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Biomedical subjects

P Montastruc

Publications and source records attributed to P Montastruc.

At least 19 recordsLinked to original sources
PubMed1992

Release of neuropeptide Y and noradrenaline during afferent nerve stimulation.

The present study was carried out to investigate the possibility that noradrenaline (NA) and neuropeptide Y (NPY) are co-released after afferent vagal or saphenous stimulation (1, 5, 10 and 20 Hz) in chloralose-anaesthetized dogs. Electrical stimulation of the vagus elicited an increase in plasma NA levels for the 5, 10 and 20 (but not 1) Hz frequencies. Blood pressure only increased after a 20-Hz stimulation. In contrast, no change in plasma NPY levels was observed whatever the frequency of stimulation. Electrical stimulation of the saphenous nerve failed to change plasma NA and NPY levels. The present data suggest that (1) the release of NA varies according to the frequency of stimulation of nociceptive fibres, (2) NPY release does not seem to be involved in the pressor effect elicited by the stimulation of nociceptive-sensitive fibres, and (3) NPY and NA release are not necessarily linked.

Animals↗
PubMed1992

Naloxone or haloperidol but not yohimbine reverse apomorphine-induced respiratory depression.

Intravenous injection of low doses of naloxone was found to reverse the respiratory depression induced by apomorphine in chloralose-anesthesized dogs. Similar results were obtained with haloperidol, whereas yohimbine remained ineffective. These data suggest that apomorphine depresses respiratory rate through a mechanism involving both dopamine and opiate mechanisms but not alpha 2-adrenoceptors. Respiratory arrest induced by overdosages of apomorphine can be treated with naloxone.

Animals↗
PubMed1992

Is yohimbine-induced increase in salivary secretion a kinin-dependent mechanism?

We have previously reported that the alpha 2-adrenoceptor antagonist yohimbine induced a significant increase in both salivary flow rate and kallikrein output. In order to assess the possible role of the kinin-kallikrein system in the increase in salivary secretion elicited by yohimbine, the effects of aprotinin, an inhibitor of kallikrein activity, were investigated in yohimbine-treated conscious dogs. Aprotinin (at a dose, 5000 IU/kg iv, which reduced both resting and yohimbine-induced increase in kininogenase and amidolytic activities of saliva) which remained inactive alone, failed to modify the increase in salivary volume elicited by yohimbine (0.5 mg/kg iv). These results show that the rise in salivary flow rate observed under alpha 2-adrenoceptor antagonist is not induced by the kinin-kallikrein system. The release of kallikrein into saliva observed after yohimbine is rather the consequence than the cause of the increase in salivary secretion.

Animals↗
PubMed1992

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

1. Plasma levels of noradrenaline (NA) and neuropeptide Y (NPY) were evaluated in two experimental models associated with an increase in sympathetic tone: conscious dogs which were subject to either sinoaortic denervation or acute administration of the alpha 2-adrenoceptor antagonist yohimbine. 2. Dogs that had undergone sinoaortic denervation exhibited a two fold increase in plasma NA without any change in NPY levels. 3. Yohimbine (0.05 mg kg-1 i.v. as a bolus) produced similar effects. A higher dose of yohimbine (0.5 mg kg-1 i.v.) increased both plasma NA (7 fold) and NPY (6.5 fold) levels. 4. The present results indicate that changes in plasma catecholamines and NPY are not always concomitant. They suggest that the simultaneous release of NA and NPY is only observed under in vivo conditions for a marked increase in sympathetic tone.

Animals↗
PubMed1992

[Beta adrenergic receptors and experimental left ventricular hypertrophy].

