Possible role of central α1-adrenoceptors in the control of the autonomic nervous system in normotensive and spontaneously hypertensive rats

Huchet, Anne Marie; Doursout, Marie–Françoise; Chelly, Jacques E.; Schmitt, Henri

doi:10.1016/0014-2999(82)90474-5

Cited by 22 publications

(5 citation statements)

References 8 publications

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“…This fact has been observed for several a1-blocking agents and has been Therefore, they do not interact with presynaptic a2-adrenoceptors, which modulate reflex phenomena. This also agrees with the known fact that central a3-adrenoceptors blockade may contribute to the inhibition of reflex tachycardia (21,22). More precise studies, however, are necessary in our case to confirm and quantify this a3blocking action.…”

Section: Results and Discussion Chemistrysupporting

confidence: 91%

Pharmacological and Phytochemical Studies ofCephäelis axillaris

Martı́n

Gupta²,

Urbina³

et al. 1994

Planta Med

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also occurs in the West Indies. Because of the chemotaxonomic and ethnomedical importance of Cephäelis species and due to positive results of testing for the presence of indole alkaloids in this plant, we decided to investigate C. axillaris, as no previous studies had been reported on this species. Materials and Methods General experimental procedures 1D-and 2D-NMR spectra were performed at 200 (250) MHz for 1H and 50MHz for 13C on a Bruker WP 200 SY (AC-250) spectrometer, in DMSO-d6 solution with TMS as internal standard. IR and LV spectra were run in CHC13 solutions.

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Section: Results and Discussion Chemistrysupporting

confidence: 91%

Pharmacological and Phytochemical Studies ofCephäelis axillaris

Martı́n

Gupta²,

Urbina³

et al. 1994

Planta Med

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“…The induced fall in blood pressure was not associated with a change in cardiac output or heart rate in either strain, suggesting an inhibition of the baroreceptor reflex response to arteriolar vasodilation. 21 In addition to the pronounced decrease in systemic vascular resistances, a significant increase in arterial compliance was observed, which is the main focus of this study. The systemic arterial compliance, as measured in these experiments, was considerably smaller in SHR than in WKY rats under control conditions.…”

Section: Discussionmentioning

confidence: 99%

Effects of alpha 1-blockade on arterial compliance in normotensive and hypertensive rats.

1991

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The effects of blockade of cq-adrenergic receptors on the mechanical properties of the arterial wall were studied in 10 spontaneously hypertensive rats (SHR) as compared with 10 matched normotensive Wistar-Kyoto (WKY) rats. Ascending aortic pressure and flow were recorded in open-chest anesthetized rats, and the systemic arterial compliance was calculated. Intravenous injection (1 mg/kg) of Urapidil, a selective «,-adrenergic antagonist, induced a significant decrease in arterial pressure (-26%, p<0.01 and -37%, p<0.001 in WKY rats and SHR, respectively) without significant changes in cardiac output. In control conditions, systemic arterial compliance was lower in SHR (3.29 ±1.52 /il/mm Hg) than in WKY rats ( 4 J 5 ± U 5 fil/mm Hg, p<0.01). Urapidil injection induced significant increases in systemic arterial compliance values in both strains (p<0.001). In another set of experiments (15 WKY rats and 15 SHR), the carotid compliance (filjmm Hg) was determined from the arterial volumepressure relation under control conditions, after local incubation with Urapidil, and after total abolition of the vascular smooth muscle by KCN. In WKY rats, the carotid compliance increased markedly after incubation with Urapidil at doses corresponding to 1 mg/kg (+31%, p<0.01). A further increase in the carotid compliance was observed after KCN poisoning (+11%, p<0.05). In SHR, incubation with Urapidil at doses corresponding to 2 mg/kg were necessary to induce a significant increase in compliance (+38%). At this dosage, there was no further increase in compliance after KCN poisoning. The present study suggests that (^blockade influences the arterial compliance in normotensive and hypertensive rats independently of its effects on the arterial blood pressure. (Hypertension 1991;17:534-540)

