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S Carney

Publications and source records attributed to S Carney.

At least 37 records · Page 2Linked to original sources
PubMed1993

Somatostatin as a modulator of distal nephron water permeability.

1. Experiments in vivo and in vitro were performed in the rat to define the role of somatostatin in modulating the hydro-osmotic action of arginine vasopressin. 2. Somatostatin had a biphasic effect on basal collecting duct diffusional water permeability with 10(-9) mol/l somatostatin producing a 14% reduction in permeability, whereas concentrations of 10(-6) and 10(-5) mol/l significantly increased basal water permeability by 13% and 22%, respectively. Somatostatin (10(-9) mol/l) also inhibited the increase in water permeability produced by arginine vasopressin, although this inhibitory effect was reduced by a 10-fold increase in arginine vasopressin concentration (5 ng/ml). 3. In the anaesthetized water-diuretic rat, low dose somatostatin (60 micrograms/h) increased free water clearance by 23% (P < 0.01), whereas increasing the somatostatin concentration (600 micrograms/h) produced a transitory 40% fall in free water clearance (P < 0.01). As in the experiment in vitro, somatostatin inhibited the action of arginine vasopressin, although a very high concentration of arginine vasopressin (250 ng/h) partly overcame this effect. 4. Glomerular filtration rate and renal electrolyte excretion (sodium, potassium, calcium, magnesium) were not altered by somatostatin, although renal inorganic phosphate excretion was increased. The papillary solute gradient was unaltered by somatostatin. 5. These results suggest that circulating somatostatin may have a physiological role in modulating distal nephron water transport with a low concentration directly inhibiting and a high concentration facilitating water transport. There is also evidence of competitive binding between somatostatin and arginine vasopressin which antagonizes the hydro-osmotic action of arginine vasopressin.

Animals↗
PubMed1993

What syndrome is this? Sjögren-Larsson syndrome.

Sjögren-Larsson syndrome is an inborn error of metabolism with its primary clinical manifestations being congenital ichthyosis, spastic hemiplegia or quadriplegia, and moderate to severe mental retardation. Definitive diagnosis can be made by measuring fatty aldehyde dehydrogenase activity in cultured skin fibroblasts. Treatment of dermatologic manifestations is best accomplished with topical emollients and frequent bathing or showering. Some evidence supports medium-chain triglyceride diets and oral retinoids. These modalities, however, remain controversial.

Child↗
PubMed1993

Hypertension education: patient knowledge and satisfaction.

Education of patients with various diseases, including hypertension, usually occurs at an individual level through a patient's doctor as well as via various media campaigns which also includes general community education. To evaluate their effects, the knowledge of 84 patients with hypertension was evaluated by a simple 13 question true/false questionnaire and the results compared with 58 normotensive subjects matched for sex, age and educational status. A significant difference in knowledge about hypertension could not be elicited between the two groups even when compared for sex or educational status. However, subjects > 70 years of age (hypertensives and controls) demonstrated a lower level of knowledge (P < 0.05). Further questioning of the hypertensive group elicited a high level of satisfaction with their doctor's educational skills (68%) and 57% were satisfied with their own knowledge. Nevertheless, 70% requested more information about their disease. These results suggest a reasonable level of knowledge within the general community presumably reflecting community education programmes. While hypertensive patients were not more knowledgeable under the test conditions, they were reasonably satisfied with their knowledge which they stated came primarily from their doctor. Nevertheless, these findings question the effectiveness of some current patient education initiatives.

Female↗
PubMed1990

A mycobacterial 65-kD heat shock protein induces antigen-specific suppression of adjuvant arthritis, but is not itself arthritogenic.

A recombinant (r)65-kD protein from Mycobacterium leprae, at levels far in excess of those present in whole mycobacteria, was unable to induce arthritis. Even when combined with a synthetic adjuvant, CP20961, to mimic the peptidoglycan adjuvant component of the mycobacterial cell wall, the r65-kD protein failed to induce arthritis. Pretreatment with as little as 1 microgram r65-kD protein protected rats against arthritis induced by M. tuberculosis, but this r65-kD protein was markedly less able to protect against arthritis induced by the synthetic adjuvant, CP20961, or type II collagen. The r65-kD protein appears, therefore, to produce an antigen-specific protection against arthritis induced by bacterial cell walls containing the 65-kD protein. Such protection can be overcome, however, by arthritogenic T lymphocytes, suggesting that protection occurs by preventing clonal proliferation of autoreactive T lymphocytes that are induced by the adjuvant properties of mycobacterial cell walls. How the r65-kD protein abrogates this particular adjuvant activity, and the nature of the arthritogenic self antigen(s), remain to be elucidated.