The effects of sinoaortic denervation (SAD) on the development of left ventricular hypertrophy (R: heart weight/total body weight; LVT : left ventricular thickness), myocardial beta-adrenergic receptivity ([125I]CYP binding; adenylate cyclase activity) and plasma catecholamine levels (HPLC) were investigated in both normotensive (group 1) and hypertensive dogs evaluated (group 2) 1 and 18 months (group 3) after SAD. Noradrenaline (NA) and adrenaline (A) plasma levels were 461 +/- 54 and 85 +/- 45 pg/ml in controls, 861 +/- 185 and 191 +/- 23 pg/ml in group 2 (P < 0.05) and were normal in group 3 (426 +/- 132 and 110 +/- 16 pg/ml). R and LVT values were higher (p < 0.05) in SAD dogs (R = 7.7 +/- 0.1 and 7.8 +/- 0.2; LVT = 13.6 +/- 1.3 and 14.2 +/- 0.9 mm in groups 2 and 3 respectively) than in group 1 (R = 6.7 +/- 0.1, LVT = 9.3 +/- 0.8 mm). In group 1, the total number of beta-adrenoceptors (beta-AR) was 37 +/- 11 and 29 +/- 6 fmol/mg prot in left ventricule (LV) and right auricle (RA) respectively. Bmax was significantly lower in group 2 (LV: 10 +/- 3; RA: 13 +/- 2 fmol/mg prot, p < 0.05) than in group 1 but was normal in group 3 (LV: 37 +/- 3 and RA: 31 +/- 3 fmol/mg prot).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1992

[Differential regulation of the release of norepinephrine and neuropeptide Y].

The release of catecholamines and their co-neurotransmitter neuropeptide Y was investigated in conscious dogs with neurogenic arterial hypertension elicited by sinoaortic denervation. One month after denervation, an elevation of catecholamine levels (measured by HPLC) without elevation of neuropeptide Y levels in plasma (evaluated by RIA) has been found. This dissociation could be explained by a transient release of neuropeptide Y during the first weeks after surgery; a depletion of neuronal neuropeptide Y due to the permanent sympathetic stimulation; or an insufficient increase in sympathetic tone. To test these three hypotheses, we investigated the time courses of catecholamine and neuropeptide Y levels in arterial plasma during the first five weeks after sinoaortic denervation; and the responses to yohimbine (an alpha 2 antagonist which enhances transmitter release). Resting neuropeptide Y levels in plasma remained normal during the first five weeks after sinoaortic denervation. In normal dogs, a high dose of yohimbine (0.5 mg/kg i.v.) elevated both catecholamine (6-fold) and neuropeptide Y levels (1.5-fold), whereas a lower dose (0.05 mg/kg i.v.) induced a two fold elevation of catecholamine levels without changing neuropeptide Y concentrations. In sinoaortically denervated dogs, yohimbine elicited elevation of both catecholamines and neuropeptide Y whatever the dose used. Thus, neurogenic arterial hypertension in dogs seams to involve catecholamines but not neuropeptide Y. Moreover, the present work suggests that a high level of sympathetic stimulation is required for a co-release of catecholamines and neuropeptide Y.

Animals↗
PubMed1991

Anorectic effect of alpha 2-antagonists in dog: effect of acute and chronic treatment.

Acute oral administration of alpha 2-antagonists (yohimbine, RX 821002, atipamezole: 1 mg/kg each) reduced dog food intake. Yohimbine reduced food intake over 20 hours, while the effect of the two other drugs lasted only 2 hours. Yohimbine (0.4 or 1 microgram/kg) gave the same results. At these doses, it promoted a lasting durable increase in plasma nonesterified fatty acids and catecholamines levels and a transient elevation of plasma insulin levels. The beta-antagonist nadolol (4 mg/kg per os) suppressed the yohimbine-induced lipid mobilization without modifying its anorectic effect. Chronic oral yohimbine (0.4 mg/kg/day during 14 days) reduced food intake and promoted a weight loss. Normal food intake was recovered two days after yohimbine withdrawal. No change was observed in the number of platelet alpha 2-adrenergic receptors. In addition to their lipid mobilizing action and sympathetic tone stimulation, alpha 2-antagonist compounds reduce food intake.

Adrenergic alpha-Antagonists↗
PubMed1991

Clonidine but not propranolol decreases plasma neuropeptide Y (NPY) levels.

