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Biomedical subjects

S L Carney

Publications and source records attributed to S L Carney.

69 records · Page 4Linked to original sources
PubMed1984

Effect of dietary sodium restriction on patients receiving antihypertensive medication.

Twenty-four patients receiving medication for moderate to severe hypertension were studied during a six week normal diet and a six week low sodium period. Mean urinary sodium excretion was reduced from 169 +/- 13 to 92 +/- 7 mmol/24 hour yet with the exception of a small reduction in the mean erect systolic blood pressure 140.7 +/- 2.5 to 135.1 +/- 2.6; p less than 0.05) no significant alteration in the patients blood pressure was noted. Urinary potassium excretion and body weight remained unaltered. However, evaluation of the patient data when the patients were grouped into those taking thiazide diuretics (n = 14) and those not taking diuretics (n = 10) revealed a significant reduction in the mean supine systolic and diastolic and erect systolic blood pressure in the thiazide group. Significant changes in blood pressure were not recorded in the non-diuretic group. It is suggested that moderate dietary sodium restriction in combination with thiazide diuretics is of value in the treatment of moderate to severe hypertension.

Adult↗
PubMed1981

Relationship between plasma and cellular potassium content during potassium repletion.

The simultaneous effect of two weeks of potassium repletion therapy on the plasma concentration and total body content of potassium was assessed in seven patients with hypokalaemia. Glomerular filtration rate, renal plasma flow, and maximal urinary concentration were also measured both before and after therapy with potassium chloride. While the plasma potassium concentration quickly returned to normal, total body content of potassium remained depressed, emphasizing the unreliability of the plasma potassium concentration as an indicator of total body potassium status. Parameters of renal function measured in this study, which were depressed by potassium depletion, also did not alter with correction of the plasma potassium level. This suggests that these functions are primarily affected by cellular potassium content.

Aged↗
PubMed1981

Effect of magnesium deficiency and excess on renal tubular potassium transport in the rat.

1. Dietary magnesium deficiency is commonly associated with significant potassium depletion although the mechanisms responsible are unknown. Because the kidney has an important role in both magnesium and potassium homeostasis, clearance and micropuncture experiments were performed on thyroparathyroidectomized magnesium-deficient, normal and hypermagnesaemic rats to study the effect of body magnesium status on renal potassium handling. 2. Dietary magnesium restriction that reduced total-body magnesium by 30% did not alter renal potassium excretion despite a 10% reduction in total-body potassium. Graded magnesium infusions increased the fractional excretion of potassium in both magnesium-depleted and normal rats. However, the increase in the dietary depleted group was significantly less than in the control group (5-10 and then 13% compared with 7-19 and then 28% respectively). These changes in urine potassium excretion followed alterations in distal-tubule function. Parathyroid hormone did not alter potassium excretion in any of the experimental groups in contrast with its effect on magnesium excretion. 3. These data support the concept of distal tubular control of renal potassium homeostasis. The body magnesium status appears to exert some control over cellular potassium content and to alter indirectly distal-tubule potassium excretion.

Animals↗
PubMed1980

Effect of parathyroid hormone on renal calcium and magnesium reabsorption in magnesium deficient rats.

Tubular magnesium reabsorption was investigated by recollection micropuncture and in vivo microperfusion techniques in acutely thyroparathyroidectomized rats made magnesium deficient by dietary deprivation. Henle's loop which normally reclaims the major portion of filtered magnesium was examined by elevation of intraluminal magnesium concentration. The transport capacity in these conditions was significantly lower in magnesium deficient rats (41%) compared to normal animals (71%) at comparable magnesium delivery rates. Acute infusion of MgCl2 further depressed loop magnesium reabsorption independent of intraluminal magnesium delivery. Parathyroid hormone did not alter magnesium transport capacity in magnesium deficient rats but resulted in enhanced transport in acutely hypermagnesemic deficient rats. Calcium reabsorption followed a similar qualitative pattern as magnesium with respect to loop function and urinary excretion. These results are consistent with a depressed transport capacity for magnesium in the loop of Henle of magnesium deficient rats which is independent of intraluminal magnesium delivery and circulating parathyroid hormone level.

Absorption↗
PubMed1980

Effect of magnesium deficiency on renal magnesium and calcium transport in the rat.

