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Biomedical subjects

D E Uehlinger

Publications and source records attributed to D E Uehlinger.

At least 37 records · Page 2Linked to original sources
PubMed1989

Cardiovascular regulation and lipoprotein profile during administration of co-dergocrine in essential hypertension.

Co-dergocrine has recently been demonstrated acutely to lower plasma norepinephrine (NE) and blood pressure (BP) in patients with essential hypertension, and similar results have been obtained during chronic administration of co-dergocrine to healthy men. The present study investigated the effect of 3 weeks of treatment with co-dergocrine 4 mg/day on BP, plasma catecholamines, certain other BP-regulating factors and serum lipoproteins in patients with essential hypertension. Compared to placebo conditions, co-dergocrine decreased supine BP and heart rate by -7% and the upright plasma NE level by -24%. Supine plasma NE also fell (-24%). Total cholesterol and the LDL + VLDL-cholesterol lipoprotein fraction were lowered by -6%. No significant change was observed in plasma renin activity, angiotensin II, aldosterone and epinephrine levels, whole blood and plasma volume, exchangeable sodium, and the cardiovascular responsiveness to NE, angiotensin II and isoproterenol. The findings suggest that in patients with essential hypertension, chronic treatment with co-dergocrine may slightly decrease sympathetic outflow and, at least in the short-term, lower the potentially atherogenic serum LDL + VLDL - cholesterol fraction.

Adult↗
PubMed1989

Antihypertensive contribution of sodium depletion and the sympathetic axis during chronic angiotensin II converting enzyme inhibition.

The known physiological adaptation of cardiovascular sensitivity to variations in angiotensin II (Ang II) levels would predict that the blood pressure (BP)-lowering effect of Ang II inhibition might be at least partly counterbalanced by enhanced Ang II reactivity. Therefore, factors other than Ang II inhibition per se may contribute to the antihypertensive mechanisms of angiotensin converting enzyme (ACE) inhibitors. In order to further investigate this, the body sodium-blood volume state as well as the pressor reactivity to infused Ang II or norepinephrine (NE) were assessed in 12 normal subjects and 16 patients with essential hypertension given a placebo, and after 6 weeks of intervention with enalapril (20-40 mg/day). Enalapril produced in both groups similar falls in plasma ACE activity (P less than 0.0001) and upright plasma aldosterone (P less than 0.01), and a rise in plasma renin activity (PRA; P less than 0.05). BP decreased from 156/107 +/- 3/2 (mean +/- s.e.m.) to 142/94 +/- 5/3 mmHg (P less than 0.001) in the hypertensives and from 118/84 +/- 4/2 to 111/73 +/- 4/3 mmHg (P less than 0.01) in the normal subjects. In the hypertensive patients only, the Ang II pressor reactivity relative to Ang II plasma levels during Ang II infusion was increased (P less than 0.01), while the NE pressor reactivity relative to NE plasma levels during NE infusion (P less than 0.01) as well as the exchangeable body sodium (-5%, P less than 0.001) were reduced significantly. Blood and plasma volume, levels of plasma atrial natriuretic factor and catecholamines, and the heart rate and its response to isoproterenol were unchanged in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Distinct hemodynamic and renal effects of calcitonin gene-related peptide and calcitonin in men.

Cardiovascular and renal actions of human calcitonin gene-related peptide II (or beta) (CGRP) and of human calcitonin (CT) infused intravenously for 1 h each (79 and 263 pmol.kg-1.h-1) have been compared in normal men (n = 10 for CGRP, n = 6 for CT and vehicle alone). CGRP lowered diastolic blood pressure by 26% and increased the heart rate by 35% and raised plasma levels of norepinephrine, epinephrine, and dopamine and renin activity (P less than 0.01). The fractional excretion rates (FE) of sodium and chloride were doubled (P less than 0.05-0.01) in the presence of an unaltered glomerular filtration rate. CT, on the other hand, did not affect the diastolic blood pressure, but the stimulation of diuresis and of the FE of sodium and chloride was more pronounced with CT than with CGRP (P less than 0.01). Moreover, CT lowered serum calcium levels and stimulated urinary adenosine 3',5'-cyclic monophosphate and phosphate excretion (P less than 0.01). In conclusion, the cardiovascular effects of CGRP are contrasted by weaker renal tubular actions of the neuropeptide in relation to CT.

