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Biomedical subjects

C C Lang

Publications and source records attributed to C C Lang.

At least 73 records · Page 4Linked to original sources
PubMed1993

The effect of intravenous saline loading on plasma levels of brain natriuretic peptide in man.

OBJECTIVE: Recent evidence suggests the presence of a dual natriuretic peptide system consisting of atrial natriuretic factor (ANF) from the atrium and brain natriuretic peptide (BNP) from the ventricle. Discrete roles have been postulated for these two natriuretic peptides in the control of circulatory homeostasis. We have therefore compared the release of ANF and BNP in response to an acute saline load to explore a differential pattern of release for the two natriuretic peptides in man. DESIGN: The effects of an acute saline infusion on plasma ANF and BNP concentrations were studied in 10 normal male volunteers. METHODS: Subjects were studied on two study days in the semirecumbent position. An acute intravenous saline infusion (250 ml/min) of 18 ml/kg isotonic sodium chloride-potassium chloride solution was administered on one of the two study days. No infusion was administered on the other day as a control. RESULTS: Plasma ANF concentrations increased significantly (P < 0.01) with saline loading without any detectable changes in plasma BNP concentrations up to 60 min following infusion. Heart rate and systolic and diastolic blood pressure were unchanged after saline loading. CONCLUSIONS: We have shown that an acute intravenous saline load causes an increase in plasma ANF concentrations with no detectable increase in plasma BNP at least up to 60 min after the acute saline load in man. These results support the view that the release of ANF and BNP may be regulated differently, especially with regard to the time required for the acute release of each peptide.

Adult↗
PubMed1993

Cyclosporin-induced hypertension precedes renal dysfunction and sodium retention in man.

OBJECTIVE: To study the acute effects of cyclosporin on blood pressure, renal function and hormones within the first few hours of drug ingestion in healthy man. DESIGN: A therapeutic (12 mg/kg) and a supratherapeutic (30 mg/kg) dose of cyclosporin were administered orally to 10 salt-replete normal healthy volunteers. Their renal haemodynamic parameters were assessed by inulin and para-aminohippurate clearances, and their blood pressure was recorded every 20 min. RESULTS: Cyclosporin had an acute hypertensive effect while having no effect on sodium excretion or renal function. The earliest renal effect of cyclosporin was on water handling, with a marked antidiuretic effect. CONCLUSIONS: Our findings contradict previous data and currently held views regarding the pathogenesis of cyclosporin-induced hypertension. In particular, we have demonstrated that hypertension precedes any measurable change in renal haemodynamic parameters and occurs without apparent overall alterations in renal sodium excretion. We have also found that an antidiuresis is a very early renal effect of cyclosporin.

Adult↗
PubMed1992

Prazosin attenuates the natriuretic response to atrial natriuretic factor in man.

The effect of alpha-1-adrenoceptor blockade with 0.25 mg oral prazosin on the renal response to atrial natriuretic factor (ANF) 5 pmol/kg/min was examined in eight healthy male volunteers undergoing maximal water diuresis. ANF on its own decreased mean arterial blood pressure (P less than 0.05) without altering heart rate or increasing plasma norepinephrine. ANF increased urinary sodium excretion by 130% (P less than 0.01) from baseline value with accompanying 18% decrease (P less than 0.05) in PAH clearance (ERPF) without changing inulin clearance (GFR). When compared to placebo infusion, ANF infusion caused a significant increase in fractional excretion lithium (FELi), a marker of proximal tubular function. Fractional distal delivery of sodium, another marker of proximal tubular outflow as determined by free water clearance, was also increased during ANF infusion. As expected, ANF decreased distal nephron fractional sodium reabsorption as evaluated by both the "lithium method" and by the conventional "solute-free water method." Prazosin on its own had no effect on blood pressure, renal function or hormonal parameters. When given in combination with ANF, prazosin blunted the natriuretic effect of ANF from 130% to 35% (P less than 0.01). However, prazosin pretreatment did not influence the ANF-induced fall in blood pressure or ERPF nor the ANF-induced suppression of plasma aldosterone. We have therefore found evidence to support the hypothesis that at basal levels of sympathetic tone, the natriuretic effect of ANF in man is dependent on an intact sympathetic nervous system, since sympathetic blockade by prazosin blunts its sodium excretory effects.

