Release of neuropeptide Y in response to splanchnic nerve stimulation in the conscious calf.

Allen, J.M.; Bircham, P. M. M.; Bloom, Stephen R.; Edwards, A V

doi:10.1113/jphysiol.1984.sp015507

Cited by 119 publications

(35 citation statements)

References 19 publications

(18 reference statements)

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“…Thus, exposure of rabbits to cold environments leads to elevation of NPY in the superior cervical ganglion, in parallel with enhanced cutaneous vasoconstrictor activity, 19 whereas reserpine treatment of rats, which increases noradrenaline synthesis rate by withdrawal of feedback inhibition, 45 also increases ganglionic NPY levels. 20 By contrast, our densitometric measurements indicated no elevation of NPY content in individual sympathetic neurons of GH rats compared with normotensive rats. Thus, our data do not suggest that there is chronically elevated activity in the vasomotor system of the GH strain, although this does not exclude the possibility that the level of activity is inappropriate to the circulatory status of the rats or that exaggerated reflex responses to specific stimuli may occur.…”

Section: Bar Graphs Showing Comparisons Of Size Distributions (Exprescontrasting

confidence: 42%

Neuropeptide Y in rat sympathetic neurons is altered by genetic hypertension and by age.

et al. 1990

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We have used immunocytochemistry to quantitate neuronai neuropeptide Y in superior cervical ganglia of a strain of nonnotensive Wistar-Otago rats and a related genetically hypertensive strain over the age range 1-60 weeks. The numbers of neuropeptide Y-immunoreactive cells and total ganglionic cell numbers were both greater in ganglia of young nonnotensive than in those of hypertensive rats. Between 10 and 60 weeks of age, peptide immunoreactivity and total cell numbers both fell in nonnotensive rat ganglia but remained constant in ganglia from hypertensive rats. Densitometric analysis showed that the concentrations of neuropeptide Y were similar in neurons of age-matched individuals of both strains, but during aging there was a substantial decline in neuronai peptide content that was similar in both strains and that was not accompanied by any decline in neuronai immunoreactivity for tyrosine hydroxylase. Our results suggest that there is a developmental abnormality of neuropeptide Y in sympathetic neurons of this strain of genetically hypertensive rat and that, furthermore, the aging process is accompanied by a selective loss of neuronai neuropeptide Y that is independent of blood pressure status. (Hypertension 1990;16:63-71) I n adult animals of both the Otago (GH) and the Kyoto (SHR) strains of rat with a hereditary predisposition to hypertension, there is biochemical and functional evidence that peripheral sympathetic activity is inappropriately high.1 -7 Furthermore, neonatal destruction of the peripheral sympathetic nervous system retards the development of hypertension and reduces the absolute extent to which both blood pressure elevation and the associated cardiovascular hypertrophy are seen in adulthood. 8 * 14Also, studies in the GH strain have shown that hypertension can be reversed completely by ganglion blocking agents until the rats are about 4 weeks of age. 15There are, therefore, several lines of evidence to suggest that elevated sympathetic drive may be an etiologic factor in the genesis of high blood pressure in these animal models for essential hypertension. In the sympathetic nervous system, neuropeptide tyrosine or neuropeptide Y (NPY) is jointly localized 23 Therefore, we compared the patterns of NPY immunoreactivity in sympathetic neurons of nonnotensive and GH hypertensive rats from the neonatal period through late adulthood. Methods AnimalsThe rats used in the present study were raised in our animal house from a normotensive white Wistar line originating in the Otago Medical School and from the GH line that was bred from the same stock.24 Breeding was from brother-sister matings, and ah 1 rats were fed a proprietary rat chow (quoted sodium content 0.5%) with water ad libitum. Periodic checks of blood pressures in conscious, prewarmed adult rats using an occlusive tail cuff and a pulse transducer confirmed that resting systolic pressures were less than 140 mm Hg in normotensive rats and at least 170 mm Hg in hypertensive rats.

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Section: Bar Graphs Showing Comparisons Of Size Distributions (Exprescontrasting

confidence: 42%

Neuropeptide Y in rat sympathetic neurons is altered by genetic hypertension and by age.

et al. 1990

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“…It is therefore likely that alterations in adrenal NPY content may be the primary cause of the differences in HPA function between these rat strains. This is entirely consistent with reports that adrenal NPY synthesis and release is controlled by the sympathetic input to the gland (Allen et al 1984, Gaumann et al 1989.…”

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Intra-adrenal mechanisms in the response to chronic stress: investigation in a rat model of emotionality

