The control of the suprarenal glands by the splanchnic nerves1

Elliott, T. R.

doi:10.1113/jphysiol.1912.sp001521

Cited by 195 publications

(34 citation statements)

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“…Histamine has been known for many years to be capable of inducing secretion of adrenomedullary catecholamines when given to -cats or dogs intravenously (Elliot, 1912;Szczygielski, 1932;Wada et al, 1940). In dogs, this action ofhistamine is completely abolished by transection of the splanchnic nerves or by ganglionic blockade, suggesting it is mediated indirectly by a central reflex mechanism (see Wada et al, 1940;StaszewskaBarczak & Vane, 1965) or that histamine in some way potentiates the response of the adrenal medulla to neural drive.…”

Section: Discussionmentioning

confidence: 99%

Effects of opioid peptides and morphine on histamine‐induced catecholamine secretion from cultured, bovine adrenal chromaffin cells

Livett

Marley

1986

British J Pharmacology

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IThe effect of opioid peptides and morphine on histamine-induced catecholamine secretion has been studied in monolayer cultures of dispersed, bovine adrenal chromaffin cells. 2 Histamine-induced a dose-dependent secretion of both adrenaline and noradrenaline with a threshold dose of approximately 5 nM, an EC50 of 150 nM and maximal secretion at 10 AM. 3 Catecholamine secretion induced by I tM histamine was completely dependent on extracellular calcium, was inhibited in a dose-dependent manner by mepyramine (I nM-l M), and was unaffected by cimetidine (10 M) and hexamethonium (0.1 mM). 4 Dynorphin-1-13 (1 nM-20 1M), metorphamide (O.1 nM-10-IM), morphine (I nM-0. mM) and diprenorphine (I nM -0.1 mM) each had no effect on adrenaline or noradrenaline secretion induced by 1 JAM histamine. 5 The characteristics of histamine-induced catecholamine secretion from bovine adrenal chromaffin cells were similar to those reported previously for cat and rat adrenal medulla being calcium-dependent and mediated by HI histamine-receptors. The results with opioid peptides and morphine suggest that endogenous adrenal opioid peptides do not act on the opioid binding sites found on adrenal medullary chromaffin cells to modify their secretory response to histamine.

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Section: Discussionmentioning

confidence: 99%

Effects of opioid peptides and morphine on histamine‐induced catecholamine secretion from cultured, bovine adrenal chromaffin cells

Livett

Marley

1986

British J Pharmacology

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“…Later Lehndorff (1908) investigated a two-part rise of blood pressure, confirming that the initial rise was due to vasoconstriction of the splanchnic area, and the second due to increased heart rate. Four years later, Elliott (1912) demonstrated that the second rise was caused by secretion of adrenalin. Then, von Anrep (1912) established the link between accelerated heart rate and the secretion of adrenalin found by Elliott (1912).…”

Section: Cardiac Inotropic Reservementioning

confidence: 99%

“…Four years later, Elliott (1912) demonstrated that the second rise was caused by secretion of adrenalin. Then, von Anrep (1912) established the link between accelerated heart rate and the secretion of adrenalin found by Elliott (1912). These findings were extended by Starling (1920) who noted that secretion of adrenalin dramatically increases Bthe energy available at each contraction.^, i.e.…”

Section: Cardiac Inotropic Reservementioning

confidence: 99%

Historical perspective on heart function: the Frank–Starling Law

Sequeira

Velden

2015

Biophys Rev

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More than a century of research on the FrankStarling Law has significantly advanced our knowledge about the working heart. The Frank-Starling Law mandates that the heart is able to match cardiac ejection to the dynamic changes occurring in ventricular filling and thereby regulates ventricular contraction and ejection. Significant efforts have been attempted to identify a common fundamental basis for the Frank-Starling heart and, although a unifying idea has still to come forth, there is mounting evidence of a direct relationship between length changes in individual constituents (cardiomyocytes) and their sensitivity to Ca 2+ ions. As the Frank-Starling Law is a vital event for the healthy heart, it is of utmost importance to understand its mechanical basis in order to optimize and organize therapeutic strategies to rescue the failing human heart. The present review is a historic perspective on cardiac muscle function. We Brevive^a century of scientific research on the heart's fundamental protein constituents (contractile proteins), to their assemblies in the muscle (the sarcomeres), culminating in a thorough overview of the several synergistically events that compose the Frank-Starling mechanism. It is the authors' personal beliefs that much can be gained by understanding the Frank-Starling relationship at the cellular and whole organ level, so that we can finally, in this century, tackle the pathophysiologic mechanisms underlying heart failure.

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“…5) Effect of morphine on the sympathetic system. Morphine was tried as a stimulant for the sympathetic system because it is known to excite the sympathetic centres of the cat (Elliott, 1912). Small doses given intravenously had an uncertain effect on the efferent outflow; some enhancement was apparent but the origin of the effect was in doubt, since morphine is a respiratory depressant and the increased outflow might in part have been secondary to under-ventilation arising from this depression.…”

Section: Normal Catsmentioning

confidence: 99%

Preganglionic sympathetic activity in normal and in reserpine‐treated cats

Iggo¹,

Vogt²

1960

The Journal of Physiology

168

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Reserpine causes a loss of noradrenaline and of 5-hydroxytryptamine from the brain, and many attempts have been made to correlate the clinical effects of reserpine with this loss. One of the difficulties in attempting such a correlation lies in the lack of knowledge about the part played by noradrenaline and 5-hydroxytryptamine in normal brain function. Regions containing the central representation of the sympathetic system (hypothalamus, reticular formation of mid-brain and of medulla) are rich in both these amines. If the stores of the amines have an essential role in central sympathetic activity, one might expect such activity to be impaired after the administration of reserpine. The following observations would appear to support such a possibility: peripheral adrenergic neurones fail to excite the tissues they innervate when reserpine has reduced their stores of amines to 10 % or less (Muscholl & Vogt, 1958); continued sympathetic activity, elicited by drugs which stimulate the sympathetic centres, is accompanied by a reduction in the noradrenaline content of these centres, a fact which demonstrates some connexion between nervous activity and noradrenaline turnover (Vogt, 1954).The object of this work, on which a preliminary note has been published (Iggo & Vogt, 1959), was to test central sympathetic activity in cats in which reserpine administration had reduced the cerebral noradrenaline and 5-hydroxytryptamine to very low figures. Efferent discharge of the preganglionic fibres of the cervical sympathetic was used as a measure of central sympathetic activity. In order to assess possible changes produced by reserpine, it was necessary first to observe the preganglionic sympathetic activity of normal cats in the same experimental conditions, and to devise some simple means of eliciting reproducible changes in activity.

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The control of the suprarenal glands by the splanchnic nerves1

Cited by 195 publications

References 0 publications

Effects of opioid peptides and morphine on histamine‐induced catecholamine secretion from cultured, bovine adrenal chromaffin cells

Effects of opioid peptides and morphine on histamine‐induced catecholamine secretion from cultured, bovine adrenal chromaffin cells

Historical perspective on heart function: the Frank–Starling Law

Preganglionic sympathetic activity in normal and in reserpine‐treated cats

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