Evidence that transmitter release in sympathetic nerves is not set by feedback via presynaptic receptors

1983 ◽  
Vol 61 (10) ◽  
pp. 1197-1201 ◽  
Author(s):  
Stanley Kalsner
Keyword(s):  
Guinea Pig ◽  
Negative Feedback ◽  
Noradrenaline Release ◽  
Transmitter Release ◽  
Feedback Regulation ◽  
Feedback System ◽  
Sympathetic Nerves ◽  
Presynaptic Receptors ◽  
Negative Feedback Regulation

The possibility of negative feedback regulation of noradrenaline release was studied in the sympathetically innervated ureters of the guinea pig mounted in vitro. Tissues were transmurally stimulated with 300 pulses at 2 Hz over a range of voltages, from 10 to 60 V. It was determined that the output of transmitter increased with increasing voltage but that the effects of supposed presynaptic antagonism by yohimbine and presynaptic agonism by added noradrenaline did not fulfill the requirements of presynaptic theory governing negative feedback. It is concluded that the presynaptic effects of these drugs is neither linked to the operation of a negative feedback system nor sensitive to the perineuronal concentrations of free and active neurotransmitter.

scholarly journals The Pituitary Function of Androgen Receptor Constitutes a Glucocorticoid Production Circuit

2007 ◽  
Vol 27 (13) ◽  
pp. 4807-4814 ◽  
Author(s):  
Junko Miyamoto ◽  
Takahiro Matsumoto ◽  
Hiroko Shiina ◽  
Kazuki Inoue ◽  
Ichiro Takada ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Negative Feedback ◽  
Late Onset ◽  
Feedback Regulation ◽  
Feedback System ◽  
Cell Types ◽  
Positive Control ◽  
Negative Feedback Regulation ◽  
Pituitary Glands ◽  
Glucocorticoid Production

ABSTRACT Androgen receptor (AR) mediates diverse androgen actions, particularly reproductive processes in males and females. AR-mediated androgen signaling is considered to also control metabolic processes; however, the molecular basis remains elusive. In the present study, we explored the molecular mechanism of late-onset obesity in male AR null mutant (ARKO) mice. We determined that the obesity was caused by a hypercorticoid state. The negative feedback system regulating glucocorticoid production was impaired in ARKO mice. Male and female ARKO mice exhibited hypertrophic adrenal glands and glucocorticoid overproduction, presumably due to high levels of adrenal corticotropic hormone. The pituitary glands of the ARKO males had increased expression of proopiomelanocortin and decreased expression of the glucocorticoid receptor (GR). There were no overt structural abnormalities and no alteration in the distribution of cell types in the pituitaries of male ARKO mice. Additionally, there was normal production of the other hormones within the glucocorticoid feedback system in both the pituitary and hypothalamus. In a cell line derived from pituitary glands, GR expression was under the positive control of the activated AR. Thus, this study suggests that the activated AR supports the negative feedback regulation of glucocorticoid production via up-regulation of GR expression in the pituitary gland.

Adrenergic presynaptic receptors: Examination of a hypothesis in guinea pig vas deferens

1979 ◽  
Vol 57 (7) ◽  
pp. 717-724 ◽  
Author(s):  
Stanley Kalsner
Keyword(s):  
Guinea Pig ◽  
Negative Feedback ◽  
Vas Deferens ◽  
Mechanical Response ◽  
Relative Effectiveness ◽  
Feedback System ◽  
Presynaptic Receptors ◽  
Adrenergic Nerve ◽  
Receptor Sites ◽  
Physiological Relevance

The hypothesis was examined that phenoxybenzamine enhances both the overflow of noradrenaline and the mechanical response in guinea pig vas deferens by blockade of presynaptic inhibitory receptors located on adrenergic nerve terminals which serve a negative-feedback function. Preparations were stimulated with a constant small number of pulses but at three different frequencies (1, 5, and 15 Hz) and the relative effectiveness of phenoxybenzamine in enhancing overflow assessed. According to the presynaptic receptor hypothesis inhibition of transmitter output should increase with increasing frequency due to increased activation of receptor sites by endogenously released noradrenaline. The antagonist enhanced the overflow of tritium but did so to a similar extent at all three frequencies, regardless of the length of the interval between pulses. Similarly, no evidence for a greater sensitization of the mechanical response by phenoxybenzamine at the higher frequencies was obtained. The conditions of the present experiment were considered optimal for the operation of the negative-feedback system and the results indicate that the physiological relevance of such a system is questionable.

