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Biomedical subjects

A F Muller

Publications and source records attributed to A F Muller.

At least 91 records · Page 5Linked to original sources
PubMed1982

Role of sodium concentration of the cerebrospinal fluid in the salt appetite of sheep.

The role of sodium concentration of the cerebrospinal fluid (CSF[Na]) in the initiation and/or satiation of Na appetite of Na-deplete or Na-replete sheep was investigated. Slow infusion (1 ml/h) into a lateral brain ventricle of an artificial sheep CSF solution was begun 0-60 min prior to and continued until the end of the Na access period (30-120 min). In Na-deficient sheep, increasing CSF[Na] caused a decrease in Na intake. In both Na-deficient and Na-replete sheep, decreasing CSF[Na] caused an increase in Na intake. The appetite was observed within 25 min of beginning infusion, which represents the most rapid induction of Na appetite yet observed. In Na-replete sheep, the appetite induced by decreasing CSF[Na] was predominantly for Na-containing solutions. A decrease in CSF[Na] of only 4-6 mmol/l was sufficient to induce Na appetite. The results derived by use of different Na, saccharide, or urea containing artificial CSF solutions suggest that there are sensors within the neuropil that respond to change of [Na] and influence salt appetite. They can be accessed by inducing change in [Na] of cerebroventricular CSF.

Animals↗
PubMed1982

Binding and activation properties of angiotensin II in dispersed rat anterior pituitary cells.

The properties of angiotensin II receptors were studied in isolated rat anterior pituitary cells prepared by trypsin digestion. Angiotensin II bound in a time- and temperature-dependent manner to pituitary cells, with Kd of 4.1 x 10(-9) M. The heptapeptide, des-Asp1-angiotensin II, had only one-tenth of the affinity of the octapeptide (Ki = 5.5 x 10(-8) M). These two peptides displayed a similar potency ratio in their ability to stimulate ACTH release from pituitary cells. These results indicate that angiotensin II may play a regulatory role in controlling ACTH secretion from the pituitary gland.

Angiotensin II↗
PubMed1981

Sodium appetite in sheep induced by cerebral ventricular infusion of angiotensin: comparison with sodium deficiency.

Intraventricular administration of supraphysiological amounts of renin, nerve growth factor preparation, or angiotensin II greatly increased the consumption of water and hypertonic sodium bicarbonate solution by sheep. These effects were antagonized by intraventricular administration of drugs that prevent the formation of angiotensin II or block its receptors. The fact that these angiotensin-blocking drugs did not change the sodium intake of sodium-deficient sheep challenges the idea that central angiotensin action is involved in sodium appetite due to a deficiency.

Angiotensin II↗
PubMed1980

Pressure natriuresis in isolated kidneys from hypertension-prone and hypertension-resistant rats (Dahl rats).

Dahl described a strain of rats with genetically controlled propensities for hypertension. Chronic excess salt feeding increased blood pressure in sensitive (s) rats, whereas resistant rats (R) remain normotensive. We tested the pressure natriuretic function (urinary sodium excretion versus perfusion pressure) in isolated kidneys perfused with a cellular medium: in sodium-restricted normotensive sensitive (S0) and resistant (R0) animals; in sensitive rats receiving a high-salt diet for 3 weeks (S3): and in both S and R animals exposed to excess sodium for 7 weeks (R7 and S7). The aim of these studies was to determine if a preset alteration of the pressure natriuretic function might be present in S animals prior to the development of hypertension. Systolic blood pressure in S0, S3, and S7 animals were 123 +/- 4, 136 +/- 2, and 162 +/- 4 mm Hg, respectively, whereas that of R0 and R7 were 121 +/- 5 and 126 +/- 5 mm Hg. An increase of the perfusion pressure of isolated kidneys from 105 to 185 mm Hg in stepwise fashion resulted in a pressure natriuresis whose slope was similar in R0 and S0 animals. Of interest was that the pressure natriuretic function slope of kidneys from R0 (low sodium) and R7 (high sodium) rats was as predicted by the Guyton system analysis of normal blood pressure control Micropuncture of the proximal nephrons demonstrated that the origin of the natriuresis resulted from a site beyond the accessible proximal tubule. Results from S7 kidneys contrasted with all others in that the natriuretic response was depressed (P less than 0.01), which resulted from significantly lower filtration rates at higher perfusion pressures. We concluded (1) in normal R rats, the pressure natriuretic function is that predicted by the Guyton hypothesis, (2) Dahl S animals have no preset abnormality of this function until hypertension is present for some time, and (3) a depression of the pressure natriuretic function may aggravate hypertension in S rats once high blood pressure has persisted.

Animals↗
PubMed1979

[Cholestyramine and digoxin intoxication: therapeutic efficacy?].

Plasma levels of digoxin were measured in a patient after massive intoxication. Pharmacokinetic analysis of the data as compared with other cases of digoxin intoxication reveals that in these situations oral administration of cholestyramine may be of benefit to the patient.

Cholestyramine Resin↗
PubMed1977

Refractory sideroblastic anemia secondary to autoimmune hemolytic anemia.

A 75-year-old woman was hospitalized with autoimmune hemolytic anemia. During a period of 22 months the patient had six hemolytic crises which responded to treatment with prednisone and azathioprine. During the last admission the patient presented a sideroblastic anemia with 98% of 'ring sideroblasts' in the bone marrow. This association has never, to our knowledge, been reported before. It is possible that the immunosuppression played a definite role in the development of this sideroblastic anemia.

Aged↗
PubMed1976

Effect on plasma aldosterone, renin activity and cortisol of acute volume depletion induced by ethacrynic acid under constant infusion of angiotensin II and dexamethasone in man.

The influence on plasma aldosterone of acute volume depletion induced by ethacrynic acid was studied in man. The experiments were performed during the morning in supine healthy males receiving a control infusion of 5% glucose or an infusion of angiotensin II (AII) to suppress endogenous renin production or an infusion of dexamethasone to suppress endogenous ACTH. Ethacrynic acid induced in all circumstances a similar diuresis and volume depletion. The rise of plasma renin activity (PRA) was effectively suppressed by AII and the rise of plasma cortisol by dexamethasone. Plasma aldosterone (PA) rose markedly even when the elevation of PRA or cortisol were suppressed. Yet when both endogenous renin and ACTH secretion were blocked, PA rose much less after ethacrynic acid. This residual increase could be attributed mainly to a decrease of the metabolic clearance rate (MCR) of aldosterone which had been measured before and after ethacrynic acid administration. The data presented indicate that multiple factors influencing PA after acute volume depletion could be dissected out and that renin, ACTH and a decrease of the MCR each contribute to the elevation of PA.

Adrenocorticotropic Hormone↗