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Regulation of Sympathetic Nerve Activity in Humans: New Concepts Regarding Autonomic Adjustments to Exercise and Neurohumoral Excitation in Heart Failure
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
David W. Ferguson, Allyn L. Mark
During the initial stages of exercise and during low-level (nonfatiguing) exercise, central command appears to dominate without sufficient muscle acidosis to engage the metaboreflex. Under these conditions, the pressor response appears to be mediated primarily by tachycardia (parasympathetic withdrawal) and increases in cardiac output without significant sympathetic vasoconstriction in skeletal muscle. The lack of significant increases in muscle SNA at the onset or with low levels of exercise would seem to subserve perfusion of the exercising muscle. Specifically, if central command or mechanoreflexes were to increase muscle SNA during the initial stage of exercise or during nonfatiguing exercise, the increase in muscle SNA could occur before or in the absence of appreciable accumulation of ischemic metabolites in the exercising muscle. Under these conditions, the increased muscle SNA might constrict vessels and impair perfusion of the exercising as well as resting muscle.
Evaluation of Autonomic Failure
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
D) Some authors have observed an increased pressor response in subjects with atherosclerosis, or, in contrast, a minimal response in normal individuals (Robertson, 1981). An increased response is typical of baroreflex failure. Another drawback of this test is that the cold stimulus is often considered very painful and a majority of the subjects are reluctant to have it repeated.
Cardiovascular receptors, reflexes and central control
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
In human studies, both metaboreceptors and mechanoreceptors can be blocked by a local anaesthetic (epidural anaesthesia), while essentially preserving motor axon function. This markedly reduces the exercise pressor response, but does not abolish the overall blood pressure response completely (Figure 16.13) illustrating the importance of both central command and peripheral reflex control. However, this experiment is difficult to interpret because epidural anaesthesia also decreases sympathetic efferent drive to muscle, causing vasodilatation as sympathetic vasoconstrictor tone is lost (the legs feel warm).
Cardiovascular diseases, cold exposure and exercise
Published in Temperature, 2018
In summary, hypertension results in aggravated [61,76] or comparable [38,42,43,63,65] increase in cardiovascular strain during whole-body cold exposure compared with controls. Local cooling suggest upregulation of pathways related to endothelial dysfunction of the microcirculation in essential hypertension. The variation in responses may partially depend on whether cooling of the head is involved or not, but also be related to differences in study populations (e.g. diseases progression, use of medication) and protocols. The higher cardiac workload observed in cold is primarily due to the increase in sympathetic activity and its effect on vasoconstriction and augmented BP [76]. The higher baseline BP together with its cold response among hypertensive subjects may more often involve an increased risk of cardiovascular events. For example, cold exposure affecting mainly the face increased SBP momentarily above 200 mmHg among untreated mildly hypertensive patients [38]. Antihypertensive medication lowers BP levels, but do not affect responsiveness to cold during whole body cooling [63–65] or the cold pressor test [40]. Appropriate protection in the cold may reduce the pressor response.
When Blood Pressure Increases with Standing: Consensus Definition for Diagnosing Orthostatic Hypertension
Published in Blood Pressure, 2023
Jens Jordan, Italo Biaggioni, Guido Grassi, Artur Fedorowski, Kazuomi Kario
Blood pressure measurements in the supine and in the upright position, while considered routine part of a physical examination in patients with cardiovascular disease, are rarely conducted in clinical practice. Abnormalities in blood pressure responses to standing, be it orthostatic hypotension or orthostatic hypertension identify patients at an increased cardiovascular risk and may affect therapeutic decisions. Yet, more research on mechanisms, epidemiology, and clinical management of patients with orthostatic hypertension is required. A consensus definition for an exaggerated orthostatic pressor response and orthostatic hypertension is an important step to make future research more comparable and applicable in the clinic.
Mechanisms involved in the cardiovascular effects caused by acute osmotic stimulation in conscious rats
Published in Stress, 2020
Eduardo Albino Trindade Fortaleza, Cristiane Busnardo, Aline Fassini, Ivaldo Jesus Almeida Belém-Filho, Gislaine Almeida-Pereira, José Antunes-Rodrigues, Fernando Morgan Aguiar Corrêa
As a first approach, the result showing that ganglion blockade only affected the initial component of the pressor response to i.p. OS indicated a minor involvement of the vascular sympathetic system acting mainly on its initial component, which is under influence of the psychological stress due to handling and injection procedure, as well as the no sympathetic involvement in the subsequent long-lasting pressor response concomitant to plasma osmolality increase caused by the OS. In agreement, ganglion blockade was reported to reduce markedly the pressor response to restraint stress (RS), a predominantly psychologic stimulus (Dos Reis et al., 2014).