Plasma vasopressin concentration in the anaesthetized dog before, during and after atrial distension.

Ledsome, J. R.; Ngsee, Johnny K.; Wilson, N.

doi:10.1113/jphysiol.1983.sp014680

Cited by 22 publications

(12 citation statements)

References 23 publications

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“…This change in left atrial pressure is within the physiological range; conscious dogs have increases in left atrial pressure of 4-6 cm H20 following a high salt meal (Kaczmarczyk et al 1979). We have previously reported that a change in atrial pressure of this magnitude causes a decrease in plasma concentration sf AVP, which is dependent upon stimulation of left atrial receptors by the increased left atrial pressure (Ledsome et al 1983). HR-ANP could have been released from the heart by a direct effect of atrial stretch or by a neural or humoral mechanism dependent upon stimulation of left atrial receptors.…”

Section: Discussionmentioning

confidence: 97%

“…These authors also found that ANP could be released from the atria by treatment with vasopressin. This is unlikely to be the mechanism by which atrial distension releases IR-ANP since atrial distension decreases plasma AVP and since the changes in AVP associated with atrial distension are abolished by vagotomy (Ledsome et al 1983). The finding that a large increase in heart rate induced by sympathetic stimulation did not increase plasma IR-ANP was surprising because tachycardia in both humans (Tikkanen et al 1985) and in rabbits (Rankin et a%.…”

Section: Discussionmentioning

confidence: 97%

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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: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 97%

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 D. BANKS AND M. C. HARRIS addition, it is known that baroreceptor activation leads to depression of supraoptic neurones (Kannan & Yagi, 1978;Yamashita & Koizuma, 1979;Harris, 1979), and that stimuli which activate baroreceptors depress the liberation of vasopressin (Ledsome, Ngsee & Wilson, 1983).…”

Section: Introductionmentioning

confidence: 99%

Lesions of the locus coeruleus abolish baroreceptor‐induced depression of supraoptic neurones in the rat.

Banks¹,

Harris²

1984

The Journal of Physiology

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SUMMARY1. Urethane-anaesthetized rats were used to investigate the influence of lesions within the locus coeruleus on the inhibition of phasically discharging supraoptic neurones that normally follows the activation of arterial baroreceptors.2. Carotid sinus baroreceptors were stimulated by the inflation of a blind sac of the carotid bifurcation. A general activation of arterial baroreceptors was evoked by increasing arterial blood pressure following the intravenous injection of the pure oc-adrenoreceptor agonist phenylephrine.3. The locus coeruleus of one side only was destroyed either by thermal (radiofrequency) lesions, or by the injection of 6-hydroxydopamine (1 PI, 05 mg/ml). The extent ofeach lesion was assessed histologically in stained tissue and with fluorescence histochemistry. 4. Lesions in locus coeruleus abolished all baroreceptor input to supraoptic neurones on the side ipsilateral to the lesion. The lesions had no effect on the cardiovascular responses to the stimulus, and did not abolish the excitation of supraoptic neurones after ipsilateral carotid body chemoreceptor activation.5. 6-Hydroxydopamine lesions (1 ,u, 2 mg/ml) in the rostral part of the ventrolateral Al catecholamine neurones were less consistent in their abolition of baroreceptor input to the supraoptic nucleus. When the input from ipsilateral carotid sinus baroreceptors was abolished, there was an equivalent effect on the influence of the carotid body chemoreceptors. Input from other arterial baroreceptors, activated by phenylephrine injection, was not affected.6. From these results, it is proposed that the baroreceptor-induced depression of phasically discharging supraoptic neurones is mediated via a direct noradrenergic input from the locus coeruleus.

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“…Comparison of the cardiovascular changes in the present experiments with those of Ledsome, Ngsee & Wilson (1983) suggest that the experiments of the two groups are not essentially different, while both groups also use the same anaesthetic.…”

Section: )mentioning

confidence: 70%

Evidence Against Anp as a Natriuretic Hormone During Atrial Distension

Knapp¹,

Hicks²,

Mary³

1986

Journal of Endocrinology

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To determine whether natriuresis attributable to atrial natriuretic peptides (ANP) is obtained in response to atrial stretch after blockade of the afferent input and reflex diuresis from atrial receptors, urine flow and sodium excretion were measured in response to distension of a balloon in the left atrium with the vagi at 37 and 9 degrees C. It is known that during such a distension ANP plasma concentration is increased by the same amount whether or not the afferent vagal fibres are intact. In 11 chloralose anaesthetized dogs 22 distensions with the vagi at 37 degrees C increased urine flow 117.5% and increased sodium excretion 28.7%. In 11 distensions with the vagi at 9 degrees C, urine flow did not change but sodium excretion decreased significantly (-20.9%). Thus natriuresis could not be demonstrated in response to atrial stretch in anaesthetised dogs after blockade of the atrial receptor reflex. These results imply that under these conditions, in which ANP is reportedly released into plasma, ANP is not acting as a hormone. The results must call into question the suggestion that ANP is released into plasma in a concentration capable of causing a natriuresis as its normal physiological function.

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Plasma vasopressin concentration in the anaesthetized dog before, during and after atrial distension.

Cited by 22 publications

References 23 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

Lesions of the locus coeruleus abolish baroreceptor‐induced depression of supraoptic neurones in the rat.

Evidence Against Anp as a Natriuretic Hormone During Atrial Distension

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