Recollection of micropuncture experiments were performed on acutely thyroparathyroidectomized rats rendered magnesium deficient by dietary deprivation. Urinary magnesium excretion fell from a control of 15 to 3% of the filtered load after magnesium restriction. The loop of Henle, presumably the thick ascending limb, was the major modulator for renal magnesium homeostasis. The transport capacity for magnesium, however, was less in deficient rats than control animals. Absolute magnesium reabsorption increased with acute infusions of magnesium chloride but was always less in magnesium-deficient rats than control rats for any given filtered load, which suggests either a defect of a resetting of the reabsorption mechanism. Recollection micropuncture demonstrated that this was a characteristic of the loop of Henle. Proximal magnesium reabsorption remained unchanged at 15% of the filtered load and was unaffected by magnesium deficiency or acute magnesium repletion. Distal tubular magnesium reabsorption was limited during depletion and increased to a similar extent in control and deficient rats with enhanced magnesium delivery. Calcium reabsorption was not altered in magnesium deficiency; however, elevations of extracellular magnesium resulted in a specific inhibition of calcium reabsorption within the loop of Henle. These data suggest that overall control of renal magnesium reabsorption occurs within the loop of Henle and that the proximal tubule reabsorbs a constant fraction of the filtered load despite variations in body magnesium status.

Animals↗
PubMed1980

Effect of lithium treatment on rat renal tubule function. Evidence against impaired antidiuretic hormone action.

Micropuncture and clearance studies were performed on normal untreated and polyuric lithium chloride treated rats (10-12 days). A persistent hypernatremic state quickly developed in the polyuric lithium treated rats during hydropenia resulting from an increased urinary loss of water over sodium chloride, as the fractional excretion of sodium remained at control levels. Superficial proximal tubule and loop of Henle fluid reabsorption was depressed by 8 and 17%, respectively, in lithium-treated rats during this period. By contrast, water reabsorption in the distal tubule and collecting system was significantly increased in the lithium animals, being 27% of the filtered load compared with 20% in normal rats. These results suggest that the urinary-concentrating defect induced by lithium treatment is due primarily to a depression of proximal tubule and possibly loop of Henle function, and that water reabsorption within the distal nephron may in fact be augmented: thus it is unlikely that the action of antidiuretic hormone is significantly impaired. Marked phosphaturia and hypocalciuria were also noted in the lithium-treated rats.

Animals↗
PubMed1979

Acute effects of streptozotocin diabetes on rat renal function.

Renal clearance studies were performed on rats both during the administration of streptozotocin and sequentially during the following 8 days as hyperglycemia progressed. Although GFR was depressed 30 min after the drug administration, GFR steadily rose during the following days to become 52% greater than control levels. Renal size did not change during this short period, and it is suggested that glomerular hemodynamic changes are responsible. A maximal tubular reabsorptive capacity for glucose (TmG) could not be satisfactorily demonstrated in normal rats, although glucose reabsorption was significantly depressed at high-filtered loads. At comparable filtered loads, glucose reabsorption in diabetic rats was almost complete in contrast to normal rats, and the increases in GFR and renal tubular sodium reabsorption are presumed to be the major factors. The administration of insulin to normal and diabetic rats was followed by a significant diuresis as well as an increase of 1% to 4% in the fraction of filtered sodium excreted although GFR was unaltered. This shows that even a 35% to 60% reduction in the filtered load of glucose can significantly depress renal sodium reabsorption. It is concluded that this is a good animal model in which to study the effects of diabetes on renal function as well as the in vivo interrelationships of sodium and glucose reabsorption.

Animals↗
PubMed1975

Beta-adrenergic receptor blocking drugs, hypertension and plasma renin.

1 Propranolol and pindolol reduced both the blood pressure and plasma renin activity when given chronically to hypertensive patients. 2 There was no correlation between the fall in blood pressure and the fall in plasma renin activity. 3 Neither the basal nor the random plasma renin activity predicted the patients who would respond to beta-adrenergic receptor blocking drugs. 4 Oral propranolol reduced plasma renin activity but did not reduce blood pressure within 4 h of administration; oral pindolol reduced blood pressure but did not reduce plasma renin activity within 4 h of administration. 5 The reduction of blood pressure by propranolol and pindolol does not seem to be mediated by changes in plasma renin in most patients.

Adult↗
PubMedDate not supplied

Adjunctive effect of salt restriction on antihypertensive efficacy.

The effect of dietary salt restriction on blood pressure was measured in patients with moderate hypertension receiving antihypertensive medication. Patients were studied during a randomly allocated 6 week period of moderate dietary salt restriction and during a 6 week period of normal diet. Twenty-four of twenty-eight patients achieved a reduction of salt excretion exceeding 20%. In these patients mean urinary sodium excretion fell from 169 (s.e.m. = 13) mmol/24 h to 92 (s.e.m. = 7) mmol/24 h. Potassium excretion and body weight did not change, and with the exception of the erect systolic pressure, there was no overall change in blood pressure. When the data were grouped according to the patient medication, mean supine systolic pressure fell from 148.9 (s.e.m. = 4.4) to 140.3 (s.e.m. = 5.0) mmHg (n = 14, P greater than 0.05) and mean supine diastolic pressure fell from 100.8 (s.e.m. = 2.9) to 97.0 (s.e.m. = 2.8) mmHg (n = 14, P greater than 0.05) in patients taking diuretics. Blood pressure did not change in patients whose medication did not include diuretics. Moderate dietary salt restriction may be therapeutically useful in patients with moderate hypertension treated with diuretics but is of little value in those not receiving diuretics.

