Preferential Release of Adrenaline from the Adrenal Medulla by Muscarine and Pilocarpine

Douglas, W. W.; Poisner, Alan M.

doi:10.1038/2081102a0

Cited by 151 publications

(101 citation statements)

References 8 publications

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“…Alternatively, ACTH administration could have altered the pool of cells contributing to enkephalin production. There are separate adrenaline-containing and noradrenaline-containing chromaffin cells (Hillarp & Hdkfelt, 1953) and evidence of differential activation of these depending on the physiological stimulus (Folkow & von Euler, 1954;Douglas & Poisner, 1965;Feuerstein & Gutman, 1971). Hence if a similar heterogeneity was present for enkephalin-containing cells ACTH could have favoured output from those with a lower content of 'free' met-enkephalin.…”

Section: Discussionmentioning

confidence: 99%

Effects of synthetic adrenocorticotrophin on adrenal medullary responses to splanchnic nerve stimulation in conscious calves.

Edwards¹,

Hansell²,

Jones³

1986

The Journal of Physiology

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SUMMARY1. Right medullary and various cardiovascular responses to stimulation of the peripheral end of the splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1 24, (5 ng min-kg-'). The adrenal-clamp technique was employed in conscious calves, after the pituitary stalk had been cauterized and they had recovered from anaesthesia.2. The intravenous infusion ofACTH1 24increased the plasma ACTH concentration by about 1100 pg ml-' and right adrenal venous output of cortisol by about 400 ng min' kg body weight-'. Stimulation of the splanchnic nerve at 4 Hz for 10 min had no effect on either arterial plasma ACTH concentration or the adrenal output of cortisol.3. Closely similar amounts of both adrenaline and noradrenaline were released in response to nerve stimulation in the presence and absence of exogenous ACTH. In contrast, the fall in adrenal vascular resistance of about 40 %, which normally occurred in response to splanchnic nerve stimulation, was completely abolished by ACTH.4. The adrenal produced relatively large quantities of met-enkephalin-containing peptides. During splanchnic nerve stimulation the output of these increased 20-100-fold, at which time free met5-enkephalin accounted for only 10-20 o of total. During ACTH infusion the output of free met5-enkephalin was reduced at rest and during nerve stimulation, but that of total met-enkephalin-containing peptides was unaffected. These results indicate that ACTH or an adrenal steroid may alter the processing of proenkephalin in the adrenal medulla acutely but not total opiate secretion. Alternatively, the presence ofACTH could act by influencing the population of chromaffin cells activated by splanchnic nerve stimulation.

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Section: Discussionmentioning

confidence: 99%

Effects of synthetic adrenocorticotrophin on adrenal medullary responses to splanchnic nerve stimulation in conscious calves.

Edwards¹,

Hansell²,

Jones³

1986

The Journal of Physiology

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“…In the present study, however, the inhibitory action of muscarine may have been obscured by the measurement of 'total catecholamines' rather than separate determinations of adrenaline and noradrenaline. Inasmuch as muscarinic agonists selectively enhance secretion from adrenaline-containing chromaffin cells (Douglas & Poisner, 1965), the possibility that muscarine selectivity depresses secretory responses to high K+, nicotine, or veratridine in noradrenaline-containing cells must also be examined before we can rule out an inhibitory effect for muscarine in the cat adrenal medulla.…”

Section: Discussionmentioning

confidence: 99%

“…Feldberg, Minz & Tsudzimura (1934) showed that muscarine evoked medullary secretion by activating a receptor which is not desensitized by nicotine. More recently, it has been shown that nicotine releases nearly equal amounts of adrenaline and noradrenaline, whereas muscarine and pilocarpine preferentially release adrenaline from the rat adrenal medulla (Douglas & Poisner, 1965). The secretory response to muscarine is Ca2l-dependent (Poisner & Douglas, 1966).…”

Section: Introductionmentioning

confidence: 99%

Effect of Muscarine on Release of Catecholamines From the Perfused Adrenal Gland of the Cat

Kirpekar

Prat

Schiavone

1982

British J Pharmacology

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The secretory effect of muscarine was studied in the perfused adrenal gland of the cat. During perfusion of the adrenal gland with Krebs‐bicarbonate solution containing muscarine 480 μm, the rate of catecholamine (CA) secretion was 2.02 ± 0.43 μg/2 min in the first 2 min; thereafter, CA output declined only moderately, to reach about 70% of the initial value after 10 min. Secretory responses to brief infusions of muscarine remained reproducible for at least the first 3 infusions. When the adrenal gland was perfused with muscarine (480 μm), infusions of high K+, nicotine, or veratridine produced their usual responses. A 100 fold lower dose of muscarine also failed to modify these responses. During perfusion with high K+, muscarine evoked a secretory response that was only slightly smaller than the response to muscarine alone. It is concluded that muscarine and nicotine activate CA secretion in the cat adrenal gland by independent mechanisms and that the muscarinic response, unlike the nicotinic response, is not readily desensitized.

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“…The argument supports our proposal that, indeed, there are in this preparation two types of muscarinic receptors. We believe that our finding will help in the interpretation of data on muscarine which have been difficult to understand. For example, muscarine is supposed to be devoid of any nicotinic activity and yet Douglas & Poisner (1965) found that muscarine caused a release of catecholamines from the adrenal medulla. We have made a similar observation with one of the furan analogues of muscarine (Ochillo et al, 1977a).…”

Section: Resultsmentioning

confidence: 99%

Mechanism of Action of Muscarine on the Longitudinal Muscle of the Guinea‐pig Isolated Ileum

Ochillo

Tsai

1981

British J Pharmacology

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dl‐Muscarine elicited a contraction of the ileal longitudinal muscle of the guinea‐pig and the contraction was characterized by an after‐response. Physostigmine (2.0 × 10−8 m) potentiated the contraction of the longitudinal muscle elicited by dl‐muscarine. Hemicholinium‐3 (HC‐3) caused a rightward shift of the dose‐response curve to dl‐muscarine on the ileal longitudinal muscle of the guinea‐pig ileum. β‐Bungarotoxin (10 μg/ml) significantly (P < 0.025) reduced the contraction elicited by dl‐muscarine (2.5 × 10−8 m) suggesting presynaptic release of acetylcholine as an indirect mechanism of action of dl‐muscarine. Morphine (1.0 × 10−8 m) significantly (P < 0.05) reduced the contractions elicited by dl‐muscarine (2.5 × 10−8 m) further suggesting presynaptic release of acetylcholine as an indirect mechanism of action of dl‐muscarine. A subthreshold dose of dl‐muscarine (2.0 × 10−10 m) potentiated the effect of acetylcholine (2.5 × 10−8 m) and the potentiation was blocked by β‐bungarotoxin.

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Preferential Release of Adrenaline from the Adrenal Medulla by Muscarine and Pilocarpine

Cited by 151 publications

References 8 publications

Effects of synthetic adrenocorticotrophin on adrenal medullary responses to splanchnic nerve stimulation in conscious calves.

Effects of synthetic adrenocorticotrophin on adrenal medullary responses to splanchnic nerve stimulation in conscious calves.

Effect of Muscarine on Release of Catecholamines From the Perfused Adrenal Gland of the Cat

Mechanism of Action of Muscarine on the Longitudinal Muscle of the Guinea‐pig Isolated Ileum

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