Vascular Responsiveness of Rabbit Common Carotid, Renal and Femoral Arteries to α-Adrenoceptor Agonists

Fujiwara, Toshimasa; Chiba, Shigetoshi

doi:10.1254/jjp.61.171

Cited by 9 publications

(5 citation statements)

References 21 publications

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“…Minneman and coworkers (27,28) proposed the existence of two a,-adrenoceptor subtypes, alA and alB-adrenoceptors, based on functional and bind ing studies. Recently, using the cannula insertion method, Fujiwara and Chiba (29) reported that clonidine-induced vasoconstrictions in the rabbit carotid artery were mediat ed by a,-adrenoceptors, but the same doses of clonidine did not produce any vasoconstriction in the renal and femoral arteries that had abundant a,-adrenoceptors. Therefore, the a,-adrenoceptor-related and clonidine-sen sitive vasoconstriction might suggest that al-adrenocep tors in the canine splenic artery are different in subtypes from or much richer than that in the other regional ar teries.…”

Section: Effects Of Vasoactive Agentsmentioning

confidence: 99%

Characteristics of the Responses of Isolated and Perfused Canine Splenic Arteries to Vasoactive Substances and to Periarterially Electrical Stimulation

Ren

Nakane

Chiba

1994

Japanese Journal of Pharmacology

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ABSTRACT-Pharmacological characteristics of the canine isolated splenic artery were investigated by the cannula insertion method for observing vascular responses to vasoactive agents and periarterial nerve stimulation. Four a-adrenoceptor agonists and tyramine induced vasoconstrictions in a dose-dependent manner, and the order of potency was noradrenaline (NA) > phenylephrine > clonidine > methoxamine > tyramine. Xylazine (a selective a2-adrenoceptor agonist) did not elicit any vasoconstriction. Several autacoids and KCl also constricted the splenic artery dose-dependently, and the order of potency was 5 hydroxytryptamine (5-HT) > ATP = histamine > KCI. The dose-response curves for clonidine and NA were shifted to the right by bunazosin (a selective a,-adrenoceptor antagonist), but were not affected by midaglizole (a selective a2-adrenoceptor antagonist). The parameters of electrical stimulation to elicit a clear and constant vasoconstriction were 0.2 msec of pulse duration, 6 V and 0.1 Hz. The vasoconstrictive responses to electrical stimulation at 6-12 V, 0.1-10 Hz and 0.2-1 msec of pulse duration were completely inhibited by tetrodotoxin (TTX) and strongly inhibited by guanethidine. The results in this study suggest that: 1) in contrast with other regional arteries, the canine splenic artery has an a 1-adrenoceptor-related and clonidine-sensitive vasoconstrictive response, 2) this artery has no functional postsynaptic a2-adrenocep tors, 3) it may be easier to observe the vascular responses to vasoactive agents in the isolated and perfused arterial segments, and 4) the isolated and perfused canine splenic artery is useful as a preparation to study the sympathetic nerve transmission.

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Section: Effects Of Vasoactive Agentsmentioning

confidence: 99%

Characteristics of the Responses of Isolated and Perfused Canine Splenic Arteries to Vasoactive Substances and to Periarterially Electrical Stimulation

Ren

Nakane

Chiba

1994

Japanese Journal of Pharmacology

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“…Thus, clonidine can stimulate also the activity of the vagus [8,17], which could account for the marked bradycardia. The finding that systolic blood pressure rose at 0.8 mg/kg/day while the bradycardia would induce a further reduction of blood pressure could be accounted for by vasoconstrictive actions of clonidine on peripheral alpha-adrenoceptors [18,19].…”

Section: Discussionmentioning

confidence: 98%

Drug withdrawal and rebound hypertension: Differential action of the central antihypertensive drugs moxonidine and clonidine

Rupp

Maisch

Brilla

1996

Cardiovasc Drug Ther

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To examine the antihypertensive action of the centrally acting antiadrenergic drugs moxonidine and clonidine, systolic and diastolic blood pressure as well as heart rate were monitored by radio telemetry in spontaneously hypertensive rats (SHR) with established high blood pressure. Increasing doses were administered with regular rat chow for 6-8 day periods. Moxonidine reduced (p < 0.05) diastolic blood pressure at a dose of 8 mg/kg/day and systolic blood pressure at 13 mg/kg/day. Heart rate was reduced during high activity of rats corresponding to an antitachycardiac action. After withdrawal of 18 mg/kg administered for only 1 day, blood pressure returned to pretreatment values within 8 days. Clonidine reduced systolic and diastolic blood pressure at 0.3 mg/kg/day. At 0.8 and 1.3 mg/kg/day, systolic blood pressure reduction was less pronounced, although heart rate was reduced further, reaching values that were below those of untreated sleeping rats. When 1.3 mg/kg/day clonidine was discontinued, systolic as well as diastolic blood pressure increased above pretreatment values within 1 day. A rebound was also observed in heart rate, which increased by 150 beats/ min. A comparable rebound in blood pressure was observed after withdrawal of 0.3 mg/kg/day. Since a blood pressure rebound occurred also after withdrawal of 0.3 mg/kg/day clonidine in normotensive rats, the rebound phenomenon was independent of the presence of high blood pressure. No blood pressure rebound was observed when moxonidine (8 mg/kg/ day) was administered (chow or gavage) in normotensive rats. These findings in unanesthetized undisturbed rats demonstrate distinct differences in the mode of action of moxonidine and clonidine, which can be accounted for by specific interactions of moxonidine with imidazoline I1-receptors, whereas clonidine would interact not only with I1-receptors but also with alpha2-adrenoceptors, and most probably also with the vagal activity. In view of our previous studies demonstrating a rise in blood pressure and heart rate after a hypercaloric dietary intake, the selective I1-receptor agonist moxonidine appears particularly appropriate for treating overweight hypertension associated with an enhanced sympathetic outflow of the brain. Of importance in this respect is that a moxonidine-induced reduction in sympathetic outflow was not associated with a gain in body weight but resulted in reduced caloric intake.

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“…It has an α 2 -adrenoceptor:α 1 -adrenoceptor agonist ratio of 160:1 and is reported to induce both vasoconstriction and vasodilation in canine coronary arteries. [19][20][21] The purposes of the study reported here were to determine the effects of xylazine on smooth muscle tone in isolated canine coronary arteries and identify the mechanism of action of xylazine.…”

mentioning

confidence: 99%

Effects of xylazine on canine coronary artery vascular rings

Teng¹,

Muir²

2004

ajvr

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Vascular Responsiveness of Rabbit Common Carotid, Renal and Femoral Arteries to α-Adrenoceptor Agonists

Cited by 9 publications

References 21 publications

Characteristics of the Responses of Isolated and Perfused Canine Splenic Arteries to Vasoactive Substances and to Periarterially Electrical Stimulation

Characteristics of the Responses of Isolated and Perfused Canine Splenic Arteries to Vasoactive Substances and to Periarterially Electrical Stimulation

Drug withdrawal and rebound hypertension: Differential action of the central antihypertensive drugs moxonidine and clonidine

Effects of xylazine on canine coronary artery vascular rings

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