Positive feedback regulation of noradrenaline release from sympathetic nerves: a questionable hypothesis

1982 ◽  
Vol 60 (5) ◽  
pp. 737-743 ◽  
Author(s):  
Stanley Kalsner
Keyword(s):  
Noradrenaline Release ◽  
Positive Feedback ◽  
Feedback Regulation ◽  
Feedback System ◽  
Sympathetic Nerves ◽  
Inhibitory Effect ◽  
Similar Extent ◽  
Test Conditions ◽  
Beta Receptors ◽  
Exogenous Agents

The effects of known agonists and of an antagonist on the stimulation-induced efflux of [3H]noradrenaline from left atria of guinea pigs was assessed. This was done to evaluate the hypothesis of presynaptic beta receptors mediating a positive feedback system. Isoproterenol (1.2 × 10−8 M) enhanced the efflux of tritium with 50 pulses at all four test frequencies and did so to a similar extent at three of them. Exogenous noradrenaline (1.8 × 10−6 M) inhibited efflux and isoproterenol was ineffective as an enhancer of efflux in its presence. Propranolol (1 × 10−7 M) did not reliably increase the inhibitory effect of added noradrenaline on stimulation-induced efflux nor did the antagonist by itself under a variety of test conditions decrease the stimulation-induced efflux of tritium. It is concluded that the synaptic quantities of transmitter do not determine the magnitudes of the effects of exogenous agents on tritium efflux and that positive feedback, for both theoretical and empirical considerations, does not function during neurosecretion

scholarly journals Possible action of vasohibin-1 as an inhibitor in the regulation of vascularization of the bovine corpus luteum

Reproduction ◽  
2012 ◽  
Vol 143 (4) ◽  
pp. 491-500 ◽  
Author(s):  
Koumei Shirasuna ◽  
Ayumi Kobayashi ◽  
Akane Nitta ◽  
Sayo Nibuno ◽  
Kiemi Sasahara ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Corpus Luteum ◽  
Negative Feedback ◽  
Physiological Mechanism ◽  
Feedback Regulation ◽  
Negative Feedback Regulation ◽  
Luteal Function ◽  
Feedback Regulator

The development of the corpus luteum (CL), which secretes large amounts of progesterone to establish pregnancy, is accompanied by active angiogenesis, vascularization, and lymphangiogenesis. Negative feedback regulation is a critical physiological mechanism. Vasohibin-1 (VASH1) was recently discovered as a novel endothelium-derived negative feedback regulator of vascularization. We therefore investigated the expression of VASH1 in the bovine CL. Expression of VASH1 mRNA and protein was predominantly localized to luteal endothelial cells (LECs). VASH1 expression in the CL was constant through the early to late luteal phases and decreased during CL regression relating with the action of luteolytic prostaglandin F2α in vivo. To investigate the role of VASH1, we determined whether VASH1 treatment affects angiogenesis and/or lymphangiogenesis using LECs and lymphatic endothelial cells (LyECs) in vitro. Vascular endothelial growth factor A (VEGFA) stimulated the expression of VASH1 in LECs but not in LyECs, and VASH1 completely blocked VEGFA-induced formation of capillary-like tube structures of LECs and LyECs in vitro. In summary, VASH1 is predominantly located on LECs in the bovine CL and inhibits the angiogenic and lymphangiogenic actions of VEGFA. Bovine CL therefore has a VEGFA–VASH1 system that may be involved in regulation of luteal function, especially in the development of the CL. The results indicate that VASH1 has the potential to act as a negative feedback regulator of angiogenesis and lymphangiogenesis in the CL in cows.

Evidence for the involvement of α1-adrenoceptors in negative feedback regulation of noradrenergic transmitter release in rat atria

1985 ◽  
Vol 68 (s10) ◽  
pp. 111s-115s ◽  
Author(s):  
D. F. Story ◽  
C. A. Standford-Starr ◽  
M. J. Rand
Keyword(s):  
Transmitter Release ◽  
Feedback Regulation ◽  
Sympathetic Nerves ◽  
Field Stimulation ◽  
Negative Feedback Regulation ◽  
Rat Atria ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Isolated Atria ◽  
Stimulation Of

1. Experiments were undertaken to determine if prejunctional α1-adrenoceptors are involved in autoinhibitory regulation of transmitter noradrenaline release in rat atria. 2. The noradrenergic transmitter stores in rat isolated atria were radiolabeled with [3H]noradrenaline and transmitter release was deduced from the efflux of the radiolabel evoked by field stimulation of the atrial intramural sympathetic nerves. 3. Phentolamine (3 μmol/l) and prazosin (0.1 and 3 μmol/l) enhanced the release of radiolabel evoked by stimulation with trains of 4, 8 and 16 pulses, whereas idazoxan (10 μmol/l) enhanced release evoked by stimulation with 8 and 16 pulses. Idazoxan and prazosin were about equieffective in enhancing the evoked release but phentolamine produced much greater enhancement than either idazoxan or prazosin. 4. Combination of idazoxan (10 μmol/l) and prazosin enhanced the stimulation-evoked release with 4, 8 and 16 pulses to the same extent as phentolamine (3 μmol/l). 5. The selective α1-adrenoceptor agonist methoxamine (10 μmol/l) inhibited stimulation-evoked release and this effect was blocked by the α1-adrenoceptor antagonist prazosin (0.1 μmol/l). 6. The findings indicate that α1-adrenoceptors may contribute to autoinhibitory feedback regulation of transmitter release in rat atria.

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