Heterologous Radioimmunoassay of Atrial Natriuretic Polypeptide in Dog and Rabbit Plasma

Wilson, N.; Ledsome, J. R.; Keeler, R.; Rankin, A. H.; Wade, J. P.; Courneya, Carol Ann

doi:10.1080/01971528608063047

Cited by 35 publications

(10 citation statements)

References 18 publications

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“…Since the antiserum used in o w experiments shows 100% cross reactivity with a-human ANP it is likely that there is a similar cross reactivity with dog ANP. We were able to show that antibodies raised to rat ANP reacted with immunoreactive substances in dog plasma and in acid extracts of dog atria (Wilson et al 1986). The values of IR-ANP found in dog plasma, which were in the range of 45-105 pg/mL, are lower than those that have been reported in the rat.…”

Section: Discussioncontrasting

confidence: 76%

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Time course of release of atrial natriuretic peptide in the anaesthetized dog

Ledsome¹,

Wilson²,

Rankin³

et al. 1986

Can. J. Physiol. Pharmacol.

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In 12 chloralose anaesthetized dogs plasma concentration of immunoreactive atrial natriuretic peptide (IR-ANP) was measured using a radioimmunoassay. Plasma IR-ANP was 74 +/- 4.8 pg/mL (mean +/- SE) and increased by 39 +/- 4.1 pg/mL when left atrial pressure was increased by 10 cm H2O during partial mitral obstruction. Observation of the time course of the changes in IR-ANP during atrial distension showed that IR-ANP was increased within 2 min of atrial distension and declined after atrial distension, with a half-time of 4.5 min. The time course of the changes in IR-ANP was unaffected by vagotomy or administration of atenolol. Maximum electrical stimulation of the right ansa subclavia failed to produce any change in IR-ANP. IR-ANP was higher in coronary sinus plasma than in femoral arterial plasma confirming that the heart was the source of the IR-ANP. The results support the hypothesis that IR-ANP is released from the heart by a direct effect of stretch of the atrial wall rather than by a neural or humoral mechanism involving a reflex from atrial receptors.

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Section: Discussioncontrasting

confidence: 76%

“…CA, RAS-8798, lot 006107). Details of the assay (Wilson et al 1986) and its application to dog plasma (kdsome et a1 . 1985) have k e n published previously.…”

Section: Wadisimmunoassaymentioning

confidence: 99%

Time course of release of atrial natriuretic peptide in the anaesthetized dog

Ledsome¹,

Wilson²,

Rankin³

et al. 1986

Can. J. Physiol. Pharmacol.

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“…Finally, we reported the time-dependent analysis of neurohormones and events using neurohormones as a binary variable, defined as activated and not activated, according to the definition used in our previous paper (c1·96 SD above the mean of normal patients) [19] . Using this definition and type of analyses we found a significant relationship between activation of norepinephrine and recurrent myocardial infarction and combined events in multivariate analyses.…”

Section: Last Neurohormone Level Prior To An Event and Prognosismentioning

confidence: 99%

“…Samples which took more than 24 h to reach the central laboratory, or which were haemolyzed or thawed, were not analysed. Previously described neurohormone assays [18,19] were used to measure plasma renin activity and plasma concentrations of norepinephrine, atrial natriuretic peptide, arginine vasopressin, epinephrine, and aldosterone. The pattern of pre-randomization neurohumoral activation and its prognostic significance have been reported previously [2,9] .…”

Section: Patientsmentioning

confidence: 99%

Two-year time course and significance of neurohumoral activation in the Survival and Ventricular Enlargement (SAVE) Study

