Localization of the central cardiovascular action of clonidine

Bousquet, Pascal; Guertzenstein, P.G.

doi:10.1111/j.1476-5381.1973.tb08532.x

Cited by 111 publications

(31 citation statements)

References 15 publications

(27 reference statements)

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“…As the bilateral area from which vasopressin release was obtained with nicotine lies 6-9 mm caudal to the trapezoid bodies the area is situated more caudally on the ventral surface of the medulla than the bilateral area from where most of the blood pressure effects have been obtained with drugs topically applied through perspex rings (Feldberg & Guertzenstein, 1972;Guertzenstein, 1973;Bousquet & Guertzenstein, 1973;Edery & Guertzenstein, 1974;Guertzenstein & Silver, 1974). For pentobarbitone sodium, glycine and clonidine, it was shown that they no longer produced their depressor effects with the rings placed so that their rostral border was 5 mm caudal from the trapezoid bodies, and the glycine-sensitive area was restricted in longitudinal direction to between 1 and 2.5 mm caudal to the trapezoid bodies.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it has been shown that a number of drugs which, on intraventricular injection affect blood pressure, heart rate, respiration or blood glucose, act in this way (Feldberg & Guertzenstein, 1972;Guertzenstein, 1973;Bousquet & Guertzenstein, 1973;Edery & Guertzenstein, 1974;Feldberg & Gupta, 1974;Guertzenstein & Silver, 1974;Dey, Feldberg & Wendlandt, 1975).…”

Section: Introductionmentioning

confidence: 99%

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Vasopressin Release by Nicotine: The Site of Action

Bisset

Feldberg

Guertzenstein

et al. 1975

British J Pharmacology

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In cats anaesthetized with chloralose the release of neurohypophysial hormones was examined after injection of nicotine into the cerebral ventricles or cisterna magna or its topical application through perspex rings to the ventral surface of the brain stem. The release was measured by assaying the hormones in samples of venous blood Injected into a lateral or the third cerebral ventricle, nicotine (0.5 to 1 mg) produced release of vasopressin without oxytocin. When the aqueduct was cannulated, preventing access to the fourth ventricle and to the subarachnoid space, this release did not occur. Vasopressin was also released without oxytocin when nicotine (0.25 to 2 mg) was injected into the subarachnoid space through the cisterna magna. With this route of administration the nicotine did not enter any part of the ventricular system. Applied through paired perspex rings placed across the ventral surface of the brain stem, nicotine again produced release of vasopressin without oxytocin. The amount of nicotine placed in each ring was usually 80 μg, but a release was obtained with 10 μg and in one experiment with as little as 5 μg. The bilateral region on the ventral surface of the brain stem where nicotine acts when producing release of vasopressin lies lateral to the pyramids and in a longitudinal direction, 6 to 9 mm caudal to the trapezoid bodies. The vasopressin release by nicotine injected intraventricularly or intracisternally, or applied topically to the ventral surface of the brain stem was not due to absorption of nicotine into the blood stream, nor to blood pressure effects. It is concluded that nicotine acts on the ventral surface of the brain stem probably by activating the central projection to the supra‐optic and possibly also the paraventricular nuclei of afferent pathways in the sinus and vagus nerves which control the release of vasopressin in response to changes in blood volume or distribution.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vasopressin Release by Nicotine: The Site of Action

Bisset

Feldberg

Guertzenstein

et al. 1975

British J Pharmacology

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“…Several years ago we demonstrated that, in the cat, the major site for the central hypotensive effect of clonidine was within the nucleus reticularis lateralis (NRL) area of the medulla (Bousquet & Guertzenstein, 1973;Bousquet et al, 1981). More recently, a structure-activity study proved that the imidazolines were able to induce such effects although catecholamines or phenylethylamines could not (Bousquet et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

Evidence for the involvement of imidazoline receptors in the central hypotensive effect of rilmenidine in the rabbit