Adult↗
PubMed1988

Human recombinant erythropoietin in anaemic patients on maintenance haemodialysis. Secondary effects of the increase of haemoglobin.

Twelve anaemic patients on haemodialysis were treated with recombinant human erythropoietin, starting with 72 IU/kg/week. The dose was doubled after 2 weeks until an increase of 2 g/dl of haemoglobin was observed. The effects on various parameters were studied during a 3-month period. Haemoglobin increased from 6.70 +/- 0.74 to 10.49 +/- 1.04 g/dl (mean +/- SD, P less than 0.001), potassium from 5.51 +/- 0.50 to 6.06 +/- 0.65 mmol/l (P less than 0.005), phosphate from 1.78 +/- 0.40 to 2.17 +/- 0.40 mmol/l (P less than 0.001) and the calcium phosphorus product from 4.3 to 5.2 (P less than 0.001). Three patients developed marked periarticular inflammation due to calcified deposits with a high calcium-phosphorus product of 6.8. An increase in arterial blood pressure was observed in three previously well-controlled hypertensive patients, one of whom developed hypertensive encephalopathy. We conclude that recombinant human erythropoietin is very effective in treating the anaemia of end-stage renal failure on haemodialysis. Regular estimations of serum potassium and phosphate are mandatory. In hypertensive individuals a further increase in blood pressure is possible.

Adult↗
PubMed1988

Calcitonin gene-related peptide is a stimulator of renin secretion.

Calcitonin gene-related peptide (CGRP) was found to stimulate renin secretion in vivo in normal human volunteers. Moreover, CGRP stimulated the release of renin in vitro from isolated rat renal juxtaglomerular cells (half-maximal effective concentration [EC50] 100 nM) concomitant with stimulation of cAMP production (EC50 60 nM). Immunoreactive CGRP was recognized in rat renal cortical nerve fibers, and intact rat CGRP was identified in extracts of the rat renal cortex. Because CGRP containing sensory nerve fibers are seen in the region of the juxtaglomerular apparatus, it would seem that the release of CGRP from these afferent nerves may be involved in the physiological control of renin secretion.

Animals↗
PubMed1988

Glucocorticoid and mineralocorticoid stimulation of atrial natriuretic peptide release in man.

To investigate the influence of a mineralocorticoid and a glucocorticoid on plasma immunoreactive atrial natriuretic peptide (irANP) and possible functional correlates, eight normal men received in random order 9 alpha-fludrocortisone acetate (9 alpha F; 0.6 mg/day), prednisone (50 mg/day), and placebo each for 9 days. Their diet contained 130 mmol sodium and 75 mmol potassium daily. The mean supine plasma irANP levels were similar on days 2, 4, and 9 of placebo treatment [25 +/- 10 (+/- SE), 27 +/- 5, and 27 +/- 6 pmol/L, respectively]. Mean plasma irANP levels were 76 +/- 42 (P less than 0.05), 89 +/- 34, and 93 +/- 29 pmol/L (P less than 0.01), respectively, on days 2, 4, and 9 during 9 alpha F administration, and 68 +/- 37 (P less than 0.05), 83 +/- 41, and 48 +/- 18 pmol/L on the same days during prednisone administration. Compared with the placebo period, sodium intake minus urinary output during 9 alpha F administration averaged +41 mmol at the time of blood sampling on day 2, +112 mmol on day 4, and +149 mmol on day 9; body weight was unchanged on day 2 and increased by 0.7 and 1.1 kg on days 4 and 9, respectively. Escape from 9 alpha F-induced renal sodium retention occurred on days 5 and 6. During prednisone administration, sodium intake minus urinary output and body weight did not change. Plasma volume and BP rose significantly during 9 alpha F (P less than 0.05) but not during prednisone administration. Plasma renin, aldosterone, and norepinephrine (NE) decreased during 9 alpha F treatment (P less than 0.05 to less than 0.01); during prednisone treatment, plasma aldosterone levels were lower on day 9 only. Cardiovascular pressor responsiveness to angiotensin II was enhanced during 9 alpha F but not prednisone administration, while blood pressure reactivity to NE was not significantly modified. These findings demonstrate that 9 alpha F and prednisone in high doses provoke remarkably similar increases in plasma irANP, but that the glucocorticoid-induced rise in plasma irANP is due to a mechanism other than sodium and volume retention.

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↗
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↗
PubMed1987

Effects of posture and ageing on circulating atrial natriuretic peptide levels in man.

