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Biomedical subjects

F C Bartter

Publications and source records attributed to F C Bartter.

At least 55 records · Page 3Linked to original sources
PubMed1980

Commentary.

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Adrenocorticotropic Hormone↗
PubMed1980

Influence of unilateral adrenalectomy on renin-angiotensin-aldosterone system in primary aldosteronism.

In a study of 14 patients (11 Japanese and 3 white North Americans) with aldosterone-producing tumor carried out within 2 to 4 weeks after unilateral adrenalectomy, both plasma renin activity (PRA) and plasma aldosterone concentration (PAC) increased almost normally with short-term sodium depletion and upright posture. Aldosterone excretion rate (AER) also increased significantly with sodium depletion, and was normally suppressed by sodium loading. Highly significant correlations were observed between PRA and PAC (r=0.89, p < 0.001) or AER (r=0.88, p < 0.001) ater operation, whereas there had been no such correlation before operation. Either physiological or laboratory findings were normalized or markedly improved in all cases although pathohistological diagnosis was made as adenomatous hyperplasia in 10 out of 11. These results indicate that within 4 weeks of operation PRA and the remaining adrenal gland can almost normally respond to stimuli such as sodium depletion and upright posture regardless of the amount of spironolactone given preoperatively.

Adrenal Gland Neoplasms↗
PubMed1979

Prostacyclin overproduction in Bartter's syndrome.

Urinary excretion of 6-keto-prostaglandin F1alpha and thromboxane B2, the major metabolites of prostacyclin and of thromboxane A2, respectively, was measured by specific radioimmunoassays in five female patients with Bartter's syndrome and in five normal female controls. The patients with Bartter's syndrome excreted about four times as much 6-keto-PGF1alpha as the controls; their excretion of thromboxane B2 was no different from that of the controls. These data suggest that overproduction of prostacyclin mediates both the hyper-reninaemia and the hyporesponsiveness of blood-pressure to pressor agents in Bartter's syndrome.

Adolescent↗
PubMed1979

Effects of prostaglandin E1 on the metabolism in rat parathyroid gland in vitro.

We investigated some effects of prostaglandin E1 on the metabolism of rat parathyroid glands using a culture system containing basal Eagle's medium supplemented with 5--10% heat-inactivated rat serum. Rat parathyroid glands incorporate [3H]fucose and 14C-labeled amino acids into cellular glycoproteins and secrete some of these into the culture medium. Gel filtration chromatography separates these glycoproteins into three classes, the smallest of which (peak 3) is secreted with immunoreactive parathyroid hormone. In cultures of 48 h, prostaglandin E1 (1 microgram/ml) specifically inhibits the secretion of peak 3 and of parathyroid hormone but has no effect on the incorporation of [3H]fucose, 14C-labeled amino acids, or [3H]uridine into parathyroid glands. Cytochalasin B inhibits the secretion of parathyroid hormone and the incorporation of isotopic fucose and amino acids. Cortisol stimulates incorporation of [3H]fucose and the secretion of parathyroid hormone even in the presence of inhibitory doses of prostaglandin E1. It is concluded that, in organ culture, prostaglandin E1 inhibits the secretion of parathyroid hormone and of a specific glycoprotein the function of which may be related to the secretion of the hormone.

Amino Acids↗
PubMed1979

Responses of plasma renin activity and dopamine-beta-hydroxylase to increased intravascular volume.

Circadian variations of plasma renin activity, plasma dopamine-beta-hydroxylase, and urinary aldosterone excretion were measured in man under conditions of high- and low-sodium intake. Plasma renin activity and urinary aldosterone excretion were maximal at 8 a.m. Plasma DBH shows small, biologically insignificant circadian fluctuations. In three subjects on low-salt diets, the values were lower than those in the same subjects on high-salt diets. Expansion of intravascular volume in supine normal volunteers lowered plasma renin and DBH activity, and also resulted in a significant natriuresis. The decline in DBH activity probably reflects a decrease in its release from autonomic nerve endings and thus demonstrates in man an effect of decreasing autonomic activity.

17-Hydroxycorticosteroids↗
PubMed1979

Prolactin in primary aldosteronism.

1. This study was done to examine the possibility that escape from the sodium retention produced by aldosterone may be associated with an inhibition of prolactin secretion. Plasma prolactin concentrations were determined in seven patients with adrenal adenoma and aldosteronism, before and after unilateral adrenalectomy, at a time when they were in balance on a sodium intake of 109 mmol/day. 2. After operation, plasma aldosterone was normal [before operation, 52.7 +/- 12.1 (supine), 64.6 +/- 9.1 ng/dl (upright); after operation, 6.8 +/- 1.5 (supine), 11.1 +/- 3.0 ng/dl (upright)], while plasma prolactin remained unchanged [before operation, 19.6 +/- 2.8 (supine), 15.5 +/- 3.3 ng/ml (upright); after operation, 23.8 +/- 2.3 (supine), 11.1 +/- 3.0 ng/ml (upright)]. 3. Our results do not support a role for prolactin in the renal response to aldosterone in man.

