Hormonal Control of Cardiovascular Reflexes
Irving H. Zucker, Joseph P. Gilmore in Reflex Control of the Circulation, 2020
The renin-angiotensin-aldosterone system can contribute to the regulation of arterial pressure through several short- and long-term mechanisms. In addition to a direct vasoconstrictor action, ANG II influences the level of arterial pressure through a retention of sodium via the direct effect of ANG II on the kidney or the release of aldosterone. The pressor response to ANG II is also influenced by actions of the peptide in the central and peripheral nervous systems. In the peripheral nervous system, the peptide facilitates the activation of sympathetic ganglia, stimulates the adrenal medulla, and enhances the release and response of norepinephrine at the neuroeffector junction. In the central nervous system, ANG II has been proposed to stimulate sympathetic nerve activity and suppress baroreflex control of the sympathetic nervous system.
Cardiorespiratory Regulation
Alan D. Miller, Armand L. Bianchi, Beverly P. Bishop in Neural Control of the Respiratory Muscles, 2019
As with ganglionic transmission, it is clear that transmission at the sympathetic neuroeffector junction is dependent on both the frequency and pattern of action potentials. Nilsson et al.48 noted that groups of impulses with high instantaneous frequencies produced contraction of mesenteric vessels that far exceeded those at a constant but equivalent average frequency. Many other similar observations have been made since.2,28 There is also evidence that the response to short burst of impulses is mediated mainly by the activation of P2x-purinoceptors and α2-adrenoceptors; however, as burst length increases the α1-adrenoceptor-mediated component becomes more significant and then dominates.37,55 Thus, the patterning of activity by central respiratory networks may have a significant impact on neuroeffector transmission.
Vascular Innervation In The Respiratory Tract With Special Reference To Neuropeptides
Geoffrey Burnstock, Susan G. Griffith in Nonadrenergic Innervation of Blood Vessels, 2019
The potentiating action of NPY seems to require the influx of Na+ and the mobilization of an intracellular sequestered Ca+ + pool.80 The possible end-result of these various actions of NPY may be an improvement in the “economy” at the sympathetic neuroeffector junction, reflected in a reduced NA demand and a suppression or shortening of the NA release process after nerve stimulation. However, most of the results obtained so far are from in vitro studies and it is unclear to what extent they apply in vivo. It is also important to keep in mind that NPY does not seem to evoke all three effects at every sympathetic neuroeffector junction. One of the effects may be manifested in one target and the other effects in another, possibly reflecting differences in the localization of receptor subtypes. Secondly, the potentiating effect of NPY is not limited to NA, since the effects of histamine, for example, are also enhanced. Finally, NPY is not the only peptide that is capable of exerting the three actions at the sympathetic neuroeffector junction. Its chemical relative peptide YY (PYY) and to some extent pancreatic peptide are also capable of inducing the same effects, and it is therefore still difficult to define a physiological role for NPY as such at the sympathetic neuroeffector junction. Certainly, however, the effects produced by NPY and PYY are manifested at concentrations which makes it very attractive to speculate on their physiological significance.
Influences of ovarian hormones on physiological responses to cold in women
Published in Temperature, 2022
Andrew M. Greenfield, Nisha Charkoudian, Billie K. Alba
In addition to central reflex mechanisms, cutaneous vasoconstriction is mediated by local mechanisms (i.e., the direct effects of local temperature on the neuroeffector junction and blood vessels themselves). These mechanisms also include adrenergic and nonadrenergic components [29,30]. The initial local vasoconstrictor response is primarily mediated by the translocation of intracellular α2C-receptors to the smooth muscle cell membrane and subsequent activation by NE [31]. Alpha2C-receptor translocation during local cooling is stimulated by reactive oxygen species (ROS)-induced activation of ROCK [28,32–34]. As skin temperature continues to decline, local mechanisms suppress the nitric oxide (NO) system by inhibiting NO synthase and downstream NO-dependent signaling, further enhancing the vasoconstrictor response during prolonged cooling [29].
Related Knowledge Centers
- Autonomic Nervous System
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- G Protein
- Gap Junction
- Metabotropic Receptor
- Neuromuscular Junction
- Synapse
- Neurotransmitter
- NON-Noradrenergic, NON-Cholinergic Transmitter