A Central Vasodepressor Effect of Dyflos

Edery, H.; Guertzenstein, P.G.

doi:10.1111/j.1476-5381.1974.tb08581.x

Cited by 17 publications

(6 citation statements)

References 17 publications

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“…The persistence of the hypotensive action of oxotremorine following decerebration and its absence in spinal cats suggests a site of action in the brain stem. This is consistent with the observations of Guertzenstein (1973) and Edery & Guertzenstein (1974) that carbachol decreased blood pressure when applied locally to a discrete area on the ventral surface of the brain stem.…”

Section: Discussionsupporting

confidence: 92%

A Centrally Mediated Prolonged Hypotension Produced by Oxotremorine or Pilocarpine

Dage¹

1979

British J Pharmacology

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1 Oxotremorine, methyloxotremorine, pilocarpine or arecoline were given intravenously to anaesthetized cats, dogs or rats, and intraperitoneally to conscious normotensive and spontaneously hypertensive rats, pretreated with doses of methylatropine that completely blocked peripheral muscarinic receptors, to ascertain their effects on blood pressure and heart rate. 2 Oxotremorine but not methyloxotremorine produced a prolonged hypotension in cats and dogs but not in rats. Heart rate was not changed. Pilocarpine, although less potent, produced an identical effect, whereas the effect of arecoline was short by comparison. The hypotensive effect of these drugs was reversed by atropine. 3 In dogs, oxotremorine produced a prolonged hypotension with no change in heart rate or cardiac output.4 A decrease in spontaneous sympathetic nerve activity accompanied the hypotension in cats. Both effects were reversed by atropine but could be reinvoked by large doses of oxotremorine. 5 The oxotremorine-induced hypotension in cats was not altered by decerebration but was abolished by high cervical spinal section. 6 The results indicate that the prolonged hypotension elicited by oxotremorine is mediated by an action at muscarinic receptors in the brain stem resulting in a decrease in sympathetic nerve activity and peripheral resistance but not heart rate or cardiac output.

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Section: Discussionsupporting

confidence: 92%

A Centrally Mediated Prolonged Hypotension Produced by Oxotremorine or Pilocarpine

Dage¹

1979

British J Pharmacology

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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%

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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“…Previously it was shown that a number of drugspentobarbitone sodium, glycine, clonidine, physostigmine, dyflos and carbacholproduced a fall in arterial blood pressure in anaesthetized cats when applied topically to the ventral surface of the brain stem through paired Perspex rings placed across the medulla. These depressor effects were obtained when the areas covered by the rings had their uppermost limits just, and their lowest limits about 4 mm, caudal to the trapezoid bodies (Feldberg & Guertzenstein, 1972;Guertzenstein, 1973;Bousquet & Guertzenstein, 1973;Edery & Guertzenstein, 1974). These areas are indicated by the ovals A of the diagram of Fig.…”

mentioning

confidence: 92%

Vasodepressor effects obtained by drugs acting on the ventral surface of the brain stem.

Feldberg¹,

Guertzenstein²

1976

The Journal of Physiology

142

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SUMMARY1. In cats anaesthetized with i.P. pentobarbitone sodium and atropinized with intravenous atropine methyl nitrate, the effects on arterial blood pressure were examined of nicotine, physostigmine, carbachol, glycine and pentobarbitone sodium applied to the exposed ventral surface of the brain stem by means of paired Perspex rings placed across the medulla.The drugs were placed inside each ring in a volume of 10 ,uJ.2. Nicotine (0-5-6 mg/ml.) produced a fall in blood pressure when the upper limit of the areas covered by the rings was about 5-6 mm caudal, but not when it was just caudal to the trapezoid bodies. The depressor effect was obtained both on bilateral and unilateral application. After application the nicotine sensitive area became for several minutes insensitive to its renewed application.3. The depressor effect of nicotine was sensitive to hexamethonium (50 mg/ml.) but resistant to atropine (50 mg/ml.) similarly applied.4. When the nicotine sensitive areas had become insensitive to nicotine, bilateral carotid occlusion produced its normal sustained pressor response.5. By applying the nicotine through a single Perspex ring which could be moved stepwise along and across the medulla, the nicotine sensitive area was localized and the highest sensitivity was found in a region around and a little caudal to the rootlets of the XIIth cranial nerve.6. Physostigmine (25 and 50 mg/ml.) and carbachol (6 mg/ml.) produced a fall in blood pressure when the uppermost limits of the areas covered by the paired rings were 5-6 mm caudal to and also when they were just caudal to the trapezoid bodies. From both regions the effects were obtained on bilateral and unilateral application. Their depressor effects were sensitive to atropine but resistant to hexamethonium similarly applied.

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A Central Vasodepressor Effect of Dyflos

Cited by 17 publications

References 17 publications

A Centrally Mediated Prolonged Hypotension Produced by Oxotremorine or Pilocarpine

A Centrally Mediated Prolonged Hypotension Produced by Oxotremorine or Pilocarpine

Vasopressin Release by Nicotine: The Site of Action

Vasodepressor effects obtained by drugs acting on the ventral surface of the brain stem.

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