Feldman

Tibiriçá

Bricca

et al. 1990

British J Pharmacology

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104

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1 Rilmenidine has recently been introduced as a new centrally-acting antihypertensive agent. We examined its cardiovascular effects after intracerebral injection to anaesthetized rabbits. Cumulative doses of rilmenidine injected intracisternally (1 to 300pgkg-1) led to dose-dependent decreases in arterial blood pressure and heart rate. The effective doses of rilmenidine were lower when injected centrally than when injected intravenously. 2 Pretreatment with the same dose of yohimbine or idazoxan shifted the rilmenidine dose-response curves for its hypotensive and bradycardic effects to the right. Idazoxan, which has an imidazoline structure, proved to be a more active antagonist than yohimbine of rilmenidine centrally-mediated cardiovascular effects. 3 The dose-response curve for the central hypotensive effect of rilmenidine was also shifted to the right after pretreatment with a bovine brain extract. This extract contains the endogenous ligand of the imidazoline-preferring receptors which is not a catecholamine. 4 Rilmenidine, like clonidine, proved to be active when micro-injected into the rabbit nucleus reticularis lateralis region. 5In conclusion, rilmenidine exhibited in the rabbit a central hypotensive effect which originated in the same area as where clonidine acts. Specific imidazoline-preferring receptors appear to be involved in this hypotensive effect.

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“…Several authors have suggested a centrally mediated pressor action of clonidine (Bousquet and Guertzenstein 1973;Trolin 1975;Kawasaki and Takasaki 1986). We recently observed in conscious rat that the hypotension induced by i.c.v.…”

Section: Discussionmentioning

confidence: 97%

“…yohimbine, and this might suggest the existence of a centrally mediated hypertensive action of clonidine (Imai et al 1986). The existence of a suprabulbar pressor center involving by alpha-adrenergic mechanisms has been suggested by several authors (Przuntek et al 1971;Bousquet and Guertzenstein 1973;Korner et al 1981). Trolin (1975) reported that the hypotensive effect of i.v, clonidine in conscious rat was potentiated by pentobarbital anesthesia and decerebration, and concluded that a pressor effect of clonidine, mediated by a suprabulbar pressor center was easily suppressed by pentobarbital anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Modulation of cardiovascular depressant action of clonidine by pentobarbital anesthesia in rats.

Imai

Abe

Sasaki

et al. 1989

Tohoku J. Exp. Med.

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The influence of pentobarbital anesthesia (5 mg 100 g, i.p.) on the cardiovascular depressor effect of clonidine administered intracerebroventricularly (i.c.v.) and intravenously (i.v.) was examined in rats. In conscious rats the hypotensive potency of i.v. clonidine [effective dose of clonidine which induced a decrease in blood pressure of 15 mmHg ; ED15 = 7 (pg/kg)] is greater than that of i.c.v. clonidine (ED15 =24.3), while in anesthetized rats that of icy. clonidine (ED15 -0.7 pg/kg) was greater than that of i.v. clonidine (ED15 = 3.5 p g/kg). Pentobarbital anesthesia potentiated the hypotensive potency of i.c.v. clonidine in conscious rats by 50 times, while it potentiated that of i.v. clonidine only by 2 times. The bradycardic potency of i.v. and i.c.v, clonidine was also potentiated by pentobarbital anesthesia. These pieces of evidence suggest that in conscious rat, the hypotensive action of i.c.v. clonidine is opposed by a centrally mediated hypertensive effect of the drug and that pentobarbital anesthesia suppresses the clonidine sensitive pressor center and so potentiates the hypotensive effect of i.c.v. clonidine blood pressure; cerebroventricular injection ; clonidine ; heart rate ; pentobarbital There is a volume of evidence to indicate that the hypotensive and bradycardic effects of clonidine are mediated by a2-adrenoceptor and/or imidazole receptor mechanisms in the depressor site of the medullary vasomotor center (Schmitt 1977;Kobinger 1978;Ernsberger et al. 1987). Studies which have shown that centrally administered clonidine caused greater hypotensive effects than the same dose given intravenously (Kobinger 1978) have been a part of that evidence which indicates a central mode of action. Such results have been obtained in several species of animal mainly under anesthetized conditions. However, there is no report of a significant difference in the hypotensive potency of clonidine via different administration route in rats, the most pupular experimental animal. We

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Localization of the central cardiovascular action of clonidine

Cited by 111 publications

References 15 publications

Vasopressin Release by Nicotine: The Site of Action

Vasopressin Release by Nicotine: The Site of Action

Evidence for the involvement of imidazoline receptors in the central hypotensive effect of rilmenidine in the rabbit

Modulation of cardiovascular depressant action of clonidine by pentobarbital anesthesia in rats.

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