Changes in plasma catecholamine and neuropeptide Y levels after sympathetic activation in dogs

Poncet, M; Damase‐Michel, Christine; Tavernier, Geneviève; Tran, Marie-Antoinette; Berlan, Michel; Montastruc, Jean‐Louis; Montastruc, P

doi:10.1111/j.1476-5381.1992.tb14232.x

Cited by 23 publications

(12 citation statements)

References 18 publications

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“…Other properties of the drug may also explain the discrepancies concerning the efficacy of yohimbine in the management of orthostatic hypotension. These data confirm previous results from our group (Poncet et al, 1992;Tavernier et al, 1992). Secondly, its cardiovascular effects depend on the mode of administration because of erratic bioavaibility in humans.…”

Section: Discussionsupporting

confidence: 90%

Effects of yohimbine, an α₂‐adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension

Verwaerde

1997

Fundamemntal Clinical Pharma

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Yohimbine has been proposed for the treatment of neurogenic orthostatic hypotension; however, no controlled trial has been performed in experimental models of orthostatic hypotension or in patients with autonomic failure. The aim of the present study was to compare the effects of yohimbine (0.05 mg/kg, intravenously [i.v.]) and placebo (saline) in a new model of neurogenic orthostatic hypotension obtained by sinoaortic denervation (SAD) in chloralose-anaesthetized dogs. Blood pressure, heart rate, noradrenaline plasma levels and systolic blood pressure and heart rate short-term variabilities (calculated on low frequency [40-50 MHz] and high frequency [390-490 MHz] bands) were measured in supine position and after a 10 min 80 degrees head-up tilting. The drugs were administered in a double-blind cross-over randomized fashion. The head-up tilting performed in normal animals increased diastolic blood pressure (+12 +/- 4 mmHg), heart rate (+39 +/- 12 beats per minute [bpm]), the low frequency band of systolic blood pressure and noradrenaline plasma level, without changing systolic blood pressure or heart rate variability. In SAD dogs, a marked fall in systolic (-80 +/- 11 mmHg) and diastolic (-43 +/- 4 mmHg) blood pressures was observed within 1 min after placebo, without modification in heart rate, systolic blood pressure and heart rate short-term variabilities and noradrenaline plasma levels. In SAD dogs, yohimbine (0.05 mg/kg, i.v.) delayed the blood pressure fall elicited by head-up tilting, but failed to modify its magnitude. These results show that, in the model of orthostatic hypotension obtained by SAD, yohimbine, at an alpha 2-adrenoceptor selective dose (0.05 mg/kg), delays the fall in blood pressure elicited by head-up tilting. The effect of yohimbine can be explained by an increase in sympathetic tone.

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Section: Discussionsupporting

confidence: 90%

Effects of yohimbine, an α₂‐adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension

Verwaerde

1997

Fundamemntal Clinical Pharma

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“…(bolus), as in previous experiments from our group [14,15]. At this dose, yohimbine acts mainly on presynaptic alpha2‐adrenoceptors [14,15].…”

Section: Methodsmentioning

confidence: 70%

“…The electrochemical detector response was linear for concentrations ranging from 10 pg/mL to 100 ng/mL. In these conditions, the detection limits is 10 pg/mL [14].…”

Section: Methodsmentioning

confidence: 99%

Changes in vascular alpha1‐ and alpha2‐adrenoceptor responsiveness by selegiline treatment

