18-hydroxycorticosterone) while conversion to products of zona fasciculata origin (17-hydroxyprogesterone, 11-deoxycortisol and cortisol) was stimulated throughout. Conversion to DOC, 18-hydroxydeoxycorticosterone and corticosterone (steroids produced by both the zona glomerulosa and the zona fasciculata) declined after initial stimulation. Within 2--3 days of the commencement of treatment, the zona glomerulosa showed a progressive decrease in cell number associated with disruption of cords and cell separation. Ultrastructurally, it was found that typical zona glomerulosa cells had almost disappeared. The majority of residual cells in this area had a structure intermediate between zona glomerulosa and zona fasciculata cells. The similarity in time-course of the alterations in both the morphological and biosynthetic characteristics suggests that the decline in aldosterone output caused by ACTH administration to sheep results from the loss of adrenal zona glomerulosa cells, predominantly due to selective cellular degeneration.

18-Hydroxycorticosterone↗
PubMed1979

Blood pressure and metabolic effects of 9-alpha-fluoro-hydrocortisone in sheep.

9 alphafluorohydrocortisone (9 alphaFF) is an analogue of hydrocortisone with both 'mineralocorticoid' and 'glucocorticoid' activity. 9 alphaFF was infused at 0.2, 0.63 and 2.0 mg/day for 5 days to intact conscious trained sheep. At high dose (0.63 and 2 mg/day) 9 alphaFF raises blood pressure in sheep, (mean arterial pressure rise 32 and 29 mm Hg respectively on the fifth day), lowers plasma [K], raises plasma [Na] and produces initial urinary sodium retention. At low dose (0.2 mg/day) blood pressure is raised (+16 mm Hg on day 5) but plasma and urinary electrolytes are unaltered. 9 alphaFF had no effect on water intake or urine output at any dose. In all animals withdrawal of 9 alphaFF was associated with a natriuresis. On the basis of its affinity for 'mineralocorticoid' and 'glucocorticoid' ovine renal receptors, 9 alphaFF at low dose may raise blood pressure by mechanisms not simply related to its 'glucocorticoid' and/or 'mineralocorticoid' action.

Aldosterone↗