The effects of acute administration of two antihypertensive drugs, clonidine and propranolol, on plasma NPY and catecholamine levels were compared in sinoaortic denervated (a model associated with a marked increase in sympathetic tone and a rise in blood pressure) and normal conscious dogs. Clonidine decreased plasma noradrenaline and NPY concentrations in both groups of animals. Propranolol failed to change plasma noradrenaline and NPY levels in sinoaortic denervated dogs but elicited a decrease in plasma noradrenaline with no change in NPY levels in normotensive animals. The present experiments show that changes in plasma noradrenaline and NPY concentrations are not always simultaneous. The decrease in plasma NPY concentrations could contribute to the sympatholytic effect of clonidine.

Animals↗
PubMed1991

Yohimbine increases submaxillary kallikrein release into the saliva in dogs: evidence for alpha 2-adrenoceptor-mediated inhibition of cholinergic pathways.

1. The effects of the alpha 2-adrenoceptor antagonist, yohimbine (0.5 mg kg-1, i.v.) on basal, sympathetic and parasympathetic stimulation-induced submaxillary kallikrein release were investigated in the anaesthetized dog. Kallikrein was measured by its kininogenase activity before and after trypsin activation which also allowed a study of the proportion of active to total enzyme. 2. Yohimbine induced a rapid, three fold increase in basal kallikrein release correlated with an increase in salivary flow rate which lasted for 60 min following injection. 3. Sectioning the chorda tympani did not affect basal kallikrein release but abolished yohimbine-induced rise in salivary kallikrein secretion. 4. Parasympathetic stimulation alone induced a 3 to 4 fold increase in basal kallikrein release correlated with an increase in salivary flow rate. Yohimbine induced a significant additional increase in parasympathetic-stimulated kallikrein release. 5. When the cervical sympathetic nerve was sectioned the basal kallikrein release decreased by 30 to 40%. 6. Sympathetic stimulation alone also induced a 3 to 4 fold increase in basal kallikrein. This was not correlated with the salivary flow and unaffected by yohimbine. 7. The results indicate that yohimbine increases submaxillary kallikrein release into the saliva by inhibition of presynaptic alpha 2-adrenoceptors located on the chorda tympani nerve endings.

Animals↗
PubMed1991

Thermogenic and lipolytic effect of yohimbine in the dog.

1. Lipid mobilization during a hypocaloric diet may be enhanced by a pharmacological approach using alpha 2-adrenoceptor antagonists since these drugs are known to increase sympathetic tone and stimulate lipolysis. Studies were undertaken in the dog in order to evaluate the effects of oral yohimbine administration (alpha 2-adrenoceptor antagonist) on heat production, metabolic, endocrinological and cardiovascular parameters. 2. Acute oral yohimbine (0.25 or 0.40 mg kg-1) provoked an increase in plasma non-esterified fatty acids. The drug increased sympathetic nervous system activity as indicated by the increased level of plasma noradrenaline. These effects persisted during the entire experimental period (4 h). The increase in plasma noradrenaline level was two fold higher with the higher dose of yohimbine (0.4 mg kg-1). The plasma adrenaline level was increased only with the higher dose. 3. Yohimbine transiently increased plasma insulin and the effect was dose-dependent. 4. Yohimbine (0.25 mg kg-1) enhanced heart rate and arterial blood pressure. 5. The effect of yohimbine on oxygen consumption, carbon dioxide and heat production was determined by indirect calorimetry. The drug (0.25 mg kg-1) increased O2 consumption and CO2 and heat production 30 min after its administration and the effect persisted over the experimental period. The respiratory quotient, rather low in the fasting animals, remained unchanged. 6. The present work indicates that thermogenesis and lipid mobilization are enhanced during fasting in the dog by alpha 2-adrenoceptor blockade. Yohimbine also induced a transient increase in plasma insulin level and increased heart rate and blood pressure. The lipid mobilization plus the action on thermogenesis observed after yohimbine draw attention to the putative interest of a2-antagonists in the pharmacological treatment of obesity during restricted calorie intake.