Possible influences of posture or age on plasma immunoreactive atrial natriuretic peptide (irANP) levels and potential correlates were assessed in 12 young (age +/- s.e.m. 24 +/- 1 year) and 12 elderly (63 +/- 8 year) healthy subjects on a liberal sodium intake. The groups did not differ significantly in their basal 24-h urinary sodium excretion (210 +/- 23 versus 180 +/- 15 mmol/l). However, plasma irANP was five- to ninefold higher in the elderly (P less than 0.05-0.01). Plasma irANP averaged 167 +/- 31 and 24 +/- 3 pg/ml in the elderly and young, respectively, during recumbency, fell (P less than 0.05) to 101 +/- 21 and 11 +/- 1 pg/ml, respectively, with upright posture, and rose (P less than 0.01) to 250 +/- 51 and 50 +/- 9 pg/ml, respectively, after intravenous (i.v.) loading with 0.9% saline (2.14 l in 3 h). Supine blood pressure (BP) and plasma norepinephrine tended to be higher while renin and aldosterone levels were lower (P less than 0.01) in the elderly; the three latter variables rose (P less than 0.001) with upright posture. These findings demonstrate that in normal humans, circulating irANP levels vary with posture and ageing. These changes may have potential physiological relevance and should be considered when interpreting plasma irANP levels in pathological conditions.

Adult↗
PubMed1987

Pressure dependence of atrial natriuretic peptide during norepinephrine infusion in humans.

The relative contribution of increased blood pressure (BP) or norepinephrine (NE), or both, to the stimulatory effect of an NE pressor infusion on circulating immunoreactive atrial natriuretic peptide (ANP) was evaluated in 10 healthy young men. They were studied during an infusion of NE, which was applied initially alone and then in combination with sodium nitroprusside. NE infusion rate was increased in four 30-minute intervals to a final dose of 200 ng/kg body weight per minute, leading to 12-fold higher plasma NE levels than were seen during control conditions. This increased mean BP (from a mean basal value of 94 +/- 3 to 119 +/- 4 [SEM] mm Hg; p less than 0.001) and plasma immunoreactive ANP (from 50 +/- 7 to 112 +/- 17 pg/ml; p less than 0.001), whereas heart rate decreased (p less than 0.001). The NE infusion was continued at the highest dose and an additional infusion of sodium nitroprusside was started to titrate mean BP in 30-minute intervals down to control values; a mean sodium nitroprusside dose of 0.95 micrograms/kg/min restored mean BP to 93 +/- 4 mm Hg (p less than 0.001), decreased plasma immunoreactive ANP to basal values (51 +/- 4 pg/ml; p less than 0.001), increased heart rate (p less than 0.001), and left plasma levels of NE largely unchanged. Plasma protein and hematocrit rose about 5 to 6% (p less than 0.001) during the NE infusion and then decreased about 3 to 4% (p less than 0.001 and p less than 0.01) when sodium nitroprusside was added.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Plasma arginine-vasopressin levels during infusion of synthetic atrial natriuretic peptide on different sodium intakes in man.

The mechanisms involved in the diuretic action of the recently discovered group of atrial natriuretic peptides (ANP) are not entirely clear. To determine whether the diuresis and the changes in blood pressure produced by alpha-human ANP (alpha-hANP) involved a concomitant modification of circulating arginine-vasopressin (arg-VP), we evaluated the effects of synthetic alpha-hANP on plasma alpha-hANP, arg-VP, electrolytes, protein, haematocrit, blood pressure and urinary sodium and water excretion in 10 normal subjects on daily sodium intakes of 16, 140 and 310 mmol, respectively. Plasma alpha-hANP levels before and during a 45-min alpha-hANP infusion (0.09 micrograms/kg per min) tended to be slightly, though not significantly, higher on 'normal' or high sodium intake than on low sodium intake. Alpha-human ANP produced a fall in diastolic blood pressure (P less than 0.001) and to a lesser extent mean blood pressure, and a rise in heart rate (P less than 0.001) at all levels of sodium intake. The induction of diuresis, natriuresis and plasma volume contraction caused by alpha-hANP was greater on a high sodium intake than on 'normal' or low sodium intakes (P less than 0.001). Plasma arg-VP concentrations were lower (P less than 0.05) on a high than on a low sodium intake, but were not altered by an alpha-hANP infusion. The data indicate that in healthy humans circulating arg-VP may tend to decrease in response to a high salt diet. However, marked changes in plasma alpha-hANP concentrations have, regardless of sodium intake, no relevant influence on circulating arg-VP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Blood levels and renal effects of atrial natriuretic peptide in normal man.

