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Biomedical subjects

H Saxenhofer

Publications and source records attributed to H Saxenhofer.

25 records · Page 2Linked to original sources
PubMed1988

Atrial natriuretic factor in mild to moderate chronic renal failure.

The relationship between kidney function and plasma immunoreactive atrial natriuretic factor (irANF) levels as well as the effects of synthetic human ANF-(99-126) were investigated in 13 patients with mild to moderate chronic renal failure. Under basal conditions, glomerular filtration rate averaged 39 +/- 5 (SEM) ml/min/1.73 m2 and blood pressure (BP) averaged 166/107 +/- 7/2 mm Hg; 12 patients were hypertensive. Plasma irANF levels were significantly increased (98 +/- 16 vs 42 +/- 4 pg/ml in healthy control subjects; p less than 0.001) and correlated (p less than 0.05-0.005) inversely with hematocrit (r = -0.65) and positively with systolic BP (r = 0.75) or fractional sodium excretion (r = 0.75). Human ANF-(99-126) infusion for 45 minutes at 0.034 microgram/kg/min augmented (p less than 0.05-0.01) diuresis and urinary sodium, chloride, calcium, phosphate, and magnesium excretion. During the subsequent 45 minutes of human ANF-(99-126) infusion at a rate of 0.077 microgram/kg/min, diuresis and electrolyte excretion remained elevated (p less than 0.05-0.01). Glomerular filtration rate and effective renal plasma flow were not significantly modified, but filtration fraction rose progressively (p less than 0.01). Human ANF-(99-126) infusion decreased BP (p less than 0.05-0.01), produced hemoconcentration (hematocrit + 7%; p less than 0.01) without negative body fluid balance, and increased (p less than 0.01-0.001) plasma norepinephrine, insulin, and serum free fatty acids; plasma aldosterone and renin activity were unaltered during but rose after cessation of human ANF-(99-126) infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Corticosteroid-induced stimulation of atrial natriuretic peptide in man.

UNLABELLED: Previously, we reported elevated plasma immunoreactive ANP (irANP) levels from the 2nd to the 9th day of administering either prednisone, 50 mg/day, or 9 alpha-fludrocortisone acetate (9 alpha F), 0.6 mg/day, to normal humans. To investigate the course of plasma irANP levels during the first 48 h of corticosteroid administration, 9 healthy men (mean age +/- SEM, 24 +/- 1 years) received in randomised sequence A) a 4-h iv infusion of prednisolone sodium tetrahydrophthalate followed by oral administration of prednisone for 2 days; or B) a 4-h infusion of aldosterone followed by oral administration of 9 alpha F for 2 days. Basal supine plasma irANP levels averaged 32 +/- 5 ng/l in study A and 30 +/- 6 ng/l in study B; they were unchanged or even deceased up to 24 h of glucocorticoid or mineralocorticoid administration, but rose (P less than 0.01) to 56 +/- 9 and 62 +/- 12 ng/l at 48 h, respectively, of the two interventions. During glucocorticoid treatment, blood pressure (BP) and indices of the sodium-fluid volume state were unchanged after 48 h. During 9 alpha F administration, body weight increased (1.1 +/- 0.3%, P less than 0.001), whereas urinary sodium excretion (63 +/- 7%, P less than 0.001), hematocrit (4.1 +/- 1.1%, P less than 0.001), and plasma renin activity (38 +/- 4%, P less than 0.001) decreased. CONCLUSIONS: The increase in circulating irANP at 48 h of administration of either a glucocorticoid or a mineralocorticoid demonstrates a distinct but slow response of the ANP system to these corticosteroids in normal humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Serum lipoproteins during treatment with antihypertensive drugs.