Animals↗
PubMed1991

[Renal adrenergic beta receptors and experimental neurogenic hypertension].

Sinoaortic denervation SAD in dog induces a permanent rise in blood pressure and heart rate leading to an experimental model of arterial hypertension. This model is associated with a marked increase in plasma catecholamine levels during the two first months. The present study investigates the changes in some renal vasoactive systems (renin activity, aldosterone and kallikrein) and cortical renal beta adrenoceptors during the development of this experimental neurogenic hypertension in dogs. SAD dogs exhibited a biphasic change in plasma renin activity and catecholamines: 1 month after SAD, plasma noradrenaline rose and renin activity decreased. These parameters return to normal values 18 months after SAD whereas blood pressure remained elevated. In contrast, plasma aldosterone levels decreased and urinary sodium increased. Urinary kallikrein was enhanced 1 month after SAD and showed a marked decrease 18 months later when compared with pre-SAD values. Cortical renal beta adrenoceptors (evaluated by 125I-cyanopindolol) exhibited a permanent decrease (Bmax) whatever the duration of arterial hypertension. These results show that SAD-induced hypertension in dog is associated with changes in renal vasoactive system involving urinary excretion of kallikrein and cortical renal beta adrenoceptors. These alterations could be involved in the maintenance of arterial hypertension in this experimental model.

Animals↗
PubMed1991

[Neuropeptide Y, orthosympathetic nervous system, hypertension and alpha-2 adrenergic receptors].

Neuropeptide Y (NPY) is coreleased with noradrenaline (NA) from sympathetic nerve endings. In vitro data suggest that NPY is coreleased during high stimulation frequencies. The present study investigates plasma levels of catecholamines and neuropeptide Y (NPY) during changes in sympathetic nervous activity in conscious dogs. Increase in sympathetic tone: arterial hypertension elicited by sinoaortic denervation induced an increase (X 2) in plasma noradrenaline (NA) but no change in NPY levels. High (0.5 mg/kg i.v.) but not low (0.05 mg/kg i.v.) doses of yohimbine rose plasma NPY concentrations. Decrease in sympathetic tone: clonidine (10 micrograms/kg i.v.) but not beta-blocking agents (propranolol or atenolol: 1 mg/kg i.v.) reduced plasma NPY levels. These results show that NPY is correleased in vivo from sympathetic nerve endings during marked and rapid increases in sympathetic tone. They suggest a lack of relationship between NA and NPY release. Alpha 2-adrenoceptors are involved in the presynaptic control of NPY release from sympathetic tone. Finally, some antihypertensive drugs (clonidine but not beta-blocking agents) are able to decrease plasma NPY levels.

Animals↗
PubMed1990

Involvement of vasopressin in the cardiovascular effects of quinpirole.

The effects of quinpirole, a specific dopamine D2 receptor agonist, were investigated on cardiovascular responses and plasma levels of catecholamines and vasopressin in two groups of conscious dogs: (1) control dogs and (2) dogs with diabetes insipidus (i.e. animals surgically deprived of vasopressin). In normal dogs, i.v. quinpirole (30 micrograms/kg) elicited a decrease in blood pressure associated with a rise in both plasma catecholamine and vasopressin levels. In dogs with diabetes insipidus, i.v. quinpirole induced a more marked decrease in blood pressure than in normal dogs. Quinpirole did not change plasma noradrenaline and vasopressin levels in dogs with diabetes insipidus. The present study demonstrates that the decrease in blood pressure elicited by quinpirole is associated with an increase in vasopressin release, which counteracts the hypotensive effect of the the dopamine D2 receptor agonist.

Animals↗
PubMed1990

Beta-adrenergic sensitivity in Parkinson's disease: effect of levodopa treatment.