Since mammalian atria were recently found to contain vasoactive and natriuretic peptides, we investigated the following in normal humans: plasma human atrial natriuretic peptide concentrations, effective renal plasma flow (ERPF), glomerular filtration rate (GFR), urinary water and electrolyte excretion, blood pressure (BP), and catecholamine, antidiuretic hormone (ADH), angiotensin II, and aldosterone levels before, during, and after intravenous administration of the newly synthetized alpha-human atrial natriuretic peptide (alpha hANP). In 10 subjects alpha hANP given as an initial bolus of 50 micrograms followed by a 45-min maintenance infusion at 6.25 micrograms/min increased plasma alpha hANP from 58 +/- 12 to 625 +/- 87 (mean +/- SEM) pg/ml; caused an acute fall in diastolic BP (-12%, P less than 0.001) and a hemoconcentration (hematocrit +7%, P less than 0.01) not fully explained by a negative body fluid balance; increased GFR (+15%, P less than 0.05) despite unchanged or decreased ERPF (filtration fraction +37%, P less than 0.001); augmented (P less than 0.05- less than 0.001) urinary chloride (+317%), sodium (+224%), calcium (+158%), magnesium (+110%), phosphate excretion (+88%), and free water clearance (from -0.76 to +2.23 ml/min, P less than 0.001) with only little change in potassium excretion; and increased plasma norepinephrine (P less than 0.001) while plasma and urinary epinephrine and dopamine, and plasma ADH, angiotensin II, and aldosterone levels were unchanged. The magnitude and pattern of electrolyte and water excretion during alpha hANP infusion could not be accounted for by increased GFR alone. Therefore, in normal man, endogenous alpha hANP seems to circulate in blood. alpha hANP can cause a BP reduction and hemoconcentration which occur, at least in part, independently of diuresis and are accompanied by sympathetic activation. An increase in GFR that occurs in the presence of unchanged or even decreased total renal blood flow is an important but not sole mechanism of natriuresis and diuresis induced by alpha hANP in man.

Atrial Natriuretic Factor↗
PubMed1986

Plasma levels and cardiovascular, endocrine, and excretory effects of atrial natriuretic peptide during different sodium intakes in man.

Endogenous plasma concentrations of human atrial natriuretic peptide (alpha hANP) as well as effects of synthetic alpha hANP on some cardiovascular, endocrine, and renal excretory parameters were investigated in 10 normal subjects during sodium (Na+) intakes of 17, 140, and 310 mmol/day, respectively. Plasma hANP was slightly but not significantly higher after 5 days of normal or high sodium intake than after 5 days of low sodium intake [54 +/- 13, 46 +/- 8, and 37 +/- 5 (mean +/- SEM) pg/ml, respectively]. alpha hANP infused at 0.1 microgram/kg X min during all Na+ intakes produced a similar fall in diastolic blood pressure (P less than 0.001) and rise in heart rate (P less than 0.001), a comparable percent increase in plasma norepinephrine (P less than 0.001), and a reduction in plasma cortisol and aldosterone (P less than 0.01-0.001) despite raised renin activity (P less than 0.05-0.001) and unchanged plasma electrolytes. alpha hANP-induced plasma volume contraction, diuresis, and natriuresis were greater during high than low Na+ intake (P less than 0.01-0.001). Therefore, in normal man different Na+ intakes are accompanied by marked modifications in renal excretory responsiveness to alpha hANP. Regardless of sodium intake, alpha hANP can promote BP reduction and hemoconcentration, elicit reflex (?) sympathetic activation, and depress basal circulating aldosterone and cortisol levels in the face of an activated renin system.

Adult↗
PubMed1986

Depressor effects and release of atrial natriuretic peptide during norepinephrine or angiotensin II infusion in man.