Adult↗
PubMed1992

Effect of haemodialysis on plasma levels of brain natriuretic peptide in patients with chronic renal failure.

1. Plasma human brain natriuretic peptide-like immunoreactivity (hBNP-li) was measured in ten patients with chronic renal failure before and after 4 h of haemodialysis. 2. Plasma hBNP-li was elevated in all patients before dialysis (mean +/- SEM 21.0 +/- 3.8 pmol/l) compared with healthy control subjects (1.3 +/- 0.2 pmol/l, n = 11), but showed considerable inter-patient variability. Before dialysis plasma hBNP-li bore no relationship to the serum creatinine level or to the mean blood pressure. 3. Plasma hBNP-li fell significantly (P = 0.04) during 4 h of haemodialysis. The fall in plasma hBNP-li correlated significantly with the degree of postural blood pressure drop (r2 = 0.44, P = 0.05) and with the fall in body weight (r2 = 0.64, P less than 0.01) after haemodialysis. In all patients, plasma hBNP-li at the end of treatment remained above that in healthy subjects. 4. There was no significant correlation between the fall in plasma hBNP-li and the fall in serum creatinine level, and between the fall in plasma hBNP-li and the fall in supine systolic or diastolic blood pressure, during haemodialysis. 5. We have shown that plasma hBNP-li is elevated in patients with chronic renal failure and is decreased during haemodialysis. The fact that the plasma hBNP-li was not reduced to normal by haemodialysis despite restoration to normovolaemia gives tentative support to the view that, in addition to hypervolaemia, another factor may also be responsible for the elevated plasma hBNP-li seen in these patients.

Adolescent↗
PubMed1992

Clearance of brain natriuretic peptide in patients with chronic heart failure: indirect evidence for a neutral endopeptidase mechanism but against an atrial natriuretic peptide clearance receptor mechanism.

1. Brain natriuretic peptide is a new natriuretic hormone with striking similarity to atrial natriuretic peptide, but there are no previous data concerning its clearance in man. Two pathways of clearance for atrial natriuretic peptide are recognized: degradation by neutral endopeptidase and binding to atrial natriuretic peptide clearance receptors. We have examined the effect of candoxatril, an inhibitor of neutral endopeptidase (dose range 10-200 mg), and the effect of an infusion of a pharmacological dose [45 micrograms (90 micrograms in two patients)] of synthetic human atrial natriuretic peptide on plasma human brain natriuretic peptide-like immunoreactivity levels in seven patients with mild to moderate chronic heart failure. 2. Plasma human brain natriuretic peptide-like immunoreactivity levels were elevated in all patients (mean +/- SEM 22.0 +/- 6.2 pmol/l) compared with healthy control subjects (1.3 +/- 0.2 pmol/l, n = 11). 3. In all patients, candoxatril increased both plasma atrial natriuretic peptide (P less than 0.05) and plasma human brain natriuretic peptide-like immunoreactivity (P less than 0.05) levels. 4. By contrast, an exogenous infusion of atrial natriuretic peptide had no effect on plasma human brain natriuretic peptide-like immunoreactivity levels despite increasing the plasma atrial natriuretic peptide concentration to 424 +/- 74 pmol/l, which is a level of atrial natriuretic peptide which would have 'swamped' all atrial natriuretic peptide clearance receptors. 5. We have therefore shown that plasma human brain natriuretic peptide-like immunoreactivity levels in chronic heart failure are increased by a neutral endopeptidase inhibitor, but are unchanged by an exogenous infusion of atrial natriuretic peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Effect of angiotensin-converting enzyme inhibition on plasma brain natriuretic peptide levels in patients with heart failure.