The beta-adrenergic sensitivity in never-treated and levodopa-treated patients with Parkinson's disease (PD) was studied through the evaluation of lymphocyte beta-adrenoceptor number ([125I]cyanopindolol binding sites) and chronotropic and metabolic (plasma nonesterified fatty acids--NEFA) responses to isoproterenol. No change was found in Bmax values or affinity constant Kd between never-treated patients, levodopa-treated patients with PD, and controls. At rest, no difference was observed in heart rate, plasma catecholamine, or NEFA levels between the three groups. Isoproterenol sensitivity (chronotropic response and plasma NEFA increase) was similar in never-treated and treated PD. The results suggest that peripheral beta-adrenergic sensitivity is unaffected either by the pathophysiological process of PD or by levodopa treatment.

Aged↗
PubMed1990

Adrenergic supersensitivity in parkinsonians with orthostatic hypotension.

The adrenergic status was studied through evaluation of platelet alpha 2-adrenoceptor number [( 3H]yohimbine binding sites), plasma catecholamine levels and blood pressure response to noradrenaline infusion in three groups of subjects (1) Parkinsonians with orthostatic hypotension; (2) Parkinsonians without orthostatic hypotension; and (3) control subjects. In Parkinsonians with orthostatic hypotension, systolic and diastolic blood pressures significantly (P less than 0.05) decreased from 144 +/- 9 and 76 +/- 6 mmHg in the lying position to 95 +/- 12 and 60 +/- 7 mmHg after 5 min standing. In these patients, noradrenaline plasma levels were significantly low (62 +/- 11 pg ml-1, (P less than 0.05) when compared with controls (219 +/- 13 pg ml-1) whereas no difference was noticed in Parkinsonians without orthostatic hypotension (195 +/- 14 pg ml-1). The noradrenaline dose required for a 25 mmHg increase in systolic blood pressure was significantly (P less than 0.01) lower in Parkinsonians with orthostatic hypotension (0.19 +/- 0.03 microgram kg-1) when compared with Parkinsonians without orthostatic hypotension (0.86 +/- 0.11 microgram kg-1) or with controls (0.68 +/- 0.1 microgram kg-1). Platelet alpha 2-adrenoceptor number was higher in Parkinsonians with orthostatic hypotension (313 +/- 52 fmol mg-1 protein) than in Parkinsonians without orthostatic hypotension (168 +/- 9 fmol mg-1 protein) or in controls (175 +/- 4 fmol mg-1 protein) with no change in Kd. This study demonstrates that in patients with Parkinson's disease, orthostatic hypotension is associated with an increase in both vascular sensitivity to noradrenaline and platelet alpha 2-adrenoceptor number.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Cardiovascular effects of central injection of acetylcholine in anaesthetized dogs: a role for vasopressin release.

1. The effect of an intracisternal injection of 20 micrograms kg-1 of acetylcholine was studied on systolic and diastolic blood pressures, heart rate, and plasma levels of noradrenaline, adrenaline, vasopressin, plasma renin activity and atrial natriuretic factor in chloralose-anaesthetized dogs, 8 of which were normal and 7 with diabetes insipidus (deprived of vasopressin secretion by surgical lesion of the hypothalamoneurohypophysial system). 2. Acetylcholine significantly increased systolic and diastolic blood pressures in both groups of animals. However, the rise in blood pressure was significantly shorter lived in the dogs with diabetes insipidus. 3. Acetylcholine significantly increased plasma levels of noradrenaline but not adrenaline in control animals and in dogs with diabetes insipidus. Noradrenaline and adrenaline responses after acetylcholine were not different in the two groups of animals. 4. Acetylcholine induced a significant increase in vasopressin plasma levels only in control animals while in dogs with diabetes insipidus vasopressin remained at nearly undetectable levels. 5. Acetylcholine significantly increased atrial natriuretic factor plasma levels only in control dogs. 6. Although plasma renin activity increased in both groups of animals after the i.c. injection of acetylcholine, this change was not significant in any group. 7. These results suggest that, in the anaesthetized dog, the central injection of acetylcholine induces a rise in blood pressure through both an increase in sympathetic outflow and a release of vasopressin.

Acetylcholine↗