Animals↗
PubMed1990

Monoclonal antibodies and arthritis.

Monoclonal antibodies to certain cell surface constituents on lymphocytes, monocytes and macrophages have been administered to Lewis rats with developing, established or adoptively transferred arthritis, to determine any immunomodulatory properties. Anti-CD4 antibodies against helper T-lymphocytes produced a dose related inhibition of developing arthritis; high dose levels completely suppressed all symptoms of arthritis and these rats were resistant to further attempts to induce arthritis. Anti-Ia (MHCII) antibodies also inhibited arthritis in a dose related manner; anti-pan T antibodies delayed the onset of arthritis, but antibodies against CD8 and IL-2 receptor positive cells were without effect. Development of type II collagen-induced arthritis was also inhibited by anti-CD4 treatment. Established arthritis could be temporarily inhibited by anti-CD4 antibodies, but rebound of arthritis invariably occurred after stopping treatment, as is the case with cyclosporin A. Similar results with anti-CD4 antibodies were obtained during treatment of arthritis adoptively transferred by arthritogenic T-lymphocytes. From these experiments it is clear that CD4 positive T-lymphocytes have a major role in the induction of adjuvant arthritis and that interaction between CD4 and Ia bearing cells is important. The rebound of arthritis that occurred after withdrawal of anti-CD4 treatment during established disease infers that cells in addition to helper T-lymphocytes are involved in the chronicity of arthritis, but these remain to be elucidated. These findings are discussed in relation to results with monoclonal antibodies in other models of arthritis and human rheumatoid arthritis; the prospects for human therapy are also discussed.

Animals↗
PubMed1989

Hypertension and asthma: psychological aspects.

Essential hypertensive and asthmatic patients, plus normal non-clinical controls, were compared on a number of psychological measures in order to identify the relationship between psychological distress, coping strategies and compliance behaviour. The hypothesised relationship between chronic clinical ailments and psychological distress was confirmed. The association between the presence of physical symptoms in the symptomatic condition, asthma, and greater psychological distress was also confirmed. The coping strategies adopted by the patients did not discriminate between the two clinical groups. Compliance with medication was negatively correlated with measures of psychological distress. Compliance with an appropriate healthy lifestyle was not correlated with medication compliance, although it too was negatively correlated with other measures of psychological distress.

Adaptation, Psychological↗
PubMed1984

Lithium administration and urinary electrolyte excretion in the rat.

The effect of lithium administration on urine eletrolyte excretion is controversial with reports of increased, unaltered and reduced excretion rates of sodium, potassium, calcium, magnesium and inorganic phosphate. Therefore rats treated with daily intraperitoneal lithium chloride for 3 weeks were studied and were found to have marked fluctuations in electrolyte excretion when compared to untreated rats. Although lithium-treated rats were always polyuric, urinary sodium, potassium and calcium excretion was significantly elevated immediately following intraperitoneal lithium but their excretion rates then returned towards normal. Magnesium excretion was initially unaltered by lithium administration (6.8 +/- 1.3 compared with 7.3 +/- 1.7 mumol/100 g/8 h) but then decreased (2.5 +/- 0.5 with 7.8 +/- 1.1 mumol of magnesium/100 g/8 h; p less than 0.01) during the final collection period. A persistent phosphaturia also occurred with lithium treatment (122 +/- 5 compared with 92 +/- 6 mumol/100 g body weight/24 h). Despite these significant changes in renal electrolyte transport with lithium administration, similar changes were also noted in rats similarly treated with equimolar doses of sodium chloride although polyuria did not occur. Thus it is postulated that lithium ions exert their effect on renal electrolyte transport in a similar manner to that of sodium.

Animals↗
PubMed1983

Effect of calcitonin on urine concentration in the rat.