Kosti

Raven²,

Renshaw³

et al. 2006

Journal of Endocrinology

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The exploratory behaviour of the genetically derived Maudsley rat model of emotionality has been well characterized. Maudsley reactives (MR) present with more 'anxious-like' behaviour than Maudsley nonreactives (MNR). Although this behaviour is assumed to be associated with altered adrenocortical function, the few studies addressing this issue have produced inconsistent findings. We therefore set out to investigate the adrenal endocrinology of the MR and MNR strains. Control Wistars, the ancestors of the Maudsleys, have been used for the first time to set the baseline for all the experiments carried out. It was found that the MNR strain had a significantly blunted adrenocorticotrophic hormone (ACTH) response to restraint stress compared with Wistars, but a normal corticosterone response. Conversely, the MR had a significantly exaggerated ACTH response to restraint stress, but a normal corticosterone response. This finding suggested that the MR adrenal is less sensitive to ACTH than the MNR. This was confirmed by investigating the corticosterone dose-response to ACTH in adrenals from the two strains incubated in vitro. Several possible intraadrenal regulators were investigated, but the only significant molecular difference in the adrenal glands from the two strains was the level of expression of neuropeptide Y (NPY), which is known to be a stress-responsive peptide in the adrenal. We propose that intra-adrenal NPY is responsible for blunting adrenocortical responses to ACTH stimulation in the MR strain. The observed changes in adrenal NPY suggest that this rat strain may serve as a model of chronic stress, with the MR phenotype representing maladaptation.

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“…These findings complement those of other workers who have investigated patterns of activity in autonomic nerve fibres and found that some fire characteristically almost continuously at low frequencies while others discharge phasically in bursts (Adrian, Bronk & Phillips, 1932;Wallin, 1981;de Groat, Booth, Milne & Ropollo, 1982;Kawamura, Matsuo & Yamamoto, 1982). Evidence that certain responses to stimulation of sympathetic nerves are enhanced by an intermittent stimulus pattern has been obtained in the case of the splanchnic nerves in respect of the release of catecholamines from the adrenal medulla (S. R. Bloom, A. V. Edwards & C. T. Jones, unpublished observations) and release of bombesin and neuropeptide Y from post-ganglionic sympathetic nerve terminals (Bloom, Edwards & Ghatei, 1984;Allen, Bircham, Bloom & Edwards, 1984) in conscious calves.…”

Section: Introductionmentioning

confidence: 99%

Effects of stimulating the sympathetic innervation in bursts on submandibular vascular and secretory function in cats.

Bloom

Edwards

Garrett

1987

The Journal of Physiology

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SUMMARY1. The effects of continuous stimulation of the peripheral end of the ascending cervical sympathetic nerve were compared with those of intermittent stimulation, so arranged as to deliver the same total number of impulses, in cats under chloralose anaesthesia.2. Continuous stimulation caused a flow of saliva at 5-10 Hz, but not at 2 Hz. In contrast, the same total number of impulses delivered intermittently in bursts elicited a prompt secretion at a frequency as low as 20 Hz for 1 s at 10 s intervals (corresponding to 2 Hz continuously) and a significantly higher rate of secretion at 50 Hz in bursts than that obtained in response to 5 Hz continuously.3. Continuous stimulation also caused a rise in submandibular vascular resistance (s.v.r.), which persisted throughout the period of stimulation, and was followed immediately thereafter by an intense but transient fall in s.v.r. During stimulation in 1 s bursts, each burst was followed first by a brief rise in s.v.r. and shortly after by a fall. The balance between these two components varied widely between individual animals but often led to an overall fall in s.v.r. during stimulation i.e. complete reversal of the mean vascular effect. A further fall in s.v.r. was then recorded when the stimulus was discontinued.4. Propranolol (1-0 mg/kg) reduced but failed to abolish the secretary response. It also altered the balance between the two phases of the vascular response slightly in favour of a rise in s.v.r. during stimulation, without apparently affecting the size of the after-dilatation.5. Pre-treatment with dihydroergotamine (1-0 mg/kg) invariably blocked secretion and revealed a small vasodilator response during sympathetic stimulation with either pattern of stimulation; it also blocked the after-dilatation.6. Following combined pre-treatment with propranolol and dihydroergotamine, to produce total adrenergic blockade, there was a small residual vasoconstrictor component which amounted to an increase in mean s.v.r. of about 20% during stimulation at 10 Hz continuously. This may have been due to release ofneuropeptide Y (NPY).7. Small but significantly greater amounts of NPY were released into the effluent S. R. BLOOM, A. V. EDWARDS AND J. R. GARRETT blood during stimulation of the ascending cervical sympathetic nerve at 70 Hz in bursts than during continuous stimulation. No significant release of vasoactive intestinal peptide (VIP), somatostatin, bombesin, substance P or calcitonin generelated peptide (CGRP) was observed during stimulation at any frequency.8. It is concluded that, in addition to a vasodilator component due to ,-adrenoceptor activation, stimulation of the sympathetic innervation to the submandibular gland in the cat elicits a vasodilator response by some pathway that depends upon a-adrenoceptor activation. This is sufficiently potent to override aadrenergic vasoconstriction during certain patterns of stimulation and is mainly responsible for the transient dilatation which occurs on cessation of stimulation. These vasodilator effects may invol...

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Release of neuropeptide Y in response to splanchnic nerve stimulation in the conscious calf.

Cited by 119 publications

References 19 publications

Neuropeptide Y in rat sympathetic neurons is altered by genetic hypertension and by age.

Neuropeptide Y in rat sympathetic neurons is altered by genetic hypertension and by age.

Intra-adrenal mechanisms in the response to chronic stress: investigation in a rat model of emotionality

Effects of stimulating the sympathetic innervation in bursts on submandibular vascular and secretory function in cats.

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