1. The aim of this study was to examine the effect of captopril, an angiotensin-converting enzyme inhibitor, on plasma levels of human brain natriuretic peptide-like immunoreactivity (hBNP-li) in patients with congestive heart failure. 2. Six male patients (aged 52-74 years) with mild to moderate congestive heart failure were studied on two occasions in the semi-recumbent position. After a 30 min rest, patients were randomized to receive oral tablets of either captopril (6.25 mg followed by 25 mg 2 h later) or placebo in a single-blind manner. Plasma hBNP-li, atrial natriuretic peptide-like immunoreactivity (ANP-li) and angiotensin II-like immunoreactivity (ANG II-li) levels and blood pressure were measured. 3. Baseline plasma hBNP-li and ANP-li levels in these patients with mild to moderate congestive heart failure were 13.5 +/- 3.2 pmol/l and 50.9 +/- 11.8 pmol/l, respectively. In 11 healthy male subjects aged 20-23 years, the peripheral plasma hBNP-li and ANP-li levels were 1.3 +/- 0.2 pmol/l and 5.6 +/- 1.7 pmol/l, respectively. In all patients, captopril decreased the plasma ANG II-li level (from 24.3 +/- 8.1 to 6.6 +/- 3.2 pmol/l, P < 0.05) and mean arterial blood pressure (from 92 +/- 3 to 80 +/- 3 mmHg, P < 0.05). Compared with placebo, captopril treatment was associated with significant reductions in plasma hBNP-li (from 14.3 +/- 3.0 to 12.8 +/- 2.1 pmol/l, P < 0.05) and in plasma ANP-li (from 53.9 +/- 1.11 to 36.8 +/- 7.6 pmol/l, P < 0.05) levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Elevated levels of brain natriuretic peptide in acute hypoxaemic chronic obstructive pulmonary disease.

1. Studies in vitro have recently shown that both atrial natriuretic peptide and brain natriuretic peptide have pulmonary vasorelaxant activity. The purpose of the present study was to evaluate for the first time whether plasma levels of brain natriuretic peptide are elevated in chronic obstructive pulmonary disease. Plasma levels of brain natriuretic peptide and atrial natriuretic peptide were therefore measured in 12 patients admitted with acute hypoxaemic chronic obstructive pulmonary disease [arterial partial pressure of O2, 6.2 +/- 0.4 kPa; arterial partial pressure of CO2, 6.9 +/- 0.1 kPa; forced expiratory volume in 1 s, 0.6 +/- 0.07 litre (27 +/- 3% of predicted)]. All but three patients had oedema on admission. 2. Plasma levels of both brain natriuretic peptide and atrial natriuretic peptide were elevated in patients with chronic obstructive pulmonary disease (31.4 +/- 4.1 pmol/l and 45.0 +/- 8.1 pmol/l, respectively) compared with healthy control subjects (1.7 +/- 0.8 pmol/l and 8.0 +/- 3.5 pmol/l, respectively). Thus, plasma levels of brain natriuretic peptide and atrial natriuretic peptide in patients with chronic obstructive pulmonary disease were increased by 18.5- and 5.6-fold respectively compared with healthy control subjects. 3. There was a significant inverse correlation between the plasma level of brain natriuretic peptide and the arterial partial pressure of O2 (r = -0.65, r2 = 0.42, P = 0.03), but not between the plasma atrial natriuretic peptide level and the arterial partial pressure of O2 (r2 = 0.07, not significant). The arterial partial pressure of CO2 did not correlate with the plasma level of either brain natriuretic peptide or atrial natriuretic peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1992

Atrial natriuretic factor improves renal function and lowers systolic blood pressure in renal allograft recipients treated with cyclosporin A.

OBJECTIVE: Atrial natriuretic factor (ANF) has several properties which suggest that it may ameliorate cyclosporin A nephrotoxicity. We therefore investigated the response to a pharmacological dose of ANF in renal transplant recipients treated with cyclosporin A. DESIGN: A single-blind randomized crossover design comparing the renal and haemodynamic effects of D-glucose (placebo) with ANF. METHODS: Seven patients with stable renal function following renal transplantation were studied under maximal water diuresis. Glomerular filtration rate and effective renal plasma flow were estimated from clearances of inulin and para-aminohippurate, respectively. RESULTS: Plasma ANF levels increased significantly in association with increased diuresis and natriuresis. Glomerular filtration rate was unchanged after placebo but increased significantly after ANF fusion. Likewise, effective renal plasma flow increased significantly with ANF infusion. There was a significant fall in systolic blood pressure, with no apparent change in heart rate and diastolic blood pressure. CONCLUSIONS: These results suggest that ANF may have beneficial effects in protecting against cyclosporin A-induced nephrotoxicity and hypertension.

Atrial Natriuretic Factor↗
PubMed1992

Prazosin blunts the antinatriuretic effect of circulating angiotensin II in man.