Pelat

Verwaerde

Tran

et al. 2001

Fundamemntal Clinical Pharma

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Pharmacoepidemiological studies have reported an excess of mortality with selegiline, a MAO B inhibitor used in the treatment of Parkinson's disease. The mechanism of this putative adverse effect remains unknown but an interaction with the sympathetic nervous system was suggested. The aim of the present study was to investigate the influence of selegiline (10 mg/daily, orally during one week) on vascular alpha1- and alpha2-adrenoceptor responsiveness in conscious unrestrained dogs. Selegiline significantly increased resting values of both systolic and diastolic blood pressures and noradrenaline plasma levels (HPLC) without changing heart rate. Moreover, spectral analysis of systolic blood pressure (Fast Fourier Transformation) showed that selegiline increased the relative energy of a low frequency band without modifying the total spectrum. ED 50 calculated from dose-pressor response curves with phenylephrine (after beta-blockade by propranolol), an index of alpha1-adrenoceptor response or with noradrenaline (after alpha1- and beta blockade by prazosin plus propranolol), an index of alpha2-adrenoceptor response, were significantly higher after selegiline. Selegiline failed to modify the number of platelet alpha2-adrenoceptors measured by [(3)H] RX 821002 binding. Yohimbine-induced increase in noradrenaline release was significantly more marked after selegiline. These results support the evidence that selegiline induces a vascular alpha1- and alpha2-adrenoceptor-hyposensitivity that can be explained by the increase in noradrenaline release elicited by the drug.

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“…The number of animals in group varied from 6 to Í VIP, vasaoactive intestinal peptide; T3, triiodothyronine; T4 thyroxine. tion of arterial blood pressure and plasma norepinephrine (26,27). Likewise, the functional responses to thyroid or splenic nerve stimulation were largely abolished by aadrenoceptor blocking agents, apparently leaving no role for a non-adrenergic mediator (12,13,28).…”

Section: Discussionmentioning

confidence: 98%

The Neuropeptides, VIP and NPY, That Are Present in the Thyroid Nerves Are Not Released into the Thyroid Vein

Michalkiewicz¹,

Dey²,

Huffman³

et al. 1998

Thyroid

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In the present study, we tested the hypothesis that the neuropeptides, vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY), which are present in the thyroid nerves, act as physiological neurotransmitters involved in the regulation of thyroid hormone secretion and thyroid blood flow. Specifically, we examined whether these neuropeptides can be released into thyroid blood vessels by electrical stimulation of the major thyroid nerves or whether their expression is altered by changes in iodine intake. Sprague-Dawley rats were used in this study. The cervical sympathetic trunk or the superior laryngeal nerve was stimulated by bipolar electrodes in anesthetized rats. During nerve stimulation, blood samples were withdrawn from the thyroid vein. Thyroid blood flow was monitored by laser Doppler blood flowmetry. Sympathetic stimulation caused a marked decrease in thyroid blood flow, which was associated with a significant increase in release of norepinephrine. However, these effects were not accompanied by any change in NPY release into the thyroid vein. Stimulation of the superior laryngeal nerve was not associated with changes in thyroid blood flow or VIP release into the thyroid vein. In a separate experiment, rats were fed a diet containing low-, high-, or normal iodine concentrations. Triiodothyronine (T3) and thyroxine (T4) levels in thyroid venous plasma were significantly reduced in rats fed a low-iodine diet but not in a separate group of rats fed a high iodine diet. However, these treatments had no effect on VIP or NPY concentrations in thyroid venous plasma or in thyroid ganglia. Thus, our results indicate that VIP and NPY, which are present in the thyroid nerves, may not be directly involved in the regulation of thyroid function.

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Changes in plasma catecholamine and neuropeptide Y levels after sympathetic activation in dogs

Cited by 23 publications

References 18 publications

Effects of yohimbine, an α₂‐adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension

Effects of yohimbine, an α₂‐adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension

Changes in vascular alpha1‐ and alpha2‐adrenoceptor responsiveness by selegiline treatment

The Neuropeptides, VIP and NPY, That Are Present in the Thyroid Nerves Are Not Released into the Thyroid Vein

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Changes in plasma catecholamine and neuropeptide Y levels after sympathetic activation in dogs

Cited by 23 publications

References 18 publications

Effects of yohimbine, an α2‐adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension

Effects of yohimbine, an α2‐adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension

Changes in vascular alpha1‐ and alpha2‐adrenoceptor responsiveness by selegiline treatment

The Neuropeptides, VIP and NPY, That Are Present in the Thyroid Nerves Are Not Released into the Thyroid Vein

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Product

Resources

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Effects of yohimbine, an α₂‐adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension

Effects of yohimbine, an α₂‐adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension