The Release of Catecholamines From the Adrenal Medulla Peptides

Staszewska-Barczak, Janina; Vane, John R.

doi:10.1111/j.1476-5381.1967.tb02172.x

Cited by 91 publications

(61 citation statements)

References 17 publications

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“…This is in accordance with the conclusions of StaszewskaBarczak & Vane (1967) Aminophylline caused a dilatation of precapillary resistance vessels and precapillary 'sphincters' manifest as a fall in vascular resistance and a rise in CFC. Falls in blood pressure on infusion of aminophylline were accompanied by rises in heart rate, and whilst the mechanism of this effect was not examined, it is possible that reflex enhancement of sympathetic vasoconstrictor tone resulting from the fall in systemic arterial pressure might have reduced the effect of aminophylline on CFC.…”

Section: Discussionsupporting

confidence: 79%

“…Histamine increases vascular permeability (Rowley, 1964;Spector & Willoughby, 1968;Clementi & Palade, 1969) Vane, 1965) or from the intestine (Everett & Mann, 1967) by the action of histamine. The fact that doses of histamine which alone cause falls in CFC, cause rises in CFC after phentolamine strongly suggests that the fall in CFC is due to ot-adrenoceptor stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…In two preparations, 25 ng kg-l min-' produced a mean fall in CFC of 50%, a mean fall in blood flow of 15%, a mean rise in systemic arterial pressure of 8% and no effect on heart rate. Because angiotensin releases suprarenal catecholamines in vitro and in vivo (Peach, Cline & Watts, 1966;Staszewska-Barczak & Vane, 1967;Robinson, 1967), three infusions of angiotensin were performed after phentolamine (2.0 mg/kg), a dose found to be adequate to block the effects of exogenous phenylephrine. There is no evidence (Table 4) that a-adrenoceptor blockade modifies the responses of the preparation to angiotensin.…”

Section: Drugsmentioning

confidence: 99%

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Drug‐induced Changes in Capillary Filtration Coefficient and Blood Flow in the Innervated Small Intestine of the Anaesthetized Cat

Richardson¹

1974

British J Pharmacology

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1 A modification of the Folkow Technique for simultaneous measurement of blood flow and capillary filtration coefficient (CFC) in the cat jejunum is described. The modification retained the sympathetic innervation of the preparation, and in the present experiments, drugs were administered intravenously. 2 There is evidence that CFC is a cardiovascular quantity independent of blood flow or regional vascular resistance in these preparations. Low doses of drugs may affect CFC without altering the blood pressure, blood flow, or heart rate. 3 Under control conditions the CFC, a measure of functional exchange vessel area, was lower than previously reported for similar, but denervated preparations.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: Drugsmentioning

confidence: 99%

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Drug‐induced Changes in Capillary Filtration Coefficient and Blood Flow in the Innervated Small Intestine of the Anaesthetized Cat

Richardson¹

1974

British J Pharmacology

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“…Substance P did not release adrenaline from the adrenal gland when injected into the coeliac artery of the cat (Feldberg and Lewis, 1964). Eledoisin produced qualitatively similar effects to those of partially pure substance P. It failed to stimulate ganglionic transmission or to release catecholamines from the adrenal medulla of the cat (Lewis and Reit, 1966;Staszewska-Barczak and Vane, 1967). However, in dogs, eledoisin was as active as bradykinin in releasing catecholamines from the adrenal medulla but, in contrast to the effect of bradykinin, this activity was abolished by ganglion blockade.…”

Section: Effects On Efferent Nervesmentioning

confidence: 65%

Substance P: Its Pharmacology and Physiological Roles

Bury

Mashford

1977

Aust J Exp Biol Med

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Summary. The recent identification and synthesis of the endecapeptide substance P has renewed interest in this naturally occurring compound. The original substance P of Euler and Gadduni was a mixture of biologically active substances, some of which were peptides. The peptide component was responsible for gut-contracting, hypotensive and sialogogic properties attributed to substance P. For almost 40 years following its discovery, substance P resisted isolation and purification. Even the most highly active preparations were heterogeneous and there was a divergence of results from experiments using preparations which were partially purified by different techniques. Nevertheless, much of the early work on the distribution and pharmacology of crude substance P has been confirmed using the synthetic endecapeptide and has stimulated research towards the elucidation of a possible functional role for substance P. Most proposed functions have been highly speculative but, at present, evidence is accumulating in support of a physiological role for substance P as a neurotransniitter in sensory pathways. DISCOVERY, PURIFICATION AND ISOLATION OF SUBSTANCE P.While investigating the distribution of acetylcholine in various tissues in 1931, Euler and Caddum detected the presence of a substance in alcoholic extracts of equine brain and intestine which stimulated contraction of isolated rabbit intestine. On intravenous administration to anaesthetized rabbits, this preparation briefly lowered the blood pressure. These effects differed qualitatively from those of acetylcholine and, in addition, were not inhibited by atropine. The active moiety found in the dried extracts was given the working designation "preparation P" and was shown to differ in its chemical and biological properties from other smooth muscle stimulating substances then known, viz. histamine and the adenine nucleotides. The new active factor, provisionally named substance P (Caddum and Schild, 1934), was first recognised as a protein-like material by Euler (1936a).

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“…If high doses are also needed to blunt the hypotensive effect of the EP-24.15 inhibitor, this would support the contention that tissue kinins are responsible for the changes in blood pressure. However, these results should be interpreted with caution, since at high doses the antagonist may stimulate the release of catecholamines 15 or have other unforeseen effects such as causing pain due to residual agonistic activity. Furthermore, when the antagonist is administered at lower doses that block the hypotensive effect of exogenous kinins by 70% or more, they do not change blood pressure; in addition, kinin antibodies that block part of the acute antihypertensive effect of ACE inhibitors do not increase blood pressure in rats not treated with the ACE inhibitor.…”

mentioning

confidence: 99%

Zinc metallopeptidase inhibitors. A novel antihypertensive treatment.

Carretero

Scicli

1991

Hypertension

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Inhibitors of two zinc metallopeptidases, angiotensin I converting enzyme (ACE) and neutral metalloendopeptidase-24.11 (EP-24.11), are antihypertensive agents. In this issue of Hypertension, Genden and Molineaux report that yet another peptidase inhibitor, metalloendopeptidase-24.15, EC 3.4.24.15 (EP-24.15), lowers blood pressure in normotensive rats. In this editorial we discuss the possible role of kinins as common mediators of part of the vasodepressor action of these peptidase inhibitors. Genden and Molineaux report that the marked fall in blood pressure caused by the EP-24.15 inhibitor is almost abolished by a kinin receptor antagonist, supporting the hypothesis that kinins play a role in the regulation of normal blood pressure. We have confirmed that the EP-24.15 inhibitor used by these investigators lowers blood pressure. Up to now, EP-24.15 has not been implicated in in vivo metabolism of kinins. Although a number of kininases have been identified, our own previous work indicated that the metabolic pathway responsible for clearing kinins from the circulation involves the action of kininase II (angiotensin I converting enzyme) and renal peptidases. Nevertheless, the main metabolic pathway involved some other unidentified enzyme, since in these experiments disappearance of kinins from the circulation was only marginally reduced by a "cocktail" of inhibitors of ACE, EP-24.11, and carboxypeptidase N. It could be that EP-24.15 is involved in kinin metabolism. However, a number of questions need to be answered with regard to the mechanism by which the EP-24.15 inhibitor lowers blood pressure. The data obtained with the EP-24.15, NE-24.11, and ACE inhibitors suggest that potentiation of vasodilator peptides is yet another possible relevant therapeutic approach to hypertension and perhaps heart failure. (Hypertension 1991;68:366-371)

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The Release of Catecholamines From the Adrenal Medulla Peptides

Cited by 91 publications

References 17 publications

Drug‐induced Changes in Capillary Filtration Coefficient and Blood Flow in the Innervated Small Intestine of the Anaesthetized Cat

Drug‐induced Changes in Capillary Filtration Coefficient and Blood Flow in the Innervated Small Intestine of the Anaesthetized Cat

Substance P: Its Pharmacology and Physiological Roles

Zinc metallopeptidase inhibitors. A novel antihypertensive treatment.

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