OBJECTIVE: The present study examines the role of alpha 1-adrenoceptors in determining the renal haemodynamic and sodium excretory responses to a physiological dose of angiotensin II in man. DESIGN: The effects of a low-dose infusion of angiotensin II (1 ng/kg per min) and a non-depressor dose of prazosin (0.25 mg), alone and in combination, on urinary sodium excretion (UNaV), effective renal plasma flow (ERPF), glomerular filtration rate (GFR) and segmental tubular function were studied in eight normal male subjects. METHODS: Subjects were studied undergoing maximal water diuresis. Clearances of inulin and para-aminohippurate were employed to estimate GFR and ERPF, respectively. Segmental tubular handling was assessed by both lithium clearance (CLi) and solute-free water methods. RESULTS: Angiotensin II decreased UNaV without altering ERPF and GFR. Angiotensin II caused a significant fall in fractional CLi, which may indicate a proximal tubular effect of angiotensin II. Angiotensin II alone also increased fractional reabsorption of sodium delivered to the distal nephron, as evaluated by both the CLi method and by estimation of solute-free water clearance. When angiotensin II was given in combination with prazosin, which on its own had no apparent effects on any renal parameters, the antinatriuretic and tubular effects of angiotensin II were significantly blunted. CONCLUSIONS: These findings suggest that low doses of circulating angiotensin II are able to modulate UNaV by increasing sodium reabsorption in the proximal and, to some extent, the distal nephron segment in man. The study also showed that a non-depressor dose of prazosin blunted the renal effects of angiotensin II, thereby providing tentative evidence of a renal interaction between alpha-adrenoceptors and angiotensin II in man.

Adult↗
PubMed1992

General practitioners' use of non-steroidal anti-inflammatory drugs in Tayside and Fife regions.

The objectives of this study were to assess the prescribing of non-steroidal anti-inflammatory drugs (NSAIDs) by general practitioners and to determine their attitudes to problems caused by this class of drugs. The study consisted of two parts. The first was a questionnaire survey among general practitioners in Fife and Tayside, and the second was an analysis of NSAID prescribing over 12 months among the doctors in the Carnoustie Health Centre, using duplicate prescriptions. In the questionnaire survey 61% of the general practitioners responded. The three most preferred drugs were buprofen (56%), naproxen (20%) and mefenamic acid (7%); choice of drug was determined by efficacy and personal experience. Gastrointestinal side effects were most frequently encountered, although there was little consensus amongst respondents as to their management. The duplicate prescription study showed that 14% of patients (1607 individuals) received at least one NSAID prescription in the year of study. Ibuprofen (31%), naproxen (20%) and piroxicam (15%) were most frequently prescribed and up to 16% of the patients were co-prescribed a gastroprotective agent; ranitidine (75%) was the most commonly prescribed. Despite the introduction of newer NSAIDs, ibuprofen and naproxen are still the most commonly prescribed drugs. Furthermore, although gastrointestinal side effects are commonly encountered, there is some uncertainty about their management.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Interactions between atrial natriuretic factor and the autonomic nervous system.

In addition to its natriuretic, hormonal and vascular actions, atrial natriuretic factor (ANF) may interact importantly with the function of the autonomic nervous system. It has been hypothesized that ANF may exert its cardiovascular and possibly renal effects by interfering with autonomic control mechanisms. In, animal experiments the hypotension that is caused by ANF is usually not associated with the expected reflex tachycardia or increased efferent sympathetic activity. Furthermore, bilateral vagotomy can attenuate the hypotensive action of ANF which suggest that ANF may stimulate sympathoinhibitory afferent vagal activity from the cardiopulmonary baroreceptor system. In man, ANF may alter reflexogenic-mediated forearm vascular responses to cardiopulmonary deactivation which suggest that ANF may have an important role as a neuromodulator of autonomic nervous function, a role that could serve to amplify or facilitate the peripheral hormonal actions of ANF. This neuromodulating influence of ANF could be due to several mechanisms: it could modulate baroreflex mechanisms or it could have direct effects on autonomic centres in the brain or it could have effects on peripheral neurotransmission. The role of the autonomic nervous system in modulating the release of ANF remains controversial. Finally, there is growing evidence to suggest that there is a reciprocal interplay between ANF and the sympathetic nervous system in peripheral target tissues which may have important pathophysiological significance.

Animals↗
PubMed1991

Effects of xamoterol in acute myocardial infarction: blood pressure, heart rate, arrhythmias and early clinical course.