Alpha-human atrial natriuretic peptide (alpha hANP) is the major circulating form of ANP in man. The potential of synthetic alpha hANP to antagonize the pressor action of norepinephrine (NE) or angiotensin II (AII) and a possible influence of NE or AII pressor infusions on circulating immunoreactive ANP (irANP) were investigated in 14 normal young subjects. After titration of doses to increase mean blood pressure by about 20 mm Hg, NE or AII was infused at a constant rate for 110 min. Mean blood pressure (BP) was similar during NE and AII infusions [109 +/- 4 (+/- SEM) and 108 +/- 3 mm Hg, respectively]. However, synthetic alpha hANP injected in stepwise increasing doses of 10, 40, and 75 micrograms caused significantly greater (P less than 0.001) BP reductions during NE infusion. alpha hANP lowered BP progressively from 147/91 +/- 5/3 to 136/70 +/- 5/3 mm Hg during NE infusion (P less than 0.001) and only minimally from 133/96 +/- 3/3 to 132/89 +/- 4/4 during AII infusion. Heart rate was elevated more (P less than 0.01) after alpha hANP injection during NE infusion. Endogenous plasma irANP increased significantly after 20 min of NE or AII pressor infusion (P less than 0.01 and P less than 0.05, respectively); this rise was more pronounced (P less than 0.05) during NE (from 25 +/- 2 to 80 +/- 20 pg/ml) than during AII (from 21 +/- 3 to 31 +/- 3 pg/ml) infusion. These findings suggest that alpha hANP interacted preferentially with noradrenergic as compared to angiotensinergic BP control. Conversely, for a given rise in BP, NE elicited a greater rise in circulating irANP.

Adult↗
PubMed1986

Cardiovascular, endocrine and renal effects of atrial natriuretic peptide in essential hypertension.

Plasma concentrations of human atrial natriuretic peptide (hANP) and effects of synthetic alpha-hANP on blood pressure (BP), on endocrine and metabolic variables, and on renal function were investigated in 10 patients with essential hypertension. Alpha-human atrial natriuretic peptide was given intravenously as a 50-micrograms bolus followed by a 45-min infusion at 0.1 microgram/kg per min. The following effects were observed: (1) a marked rise in plasma alpha-hANP, (2) a progressive fall in BP (from 181/127 to 165/109 mmHg) and plasma volume, (3) a probably baroreflex-mediated sympathetic activation, evidenced by raised heart rate and plasma norepinephrine levels, (4) an increase in serum free fatty acids and circulating insulin (+45%), (5) an enhanced diuresis (+770%) and excretion of sodium (+665%), chloride (+524%), phosphate (+518%), other electrolytes, amino acids and free water clearance, (6) biphasic responses in the glomerular filtration rate (GFR) and p-aminohippurate (PAH) clearance, with initial increases (+40 and 30%, respectively) followed by a rapid return to (GFR), or even a fall below (PAH clearance) control values, and (7) a marked rise in the filtration fraction. Plasma antidiuretic hormone and urinary prostaglandin E2, F2 alpha and dopamine levels were not modified during alpha-hANP infusion, while plasma renin increased. Discontinuation of alpha-hANP was followed by rises in plasma aldosterone, the aldosterone:renin ratio and cortisol. Compared with previously studied normal subjects, in the hypertensive patients alpha-hANP caused a distinctly greater diuresis and electrolyte excretion but lowered BP only slightly more. In essential hypertension, as in normal man, alpha-hANP circulates in the blood and may exert a wide spectrum of cardiovascular, metabolic, endocrine and renal actions.

Adult↗
PubMed1986

Plasma kinetics of synthetic alpha-human atrial natriuretic peptide in man.

Atrial natriuretic peptides (ANPs) circulate in the blood stream and may modulate the regulation of blood pressure, sodium-fluid volume state and renal function. In man, alpha-human ANP (alpha hANP) is probably the major circulating form of ANP. To evaluate its plasma kinetics, we studied in 7 healthy men plasma alpha hANP concentrations under basal conditions and at short intervals during and up to 40 min after discontinuation of a 45-min constant alpha hANP infusion at a rate of 0.1 microgram/min/kg. From basal levels averaging 75 +/- 18 pg/ml (mean +/- SEM), plasma alpha hANP concentrations increased to 1,185 +/- 321 and 1,117 +/- 175 pg/ml at 30 and 40 min during the alpha hANP infusion, respectively. After discontinuing the latter, plasma alpha hANP decreased rapidly, following first-order kinetics, with a plasma half-life of 3.2 +/- 0.4 min. This finding is in line with the brief effects of intravenously applied alpha hANP and suggests that this system may be designed for rapid minute-to-minute adjustments.

Adult↗