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Biomedical subjects

F C Bartter

Publications and source records attributed to F C Bartter.

At least 19 recordsLinked to original sources
PubMed1985

The effects of oral furosemide on the response of urinary excretion of cyclic adenosine monophosphate and phosphate to parathyroid extract in normal subjects.

We studied the effects of oral furosemide, 80 mg/day for 7 days, on the response of urinary excretion of phosphate and cyclic AMP to exogenous parathyroid extract (PTE) in 6 normal subjects. All 6 subjects had marked increases in urinary calcium and a significant increase in urinary cyclic AMP from the control to the furosemide periods: this suggests that furosemide-induced hypercalciuria produced elevated parathyroid activity. After treatment with furosemide, the response of urinary cyclic AMP and phosphate to PTE was blunted. During the subsequent calcium infusion (4 mg/kg), urinary cyclic AMP was suppressed to subnormal values, and the response to PTE returned to normal. The evidence suggests that furosemide may blunt the response to PTE, perhaps as a result of the elevated parathyroid activity produced by furosemide-induced hypercalciuria and lowering of plasma-ionized calcium. This blunting effect of furosemide on the response of urinary phosphate and cyclic AMP to PTE should be considered in the evaluation of parathyroid function in patients taking furosemide.

Calcium↗
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↗
PubMed1979

Adrenergic receptor function is different in male and female patients with essential hypertension.

As plasma norepinephrine (NE) levels may be similar in hypertensive and normotensive subjects, the sensitivity of adrenergic receptors was investigated in patients with essential hypertension and normotensive subjects of similar age and sex. Alpha-adrenergic receptor sensitivity was measured in platelets by the specific binding of [3H]dihydroergocryptine and the NE inhibition of prostaglandin E1 (PGE1)-stimulated cyclic AMP (cAMP) production. The number of alpha-adrenergic receptors in platelets from hypertensive women was 1.5 times that in the platelets from normotensive ones, with no differences between hypertensive and normotensive women or between men and women in the affinity of the alpha-adrenergic receptor for [3H]dihydroergocryptine. PGE1-stimulated cAMP production was half as great in hypertensive as in normotensive men, while NE inhibition of PGE1-stimulated cAMP production was similar in hypertensive and normotensive men and women. [3H]Dihydroergoeryptine binding in female hypertensives, and PGE1-stimulated cAMP in male hypertensives did not differ from that in sex-matched controls. The sensitivity of the beta-adrenergic receptor, measured by [3H]dihydroalprenolol binding and cAMP production was similar in hypertensive and normotensive subjects.

Cyclic AMP↗
PubMed1979

Hypophosphatemic rickets: effect of 1 alpha, 25-dihydroxyvitamin D3 on growth and mineral metabolism.

Growth retardation nearly invariably accompanies hypophosphatemic rickets. Studies were conducted in an adolescent male with this disorder as follows. Protocol I: age, 6 to 16 years; treatment per day, 5,000 to 80,000 units vitamin D2, 1,760 to 2,200 mg phosphorus, orally as buffered phosphate; growth velocity, 5 to 6 cm/year. Protocol II: age 16 to 17 years; treatment per day, 1 alpha,25-dihydroxyvitamin D3, 1 microgram; 2,200 mg of phosphorus, orally as buffered phosphate; growth velocity, 14 cm/year. The height improved from less than third percentile for the decade during study protocol I to the 25th percentile during protocol II. Mineral balance studies showed a reduction of urinary and stool phosphorus during treatment protocol II, while the patient was receiving metabolic diet. The serum phosphorus improved from 2.2 to 4.3 mg/dl and radiologic healing of rickets was documented. No hypercalcemic episode was encountered. The data support the contention that 1 alpha,25-dihydroxyvitamin D3 is the treatment of choice for hypophosphatemic rickets.

Adolescent↗
PubMed1979

Rhythmometry gauges treatment of mesor-hypertension in the seventh and eight decades of life.

Autorhythmometry of blood pressure by an individual over an age-span of 67 to 72 years showed a strong circadian rhythm superimposed upon significant circaseptan and circannual rhythms. Automatic BP monitoring with an Arteriosonde throughout 24-hour spans on 4 separate occasions, before and during treatment, also indicated a prominent circadian BP rhythm and a treatment-related reduction in circadian mesor. The concept of a blood pressure mesor reference for the antimesor-hypertensive treatment constitutes a valuable guideline in the control of "familial" mesor-hypertension.

Aged↗
PubMed1979

Schedule shifts, life quality and quantity--modeled by murine blood pressure elevation and arthropod life span.

During the span from 50 to 100 days and beyond, the male stroke-prone Okamoto rat develops systolic blood pressure measures in excess of 200 mm Hg. In the course of developing such a marked elevation in systolic blood pressure mean, this intermittently handled male Okamoto rat exhibits a statistically significant circadian rhythm with large amplitude. This amplitude may represent, at least in part, a response to intermittent handling; it is several times larger than the amplitude for spontaneously mesor-hypertensive (but not stroke-prone) female animals of the same age.

Aging↗