Because mammalian distal nephron segments with both calcitonin- and antidiuretic hormone- (ADH) sensitive adenylate cyclase activity have been described, in vivo and in vitro experiments were performed to study the effect of calcitonin on rat distal nephron water permeability. Calcitonin 1 and 0.1 U/ml, but not 0.01 U/ml, significantly increased the diffusional water permeability in the isolated papillary collecting duct by 15 and 11%, respectively. However, this effect was small when compared with a 68% increase with a supramaximal concentration of ADH (from 4.0 +/- 0.3 to 6.7 +/- 0.9 microns/s; n = 6, P less than 0.01). The normal increase in water permeability with increasing concentration of ADH (0.02 and 0.2 mU/ml) was depressed by the previous addition of calcitonin (1 U/ml) to the bath but was unaltered with the supramaximal ADH concentration (2 mU/ml). Verapamil, a compound that antagonizes cellular calcium entry, did not alter the effect of calcitonin on diffusional water permeability. Calcitonin in concentrations of 0.05, 0.5, and 5 U/ml produced a significant reduction in urine flow and free water clearance. Pretreatment with calcitonin in these concentrations inhibited the antidiuretic action of ADH. These studies suggest that calcitonin acts as a partial agonist to ADH within the distal nephron. It is unclear whether such an action represents a physiological or a pharmacological effect.

Animals↗
PubMed1982

Effect of differing concentrations of parathyroid hormone on rat renal electrolyte excretion.

Urinary clearance studies were performed on acutely thyroparathyroidectomized rats to study the effect of a range of parathyroid hormone (PTH) concentrations on renal electrolyte transport. PTH 0.1 U, prime and per hour, significantly increased the plasma calcium concentration, yet fractional calcium excretion was increased by 47.5% and inorganic phosphate excretion remained unaltered. PTH 1 U produced a similar increase in the plasma calcium concentration. However, urinary calcium excretion was unchanged when compared with control animals and a small phosphaturia occurred (from 0.1 +/- 0.1 to 0.8 +/- 0.2%; P less than 0.05). PTH 10 U decreased fractional calcium excretion by 50% and increased fractional phosphate excretion from 0.4 +/- 02. to 19.4 +/- 1.7% (P less than 0.01). Changes in urinary magnesium excretion were similar to those of calcium, being increased with the lowest PTH concentration yet decreased with a 100-fold increase in PTH concentration. These data suggest that PTH, at a low physiological concentration that acts on bone, does not directly alter renal electrolyte handling. High physiological concentrations of PTH, however, produce a brisk phosphaturia and reduce calcium and magnesium excretion. A reappraisal of the accepted role of PTH on renal calcium conservation is therefore required.

Animals↗
PubMed1981

Acute effect of calcitonin on rat renal electrolyte transport.

Renal clearance studies were performed on parathyroid-intact and acutely thyroparathyroidectomized (TPTX) rats to clarify calcitonin (CT) action on renal electrolyte transport. Although CT (0.15 U x 100 g body wt-1 x h-1) reduced fractional excretion of calcium and magnesium by 72 and 46%, respectively, in TPTX rats without altering sodium and phosphate excretion, a 10-fold increase in CT (1.5 U) caused a smaller reduction in calcium and magnesium excretion and significantly increased sodium and phosphate excretion. A higher CT dose (15 U) did not alter calcium excretion, increased magnesium excretion, and caused an even greater increase in sodium and phosphate excretion. Results in parathyroid-intact animals were similar. Despite the fall in plasma calcium following CT administration, the filtered calcium load was unaltered due to a concomitant increase in glomerular filtration rate. Calcium infusion prior to CT (0.15 U) prevented a detectable fall in plasma calcium concentration. However, a 45% fall in fractional calcium excretion occurred despite the significant increase in filtered calcium. These data suggest that the physiological role of calcitonin on the nephron is to conserve calcium. Reports of increased electrolyte excretion presumably reflect a depressant effect of pharmacological doses of CT on nephron function.

Animals↗
PubMed1979

Treatment of mild hypertension in elderly males.

1. Males, born between 1900 and 1925, with mild hypertension have been treated for periods varying from 300 to 2000 days. 2. The life and death status of all patients (except two) was known on 1st November 1978. 3. A group of patients with mild hypertension receiving treatment based on a thiazide diuretic had a greater mortality than the other drug-treated group. 4. The increased mortality was caused by an increased number of myocardial infarcts. 5. Elderly male patients with mild hypertension probably have preexisting vascular disease and therapy should not automatically be started. If therapy is started, beta-adrenoreceptor-blocking drugs may be a preferred therapy.

Adrenergic beta-Antagonists↗