Blood Pressure↗
PubMedDate not supplied

Mechanism of action of natriuretic fraction of urine.

The nature of calcium dependence of natriuretic fraction (NF)-induced contractions in the rat smooth muscle anococcygeus and a possible correlation between the effect of NF on sodium transport and its natriuretic potency was investigated. NF and noradrenaline-induced contractions were partially dependent on external calcium concentration. Ouabain and potassium (K) free solution (KoPSS)-induced contractions were totally dependent on external calcium and were more effectively inhibited by calcium antagonists than those of NF and noradrenaline suggesting pharmacomechanical coupling as the mode of calcium dependence of NF. Like other agonists which contract by pharmacomechanical coupling, NF stimulated sodium transport (86rubidium uptake) in dog saphenous vein. Such stimulation correlated positively (r = 0.495, n = 17, P less than 0.05) with the natriuretic potency of NF. NF, like noradrenaline, contracts smooth muscle by pharmacomechanical coupling and NF-induced natriuresis is associated with stimulation of the sodium pump.

Animals↗
PubMedDate not supplied

Chronic calcitonin administration and renal calcium transport in the rat.

1. While calcitonin (CT) has now been clearly demonstrated to be a renal Ca2+-conserving hormone and may share similar transport mechanisms with parathyroid hormone (PTH), the effect of prolonged CT exposure on renal Ca2+ transport has not been evaluated. 2. Consequently, a submaximal and maximal Ca2+-conserving concentration of human CT was infused into groups of anaesthetized acutely thyroparathyroidectomized rats that had been treated with twice daily subcutaneous human (h) CT at a low or high dose or vehicle for 12 days. 3. The maximal hCT infusion (10 microg bolus and per hour) produced a marked inhibitory effect on renal Ca2+ excretion in vehicle-treated rats, with the fractional excretion rate of Ca2+ being reduced from 4.49+/-0.31 to 139+/-0.23% (P<0.001). However, in rats pretreated with high concentrations of hormone (0.25 microg hCT) twice daily for 12 days, marked Ca2+ conservation was measured (fractional excretion 1.09+/-0.18%), which was not altered by the additional intravenous administration of maximal hCT. 4. Renal Mg2+ transport was similarly altered by hCT administration, without any evidence that prolonged CT inhibited renal Mg2+ transport. The increase in glomerular filtration rate caused by hCT also appeared to persist with repeated hormone administration. The fractional excretion of Na+ and PO4 was significantly increased by high- but not low-dose hCT treatment and was not altered by the addition of a maximal hormone dose at day 12. 5. The present study failed to demonstrate any down-regulation of the response to prolonged hCT administration when renal Ca2+ and Mg2+ transport was measured. If renal escape does occur with CT, as has been suggested but not proven with PTH, other mechanisms, such as hormone production or release, may be responsible.

Animals↗
PubMedDate not supplied

Effect of calcitonin on hemodialysis patients with hypercalcemia and renal osteodystrophy.

Because calcitonin administration has been shown to decrease the serum calcium level in certain hypercalcemic conditions, 10 patients on maintenance dialysis with renal osteodystrophy and persistent hypercalcemia were treated with salmon calcitonin for 3 months. While plasma calcium concentrations were reduced by calcitonin therapy in four patients, therapy was ceased in two patients due to a worsening of their hypercalcemia, although in another two patients the initial worsening of the hypercalcemia settled with continued therapy. No significant changes in calcium levels occurred in the remaining two patients. Analysis of the data suggests that a hypocalcemic effect of calcitonin was most likely in the presence of osteomalacia, while predominant osteitis fibrosa favored a hypercalcemic response. Calcitonin administration caused a mean increase in parathyroid hormone (PTH) secretion 3.6 +/- 1.5 to 6.5 +/- 1.7 ng/ml; p less than 0.05) after 6 weeks of therapy. Three patients reported improvement in their bone pain. These studies show that despite possible symptomatic and morphological effects of calcitonin, its hypocalcemic effect in patients with renal osteodystrophy and hypercalcemia is inconsistent.

Alkaline Phosphatase↗