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Hormonal Control of Cardiovascular Reflexes
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Vernon S. Bishop, Joseph R. Haywood
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.
Vascular Innervation In The Respiratory Tract With Special Reference To Neuropeptides
Published in Geoffrey Burnstock, Susan G. Griffith, Nonadrenergic Innervation of Blood Vessels, 2019
Frank Sundler, Rolf Håkanson, Anders Luts, Rolf Uddman
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.
The autonomic nervous system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Synapses between the autonomic postganglionic neuron and the effector tissue, the neuroeffector junction, differ greatly from the neuron-to-neuron synapses discussed previously in Chapter 13 (see Table 14.1). The postganglionic fibers in the ANS do not terminate in a single swelling like the synaptic knob, nor do they synapse directly with the cells of a tissue. Instead, where the axons of these fibers enter a given tissue, they contain multiple swellings called varicosities. When the neuron is stimulated, these varicosities release neurotransmitter along a significant length of the axon and, therefore, over a large surface area of the effector tissue. The neurotransmitter diffuses through the interstitial fluid to wherever its receptors are in the tissue. This diffuse release of the neurotransmitter affects many tissue cells simultaneously. Furthermore, cardiac muscle and most smooth muscle have gap junctions between the cells. These specialized intercellular communications allow for the spread of electrical activity from one cell to the next. Thus, the discharge of a single autonomic nerve fiber to an effector tissue may alter the activity of the entire tissue.
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].