Evidence for a Central Mechanism in Angiotensin Induced Hypertension.

Bickerton, Robert K.; Buckley, Joseph P.

doi:10.3181/00379727-106-26492

Cited by 342 publications

(124 citation statements)

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“…Thus, the pressor potency was reduced by treatment with the catecholamine depleting substances, reserpine and syrosingopine, and was restored by infusions of catecholamines. Similarly, inhibition of monoamine oxidase which has been shown to increase peripheral levels of catecholamines (Goldberg & Shideman, 1962;Sanan & Vogt, 1962) (Feldberg & Lewis, 1964, 1965Vane, 1969 (Bickerton & Buckley, 1961) and via central vagal inhibition (Scroop & Lowe, 1968). The failure of both pempidine and bethanidine to reduce the angiotensin pressor responses in the present experiments argues against a significant central component to the response.…”

contrasting

confidence: 38%

Role of noradrenaline in the acute pressor response to angiotensin in conscious cats

Day¹,

Owen²

1970

British J Pharmacology

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contrasting

confidence: 38%

Role of noradrenaline in the acute pressor response to angiotensin in conscious cats

Day¹,

Owen²

1970

British J Pharmacology

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“…Though it is generally assumed that the pressor effect of angiotensin is due to a direct stimulation of vascula~r smooth muscle, a number of recent studies strongly suggest a nerve-mediated component of action (Bickerton & Buckley, 1961;Laverty, 1963). The reduction of the pressor effect of angiotensin by guanethidine might be related to the adrenergic nerve blocking action of the latter.…”

Section: Discussionmentioning

confidence: 99%

Supersensitivity to Catecholamines Following Guanethidine

Gokhale

Gulati

Kelkar

1967

British Journal of Pharmacology and Chemotherapy

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“…Somlyo et al (1965) also observed slight or no response of the umbilical vessels to angiotensin. The polypeptide is a powerful vasoconstrictor, and the bulk of evidence to date suggests a strong direct musculotropic action in causing this effect, though a nerve mediated component of action has been demonstrated (Bickerton & Buckley, 1961;Laverty, 1963;Robertson & Rubin, 1962). The inactivity of angiotensin is probably due to absence of responsive sites in the umbilical artery for angiotensin.…”

Section: Discussionmentioning

confidence: 99%

Effect of Some Drugs on Human Umbilical Artery in Vitro

Gokhale

Gulati

Kelkar

et al. 1966

British Journal of Pharmacology and Chemotherapy

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Investigation of the actions of drugs on vascular smooth muscle is frequently complicated by indirect actions mediated through neural elements. However, valuable information on the direct actions of drugs on vascular smooth muscle can often be obtained from experiments on nerve-free preparations. Perfused placental vessels (von Euler, 1938;Panigel, 1962), spirally cut umbilical arterial and venous strips (Somlyo, Woo & Somlyo, 1965), chick amniotic membrane (Ferguson, 1940;Cuthbert, 1963), and rabbit ear vessels before innervation (Clark & Clark, 1943) have been employed in the past for this purpose. A nerve-free vascular smooth muscle preparation, responding uniformly to various autonomic transmitters could also be used to elucidate the nature of their storage and release.In the present study the isolated perfused human umbilical artery was used to study the direct action of drugs on the vascular smooth muscle. It was observed that with the method employed many vasoactive agents gave fairly uniform responses. Modification of these responses by other drugs could, therefore, be studied. The preparation exhibited spontaneous tone and could give a dilator response to drugs, without the previous addition of a spasmogenic agent. METHODSUmbilical cords were obtained from the Maternity Ward of Shree Sayaji General Hospital, Baroda, as soon after delivery as possible. After identifying the foetal and the placental ends, every cord was firmly tied at both ends and kept in a flask containing perfusion fluid of the following composition (g/l.): sodium chloride, 9.00; potassium chloride, 0.42; calcium chloride, 0.24, sodium bicarbonate, 0.2 and dextrose, 1.0. Tying ensured that any blood in the lumen of the vessels remained in a fluid state and could subsequently be washed out easily. In earlier experiments when the cords were not tied, many of them could not be used because of the intravascular clotting. The cords remained viable for about 5 hr after delivery. Experiments were, therefore, started soon after the collection of the cords.Before cannulation the cords were placed in fresh perfusion fluid at 34' C for 10 min. This considerably reduced the spasm of the vessels and thus facilitated cannulation. A piece of cord about 5 in. long was selected (excluding any portion with injury and pseudoknots), and this was cut at both ends with a sharp pair of scissors. One of the umbilical arteries was cannulated at the

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Evidence for a Central Mechanism in Angiotensin Induced Hypertension.

Cited by 342 publications

References 0 publications

Role of noradrenaline in the acute pressor response to angiotensin in conscious cats

Role of noradrenaline in the acute pressor response to angiotensin in conscious cats

Supersensitivity to Catecholamines Following Guanethidine

Effect of Some Drugs on Human Umbilical Artery in Vitro

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