Hypertension and certain alterations in serum lipoproteins such as a decrease in high density lipoprotein-cholesterol (HDL-C), an increase in low density lipoprotein-cholesterol (LDL-C) and perhaps also elevated triglycerides (Tg), are complementary coronary risk factors. Moreover, it has become evident that several of the drugs used for standard antihypertensive therapy may also interact with lipoprotein metabolism. The following has been observed after 1 to 12 months of treatment. Various diuretics can significantly increase LDL-C and/or very LDL-C and total C/HDL-C ratio, while HDL-C is often largely unchanged; Tg also are often elevated. LDL-C increased in diuretic-treated men and in chlorthalidone-treated postmenopausal women but not in chlorthalidone-treated premenopausal women. The latter may be protected from this side effect. Drug dosages were usually high in these studies. Indapamide, given at a dose of 2.5 mg/day, seems to exert no relevant effect on the lipoproteins. It is not established whether this difference is related to the nature of the drugs or the doses used. There is little doubt that the dose of chlorthalidone used was greater than that required for a full antihypertensive effect of this drug. Several beta-blockers given as monotherapy induce significant increases in Tg and a tendency for decreases in HDL-C. These changes are most prominent on non-selective beta 1+2-blockers without partial intrinsic sympathomimetic activity (ISA), less pronounced on highly selective beta 1-blockers without ISA, and even more discrete or absent on beta-blockers with distinct ISA. Other sympatholytics such as reserpine, methyldopa, debrisoquine, urapidil, clonidine, labetalol, or postsynaptic alpha-blockers (prazosin, trimazosin, doxazosin etc.) did not affect or, postsynaptic alpha-blockers in particular, sometimes even slightly decreased Tg or LDL-C and very LDL-C values. During combination therapy, diuretic-induced increases in LDL-C were at short term prevented or reversed by the concomitant administration of certain beta-blockers, but not by sympatholytics such as reserpine, methyldopa or clonidine. With combined diuretic-prazosin treatment, a tendency for slightly higher HDL-C was reported. Angiotensin converting enzyme inhibitors (captopril, enalapril) and calcium channel blockers (verapamil, nifedipine, nitrendipine, diltiazem) seem to be largely devoid of undesirable effects on serum lipoproteins. Monotherapy with the potent direct vasodilator carprazidil improved blood pressure and significantly increased HDL-C. Whether and to what extent the observed variations in lipoproteins may persist beyond 1 year of treatment is as yet unclear.(ABSTRACT TRUNCATED AT 400 WORDS)

Antihypertensive Agents↗
PubMed1988

[Pharmacologic effects of atrial natriuretic peptide in humans].

Since the discovery of atrial natriuretic peptide (ANP) by de Bold in 1981, several scientists (e.g. nephrologists, endocrinologists, cardiologists) have contributed to research efforts to define the physiologic and pharmacologic profile of the peptide. ANP given in pharmacologic doses seems to lower blood pressure, probably by reducing both preload and afterload. ANP increases renal water and electrolyte excretion, although the underlying mechanisms have not been entirely clarified yet. The depressor and natriuretic effect of ANP act in harmony with an inhibitory effect on the release of renin, aldosterone, and arginine-vasopressin. While the physiologic role or importance of ANP is still in question, synthetic alpha ANP has a promising pharmacologic profile in renal and cardiovascular pathologic states.

Atrial Natriuretic Factor↗
PubMed1987

[History and physiology of atrial natriuretic peptides in man].

The recent discovery of the atrial natriuretic peptide (ANP) system and its possible physiological role in man are discussed. ANPs are produced in the atria of various species, including man. In normal humans the biologically active alpha-ANP, a peptide consisting of 28 amino acid residues, is released into the circulation through cleavage from a larger prohormone which is stored in specific granules in atrial myocytes. The secretion of alpha-ANP from the heart is activated during atrial distension secondary to volume overload or increased atrial pressures. When injected intravenously, synthetic human alpha-ANP can produce a wide spectrum of hemodynamic, endocrine and renal effects. The ANP system may well play an important role in the homeostasis of (central) blood volume and blood pressure.

Amino Acid Sequence↗
PubMed1987

Plasma levels and dialysance of atrial natriuretic peptide in terminal renal failure.

Plasma immunoreactive atrial natriuretic peptide (irANP) levels, their chromatographic profile, relationship with hemodynamic variables, and responses to hemodialysis (HD) or postural changes were investigated in HD patients. Peripheral venous supine plasma irANP averaged 167 +/- 31 (+/- SEM) pg/ml in 12 normal subjects (age 63 +/- 2 yr). In 42 HD patients (mean age 65 +/- 1 yr), plasma irANP in peripheral arterio-venous fistulae was high (447 +/- 50 pg/ml, P less than 0.01) before HD and decreased (P less than 0.001) to 164 +/- 24 pg/ml after HD. The latter reduced body weight by -2.3 +/- 0.2 kg (P less than 0.001) and blood pressure from 139/77 +/- 4/2 to 126/73 +/- 4/2 mm Hg (P less than 0.01). Pre-dialysis plasma irANP in right atrium, pulmonary artery or avfistula correlated with pulmonary capillary wedge pressure (N = 10, r = 0.66 to 0.73; P less than 0.05); HD-induced changes in these variables were also correlated (r = 0.80 to 0.90; P less than 0.05 to less than 0.01). Compared with supine values, upright posture decreased plasma irANP in 12 normal subjects and 8 HD patients (-40 and -42%, respectively, P less than 0.01). IrANP clearance from plasma averaged 24 +/- 5 ml/min across the hemodialyzer (N = 6) and 46 +/- 3 ml/min across the hemofilter (N = 4). We conclude that in terminal renal failure, circulating irANP consists largely of alpha ANP, is often elevated before HD, decreases with the change from recumbency to standing, falls after removal of excess fluid, and may depend strongly on left atrial and pulmonary arterial pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