Nicotine stimulates adrenergic terminals and inhibits contractions of mouse uterine horns

✓ The Hillarp technique of fluorescent staining of monoamines was used to examine the adrenergic fibers in the cerebral vessels of rabbit brains. These fibers were found to lie wholly within the deeper layers of the adventitia and not within muscle layers. Varicosities were interpreted as representing neural transmitter substance. The basilar artery had a sparse innervation; the anterior cerebral, carotid, and middle cerebral arteries were more richly supplied by adrenergic terminals, with the most dense innervation in the superficial vessels between 100 and 300 µ in diameter. Mild trauma to the basilar artery, as well as subarachnoid blood without trauma, caused the catecholamine reaction to disappear. A marked depletion of adrenergic fibers was also noted after administration of alpha methyl tyrosine and subjection of the animals to extremes of blood pressure.

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Postnatal development of adrenergic terminals in rat locus coeruleus, with special reference to growth of noradrenergic neurons

Developmental Brain Research ◽

10.1016/0165-3806(96)00118-6 ◽

1996 ◽

Vol 96 (1-2) ◽

pp. 241-248 ◽

Cited By ~ 8

Author(s):

Naruo Saito ◽

Morimi Shimada ◽

Kunio Kitahama ◽

Toshihiro Maeda

Keyword(s):

Special Reference ◽

Locus Coeruleus ◽

Postnatal Development ◽

Noradrenergic Neurons ◽

Adrenergic Terminals

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Noradrenergic stimulation of serotonin release from rat pineal glands in vitro

Journal of Endocrinology ◽

10.1677/joe.0.1140003 ◽

1987 ◽

Vol 114 (1) ◽

pp. 3-9 ◽

Cited By ~ 19

Author(s):

V. J. Aloyo ◽

R. F. Walker

Keyword(s):

Serotonin Release ◽

Time Interval ◽

Intracellular Accumulation ◽

Differential Distribution ◽

Intracellular Compartments ◽

5 Ht Uptake ◽

Layer Chromatography ◽

Adrenergic Terminals ◽

Stimulation Of

ABSTRACT The pharmacodynamics of serotonin (5-hydroxytryptamine; 5-HT) uptake and release were studied in rat pineal glands. Initially, uptake was tested by incubating pineals with several concentrations of [3H]5-HT. The incubation media also contained [14C]mannitol to which cells are impermeable. Since [14C]mannitol accumulates only in extracellular spaces, the radio-labelled sugar was used to determine the differential distribution of [3H]5-HT in pineal compartments. Intracellular accumulation of 3H in pineal glands increased linearly as a function of time for [3H]5-HT concentrations ranging from 1 to 10 μmol/l. The ratio of 3H to 14C also increased for the same time-interval, indicating that the glands accumulated [3H]5-HT preferentially in non-extracellular spaces. [3H]5-HT accumulated in pineal glands which were denervated for more than 7 days before testing, suggesting that uptake is not restricted to adrenergic terminals but also occurs in pinealocytes. In addition to uptake, spontaneous and noradrenaline-stimulated release of [3H]5-HT was tested in perifusion and/or step-transfer systems. Spontaneous release of [3H]5-HT was biphasic consisting of rapid and slower efflux phases. In contrast, release of [14C]mannitol was monophasic, characterized exclusively by rapid efflux. Since [14C]mannitol does not enter cells, the rapid and slower phases of [3H]5-HT efflux may represent release from pineal extracellular and intracellular compartments respectively. The identity of [3H]5-HT in pineal glands and perifusion media was confirmed by thin-layer chromatography. When l-noradrenaline was added to the perifusion media, [3H]5-HT efflux during the slower phase of release was significantly increased above the non-stimulated state. In contrast, d-noradrenaline was significantly less effective than l-noradrenaline in releasing [3H]5-HT. Noradrenaline also stimulated [3H]5-HT release from denervated glands, suggesting that pinealocytes secrete 5-HT in response to noradrenergic signals. Since the pineal is innervated by fibres of the sympathetic division of the autonomic nervous system, differential release of 5-HT may occur in response to changing levels of glandular noradrenaline. J. Endocr. (1987) 114, 3–9

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The involvement of heating rate and vasoconstrictor nerves in the cutaneous vasodilator response to skin warming

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00919.2008 ◽

2009 ◽

Vol 296 (1) ◽

pp. H51-H56 ◽

Cited By ~ 63

Author(s):

Gary J. Hodges ◽

Wojciech A. Kosiba ◽

Kun Zhao ◽

John M. Johnson

Keyword(s):

Sympathetic Nerve ◽

Transmitter Release ◽

Whole Body ◽

Local Skin ◽

Axon Reflex ◽

Sympathetic Function ◽

Cutaneous Vascular Conductance ◽

Skin Temperatures ◽

Adrenergic Terminals ◽

Adrenergic Effects

Slow local skin heating (LH) causes vasodilator responses, some of which are dependent on sympathetic nerve function. It is not known, however, how the rate of LH affects either the sympathetic or the nonadrenergic components of the responses to LH and whether the adrenergic effects of LH depend on tonic sympathetic activity or whether LH stimulates transmitter release. In part 1, cutaneous vascular conductance (CVC) responses to slow and fast LH (+0.1° and +2°C/min) from 34° to 40°C were compared both at control sites and at sites pretreated with bretylium tosylate (BT; blocks transmitter release from adrenergic terminals). We confirmed, as previously found, the axon reflex (AR) response to slow LH to be blocked by BT ( P < 0.05). Pretreatment with BT reduced the AR only with fast LH. BT inhibited the peak vasodilation achieved with both rates of LH ( P < 0.05). Longer-term LH was associated with a slow fall in CVC, the classical “die away” phenomenon, at untreated sites ( P < 0.05) but not at BT-pretreated sites. Thus the LH-stimulated AR is only partially dependent on intact sympathetic function, and the “die away” phenomenon is dependent on such function. In part 2, we tested whether the conditions in part 1 (whole body and local skin temperatures of 34°C) completely suppressed sympathetic nerve activity. The infusion of BT by microdialysis did not change the CVC ( P > 0.05), suggesting the absence of tonic activity in those conditions and therefore that the adrenergic components of the responses in part 1 are via the stimulation of the transmitter release by LH.

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