Vantrimpont

Rouleau

Ciampi

et al. 1998

European Heart Journal

103

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Aims To describe the temporal evolution of neurohumoral activation in survivors of myocardial infarction with left ventricular dysfunction who are initially asymptomatic and to relate this to prognosis. Methods and ResultsPatients in the neurohumoral substudy (n=534) of the Survival and Ventricular Enlargement (SAVE) study had their neurohormones measured at baseline, 3, 12 and 24 months post-infarction, were followed 38 7 months and had these values related to prognosis. All patients had a left ventricular ejection fraction c40% early post-infarction. Atrial natriuretic peptide, aldosterone, norepinephrine and plasma renin activity decreased progressively over time. Patients with events had a persistent increase in these neurohormones with those dying within the first 24 months of follow-up having the greatest increase. Treatment with captopril affected only plasma renin activity (increase) and aldosterone (decrease). For patients who remained asymptomatic for the first 3 months postinfarction (n=471), by multivariate analyses (all neurohormones together with non-neurohumoral risk factors), 3-month plasma atrial natriuretic peptide and aldosterone were the most closely related to the development of severe heart failure or to the combined end-points (cardiovascular death, myocardial infarction, or severe heart failure). No neurohormone was related to recurrent myocardial infarction or to cardiovascular mortality. When the last neurohormone measured prior to an event was considered along with non-neurohumoral risk factors (adjusted univariate), atrial natriuretic peptide, aldosterone, norepinephrine and epinephrine were associated with prognosis indicating that a time-dependent analysis identified a closer relationship between neurohormones and events than that identified by 3-month values. However, by multivariate analyses atrial natriuretic peptide was the only neurohormone associated with an event, being associated with the development of severe heart failure (P<0·001) and the combined end-points (P=0·022). However, when neurohormones were considered as binary variables, activated or non-activated (defined as >1·96 SD above the mean of age-matched controls), an association between activation of norepinephrine prior to recurrent myocardial infarction (P<0·001) and combined end-points (P<0·01) and between activation of aldosterone and severe heart failure (P<0·05) was identified.Conclusions Neurohumoral activation decreases progressively post-infarction, but only in patients with a good prognosis. In patients with a left ventricular ejection fraction c40% and asymptomatic post-infarction plasma atrial natriuretic peptide at 3 months, aldosterone levels appeared to be the neurohormones most closely associated with prognosis. Increased levels of atrial natriuretic peptide, aldosterone and norepinephrine appear to be temporally most closely associated with events.

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“…Radioimmunoassay ofIR-ANF Plasma IR-ANF was measured according to a previously described method (Wilson, Ledsome, Keeler, Rankin, Wade & Courneya, 1986) using mouse monoclonal anti-a ANF serum in a dilution of 1 :11250000. The plasma was extracted according to a previously described method (Rankin et al 1987a).…”

Section: Treatment Of Blood Samplesmentioning

confidence: 99%

The effect of tachycardia on right atrial dynamics and plasma atrial natriuretic factor in anaesthetized rabbits.

King

Ledsome

1990

The Journal of Physiology

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SUMMARY1. The effect of tachyeardia on right atrial pressure (RAP) and dimensions (RAD) and plasma immunoreactive atrial natriuretic factor (IR-ANF) was examined in anaesthetized rabbits before and after the administration of atenolol.2. Small increases in plasma IR-ANF occurred during pacing at 6 Hz and after the administration of atenolol (0 4 mg kg-1). A significantly greater increase in IR-ANF occurred during pacing in the presence of atenolol.3. Despite a significant rise in mean RAP, systolic RAD (SRAD) and diastolic RAD (DRAD) did not change during tachyeardia. Systolic RAD increased after the administration of atenolol while both SRAD and DRAD increased during pacing in the presence of atenolol.4. Systolic right atrial wall stress (SRAS) increased during tachyeardia, did not change after the administration of atenolol, and increased during pacing in the presence of atenolol. Minute SRAS followed a similar pattern of changes except that it decreased after atenolol.5. Diastolic right atrial wall stress (DRAS) did not change during tachyeardia, and increased both after atenolol and after pacing in the presence of atenolol. Tachyeardia led to an increase in minute DRAS; a significantly greater increase in minute DRAS occurred during tachycardia in the presence of atenolol.6. The absence of alterations in RAD during tachyeardia suggests that the release of ANF in response to tachycardia is not due to simple mechanical stretch of the atria. Both systolic and diastolic atrial wall stress may be determinants of ANF release: the influence of systolic factors appears to predominate during tachycardia while diastolic factors appear to be the major determinants of the effects of atenolol.

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Heterologous Radioimmunoassay of Atrial Natriuretic Polypeptide in Dog and Rabbit Plasma

Cited by 35 publications

References 18 publications

Time course of release of atrial natriuretic peptide in the anaesthetized dog

Time course of release of atrial natriuretic peptide in the anaesthetized dog

Two-year time course and significance of neurohumoral activation in the Survival and Ventricular Enlargement (SAVE) Study

The effect of tachycardia on right atrial dynamics and plasma atrial natriuretic factor in anaesthetized rabbits.

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