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“…35 In conclusion it seems justified to state that the aadrenergic receptors in the brain stem that mediate the central hypotensive action of clonidine probably are located at postsynaptic sites; their receptor demand appears to be that of the a 2 -adrenergic receptor subtype. The central a-adrenergic receptors that facilitate the vagally mediated bradycardia most likely are also of the a,-type; however, an inhibitory role of central a,-adrenergic receptors on vagal reflex bradycardia has been suggested.…”

Section: Mode Of Action Involving Central A-adrenergic Receptorsmentioning

confidence: 96%

“…The central a-adrenergic receptors that facilitate the vagally mediated bradycardia most likely are also of the a,-type; however, an inhibitory role of central a,-adrenergic receptors on vagal reflex bradycardia has been suggested. 35 Side Effects: Pharmacological Basis…”

Section: Mode Of Action Involving Central A-adrenergic Receptorsmentioning

confidence: 99%

The hypotensive activity and side effects of methyldopa, clonidine, and guanfacine.

Zwieten¹,

Thoolen²,

Timmermans³

1984

Hypertension

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Clonidine (Catapres, Catapresan), guanfacine (Estulic), and methyldopa (Aldomet) are the prototypes of centrally acting antihypertensive drugs. Clonidine and guanfacine are lipophilic drugs that readily penetrate into the brain, where they stimulate a-adrenergic receptors in the pontomedullary region. The stimulation of these central a-adrenergic receptors has been shown to activate an inhibiting neuron, which causes a reduction of peripheral sympathetic tone and a subsequent fall in arterial blood pressure and heart rate. Both a centrally initiated reduction of vagus reflex activity and the activation of presynaptic o s -adrenergic blocking agents in the heart may contribute to the bradycardia. Studies indicate that methyldopa also penetrates into the brain, where it is converted into a-methylnorepinephrine. This amine may stimulate the same central a-adrenergic receptors as those activated by clonidine, which will result in a hypotensive effect. Possibly, a-methyldopamine might also play a role. Accordingly, the modes of action of clonidine and a-methyldopa probably are very similar at a basic level. The central adrenergic receptors probably are located postsynaptically. Their receptor demand corresponds more closely to that of the a 2 -subtype. Central a,-adrenergic receptors might possibly play a part in the modulation of vagally induced baroreflex bradycardia. A discussion on the pharmacological basis of the side effects of the centrally acting antihypertensives has been limited to those adverse reactions that are somehow related to a-adrenergic receptors. Sedation, a common side effect, appears to be mediated by central a 2 -adrenergic receptors, at least in animal models. The withdrawal syndrome, observed on abrupt cessation of treatment with clonidine, apparently also involves a-adrenergic receptors; however, why methyldopa does not precipitate a withdrawal phenomenon in the same animal model where clonidine was studied cannot be explained at present. (Hypertension 6 (Suppl. II): 11-28-11-33, 1984) KEY WORDS • methyldopa • central hypotensive activity guanfacine • a-adrenergic receptors clonidine From the Division of Pharmacolherapy. University of Amsterdam. Plantage Muidergracht 24. 1018 TV Amsterdam. The Netherlands. Address for reprints: P. A. van Zwieten. Division of Pharmacotherapy. University of Amsterdam. Plantage Muidergracht 24. 1018 TV Amsterdam. The Netherlands. 11-28 by guest on July 2, 2015 http://hyper.ahajournals.org/ Downloaded from

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Possible role of central α1-adrenoceptors in the control of the autonomic nervous system in normotensive and spontaneously hypertensive rats

Cited by 22 publications

References 8 publications

Pharmacological and Phytochemical Studies ofCephäelis axillaris

Pharmacological and Phytochemical Studies ofCephäelis axillaris

Effects of alpha 1-blockade on arterial compliance in normotensive and hypertensive rats.

The hypotensive activity and side effects of methyldopa, clonidine, and guanfacine.

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