Adrenalectomy↗
PubMed1979

Interrelationship between acetylcholine and prostaglandins in the control of sodium excretion and renin secretion in anesthetized dogs. I.

The interrelationships between acetylcholine (ACH) and prostaglandins in the control of sodium excretion (UNaV) and of renin secretion (RS) were examined in unilaterally-nephrectomized, anesthetized dogs with or without treatment with indomethacin, an inhibitor of prostaglandin synthetase. Inrarenal infusion of ACH (40 microgram/min) in control animals produced diuresis and natriuresis. UNaV was 9.2 +/- 3.1 muEq/min during control periods and was 74.7 +/- 31.6 muEq/min after 40 min of infusion of ACH (p less than 0.05). UNaV was still 48.0 +/- 16.8 muEq/min after 100 min of infusion of ACH (p less than 0.05). RS rate was 930.6 +/- 188.5 U/min during control periods, and was 737.4 +/- 220.3 U/min after 100 min of infusion of ACH (p greater than 0.1). In the dogs treated with indomethacin, the natriuresis produced by ACH could not be sustained. UNaV was 46.6 +/- 12.1 muEq/min before and was 34.7 +/- 12.8 muEq/min 100 min following the infusion of ACH (p greater than 0.1). Arterial plasma renin activity was 3.29 +/- 0.83 ng/ml/h before and was 20.97 +/- 7.78 ng/ml/h after 100 min of infusion of ACH (p less than 0.025). The data suggest that prostaglandins are involved in the sodium excretion and the renin secretion produced by acetylcholine.

Acetylcholine↗
PubMed1979

Effect of indomethacin on renal function and plasma renin activity in dogs with chronic renovascular hypertension.

The effect of indomethacin on plasma renin activity (PRA) and renal function was examined in conscious dogs with chronic renovascular hypertension before or after volume expansion. PRA did not change following the infusion of indomethacin: PRA was 5.18 +/- 1.46 ng/ml/h during control periods and was 5.01 +/- 0.95 ng/ml/h (p greater than 0.1) after 80 min of infusion of indomethacin. Mean arterial blood pressure (MABP) was 121.6 +/- 7.4 mm Hg during control periods and was 122.0 +/- 4.6 mm Hg (p greater than 0.1) after 80 min of infusion of indomethacin. Infusion of indomethacin into these dogs undergoing diuresis did not change inulin or p-aminohippuric acid clearance. Sodium excretion (UNaV) showed slight but not signifcant decreases with the infusion of indomethacin. UNaV was 109.3 +/- 25.7 muEq/min during control periods and was 69.6 +/- 21.0 muEq/min (0.05 less than p less than 0.1) after 80 min of infusion of indomethacin. The results suggest that renin release, sodium excretion, and blood pressure in the dog with chronic renovascular hypertension in uninfluenced by indomethacin.

Animals↗
PubMed1979

Effect of inhibition of prostaglandin synthesis on sympathetic nervous system function in man.

The effect of inhibition of prostaglandin synthesis by indomethacin on the function of the peripheral sympathetic nervous system was studied in eight normotensive subjects. Sympathetic nervous function was assessed by measurement of plasma norepinephrine, alpha-adrenergic receptor sites on platelet membranes, and urinary excretion of epinephrine and norepinephrine. Treatment with indomethacin for 7 days resulted in significant decreases in basal plasma norepinephrine from 134 +/- 7 to 99 +/- 6 (SEM) pg/ml (P less than 0.01), a 26% decrease. Posturally stimulated norepinephrine concentrations (337 +/- 14 pg/ml in control studies) were 255 +/- 18 pg/ml (P less than 0.02), 25% lower, with indomethacin. Plasma norepinephrine after 5-min compression of hand grip (468 +/- 47 pg/ml in control) was 331 +/- 30 pg/ml (P less than 0.005), 29% lower, with indomethacin. The number of platelet alpha-adrenergic receptor sites did not change with indomethacin, nor did prostaglandin E1-stimulated cAMP production by platelet membranes. In addition, indomethacin produced no change in urinary excretion of norepinephrine or epinephrine. It is suggested that inhibition of prostaglandin synthesis may lead, via baroreceptor feedback, to a decrease in plasma norepinephrine concentration.

Adult↗