Xamoterol is a novel partial agonist of beta 1 adrenoceptors that reduces myocardial ischaemia and improves ventricular function in patients with mild to moderate heart failure. In a double blind, randomised, placebo controlled study, the effects of xamoterol given in a dose of 200 mg twice daily were studied in 51 consecutive patients with acute myocardial infarction, including 17 receiving diuretics for left ventricular failure. Treatment was started on the third day of admission and continued for 7 days. Blood pressure was recorded at 0900 daily, and 24 hour ambulatory electrocardiogram monitoring was commenced at this time on days 1 (pre-treatment), 4, 6 and 9 of admission. Additional drug therapy was recorded daily throughout the study. One patient died prior to randomisation and three were withdrawn (1 placebo, 2 xamoterol) with ventricular arrhythmias and/or disturbances of conduction. Compared to placebo, xamoterol had no effect on the rate of ventricular premature beats or ventricular tachycardia. Xamoterol increased nocturnal heart rate (0000-0600 hrs 79 +/- 2; placebo 72 +/- beats/min; P less than 0.03) but did not change blood pressure. Three patients receiving xamoterol, and 7 on placebo, required new (after randomisation) antianginal therapy. One patient treated with placebo developed new heart failure. These results show that xamoterol can be administered safely to selected patients following myocardial infarction, including those treated for mild heart failure.

Adrenergic beta-Agonists↗
PubMed1991

Dietary sodium loading increases plasma brain natriuretic peptide levels in man.

The effect of dietary sodium loading on plasma human brain natriuretic peptide-like immunoreactivity (hBNP-li) was examined in 11 normotensive subjects aged 20-23 years. Plasma hBNP-li increased significantly with increasing dietary sodium intake, with levels of 1.33 +/- 0.17 pmol/l on day 5 of a normal-sodium diet (24-h urinary sodium excretion of 171 +/- 16 mmol) and 2.04 +/- 0.10 pmol/l (P less than 0.05, versus normal-sodium diet) on day 5 of a high-sodium diet (24-h urinary sodium excretion 503 +/- 36 mmol). Corresponding plasma atrial natriuretic factor levels were 5.6 +/- 1.7 pmol/l and 11.0 +/- 2.0 pmol/l (P less than 0.05, versus normal-sodium diet) on the normal- and high-sodium diets, respectively. These results suggest that, in addition to atrial natriuretic factor, BNP may be a new and important natriuretic peptide which regulates sodium homeostasis in man during increased sodium intake.

Adult↗
PubMed1991

Lithium does not alter the renal response to a pressor dose of tyramine in man.

Renal clearance of lithium has been used as a marker of proximal tubular function in man. Recently, lithium pre-treatment has been shown to interfere with the natriuretic actions of some natriuretic agents in man. We have therefore investigated the effects of oral lithium carbonate (500 mg) on the natriuretic response to a pressor dose of tyramine (15 micrograms kg-1 min-1) in six normal volunteers. Lithium had no effect on baseline sodium excretion, nor did it affect the tyramine-induced increase in blood pressure and subsequent natriuresis. These results show that oral lithium carbonate (500 mg) does not appear to interfere with the pressure natriuretic response to tyramine in man.

Adult↗
PubMed1991

Atrial natriuretic factor inhibits metoclopramide stimulated aldosterone release in man.

1. Atrial natriuretic factor (ANF) has an inhibitory effect on angiotensin II and ACTH stimulated aldosterone secretion in man. The selectivity of this aldosterone suppressing effect of ANF is unclear in man. The present study investigated the effect of ANF on the increase in plasma aldosterone due to metoclopramide in man. 2. Eight normal male volunteers were studied on three occasions. Metoclopramide (10 mg slow i.v.) was given on all study days and each volunteer was randomised to receive 45 min infusion of either 5% D-glucose (placebo) or ANF (99-126) 3 or 15 pmol kg-1 min-1. 3. Metoclopramide increased plasma aldosterone to approximately 170% of baseline levels (P less than 0.01). Concomitant infusion of ANF 3 pmol kg-1 min-1 and 15 pmol kg-1 min-1 significantly attenuated this rise in plasma aldosterone to approximately 130% (P less than 0.05) and 110% (P less than 0.01) of baseline values respectively. 4. It is suggested, in the light of previous findings, that the inhibitory effect of ANF represents a non-selective action of ANF on aldosterone release.

Adult↗