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Homeostasis
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
Most of the body’s compensatory homeostatic mechanisms function by way of negative feedback. This is a response that causes the level of a variable to change in a direction opposite to that of the initial change. Because the response returns the variable back to its baseline level, it has a stabilizing effect on the body. For example, when blood pressure increases, the arterial baroreceptors are stimulated and an increased number of nerve impulses are transmitted to the CNS through afferent pathways. The region of the brain regulating the cardiovascular system responds to this sensory input by altering efferent nerve activity to the heart. The result is a decrease in heart rate and, therefore, a decrease in blood pressure back to its baseline value (see Figure 2.2). In general, when some physiological variable becomes too high or too low, a control system elicits a negative feedback response consisting of one or a series of changes that returns the variable to within its normal physiological range. These compensatory mechanisms operating via negative feedback allow the body to effectively maintain homeostasis.
Physiology of Equilibrium
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Floris L. Wuyts, Leen K. Maes, An Boudewyns
The vestibular sensory epithelium is formed mainly of hair cells, which are very similar to those located in the cochlea. Two types of hair cells (I and II) can be distinguished. Type I hair cells are amphora-shaped, have a spherical nucleus and are surrounded by a chalice-like afferent nerve ending. Efferent nerve buds impinge on the afferent nerve chalice. Type II hair cells are more cylindrical, contain a cylindrical nucleus and have bud-shaped afferent and efferent nerve endings located at the distal end of the cell. The apex of the hair cells is bathed in endolymph and is surrounded by non-sensory, supporting cells and dark cells (Figure 49.19).
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
The term”neuroeffector junction” (or “neuroeffector ending”) was noted in only 5 of the 23 recent textbooks of basic neuroanatomy consulted for this discussion. Given the literal meaning of the term, it could reasonably be used to label efferent nerve-endings on any effector, whether somatic (skeletal muscle) or visceral (cardiac muscle, smooth muscle, and glands). Although the authors of two texts clearly do use the term in this broad manner (B&K, p. 41; w&G, p. 103–104, 578 [in conjunction with p. 71, 73]), authors of the other three texts use it to label efferent nerve-endings on visceral effectors only (Brod, p. 719;Chus, p. 175 [Fig. 8–9], FitzG, p. 37, 39, 41]. I don’t know whether the latter authors consider “neuroeffector junctions” to be solely visceral by definition, or whether they have instead simply not used the term to describe somatic nerve-endings because common terms such as “neuromuscular junction” are available. As additional data supporting an intent to limit “neuroeffector junctions” to visceral structures, the relevant entries in the indices of two of the texts do not indicate pages on which neuromuscular junctions are described (Chus, p. 504–505; FitzG, p. 289). In the third text, the closest relevant entry in the index is “Autonomic nervous system, neuroeffector mechanisms” (Brod, p. 1038), so references to the neuromuscular junction would be inappropriate.
Application of bulbocavernosus reflex combined with anal sphincter electromyography in the diagnosis of MSA and PD
Published in International Journal of Neuroscience, 2022
Xiaoting Niu, Yifan Cheng, WangWang Hu, Zijian Fan, Wanli Zhang, Bei Shao, Binbin Deng
The BCR examinee took a stone cutting position. A saddle-shaped surface electrode was placed at the root of the penis (male) or clitoris (female). A concentric needle recording electrode was inserted into the left and right bulbocavernous muscles successively (Figure 1). The stimulation intensity was 7 times the sensory threshold, and the electrode impedance was maintained less than 5 k Ω. Twenty reflected waves were recorded with a scanning time of 5 ms/div, a bandwidth of 100 ms, and a bandwidth of 10 Hz. Twenty reflected waves were recorded, and the average latency was calculated. The BCR index reflected the conduction function of the pudendal afferent nerve, the efferent nerve and the sacral 2-4 reflex arc. An abnormal recording was judged as (1) prolonged BCR latency or (2) if no BCR was elicited.
Renal denervation as a management strategy for hypertension: current evidence and recommendations
Published in Expert Review of Cardiovascular Therapy, 2021
Márcio Galindo Kiuchi, Revathy Carnagarin, Janis M. Nolde, Leslie Marisol Lugo-Gavidia, Natalie C. Ward, Markus P. Schlaich
There is continued interest in improving our understanding of the major mechanisms through which RDN exerts its BP lowering effects. While a detailed discussion is beyond the scope of this review, several aspects are worthwhile to be highlighted in the current context. There is clear evidence that efferent sympathetic outflow to the skeletal muscle vasculature as assessed by microneurography (19) and to the kidneys, as assessed by renal noradrenaline spillover technology (20) is significantly reduced by RDN. While the latter is a direct consequence of severing of renal efferent nerve fibers during the procedure, the effect on sympathetic outflow to muscle is most likely explained by inhibition of afferent signaling from the kidneys to brain stem nuclei that control muscle sympathetic nerve activity, thereby highlighting the contribution of afferent nerves (31). Whether re-innervation of nerves may occur is another relevant question and while animal studies indicate that sympathetic nerves can regrow, longer term human studies demonstrated sustained BP lowering over at least 3 years (24, 32), rendering a significant role for reinnervation unlikely.
Renal sympathetic denervation attenuates left ventricle hypertrophy in spontaneously hypertensive rats by suppressing the Raf/MEK/ERK signaling pathway
Published in Clinical and Experimental Hypertension, 2021
Bing Xiao, Fan Liu, Ye-Hui Jin, Ya-Qiong Jin, Li Wang, Jing-Chao Lu, Xiu-Chun Yang
Accumulating evidence has shown that hypertension is a kind of systemic disease caused by multiple risk factors, including genetic and environmental factors, or their interactions, having great associations with the high prevalence and mortality of cerebrovascular events (1,2). Left ventricle hypertrophy (LVH), one of the most important target organ damages in hypertension, has been well recognized as an independent risk factor for cardiovascular morbidity and fatality, and continuous myocardial hypertrophy may eventually result in heart failure, malignant arrhythmia or even sudden death (3,4). Thus, how to delay or even reverse the progression of LVH is a major issue in the research and development of new strategies for the prevention and treatment of myocardial diseases (5). Recent studies have indicated that renal sympathetic denervation (RSD) can efficiently decrease blood pressure (6,7). Mechanistically, RSD can specifically block the renal sympathetic nerves, i.e., the renal sympathetic afferent nerve-hypothalamus-renal sympathetic efferent nerve circuit decreases the activity of sympathetic nerves, thus decreasing blood pressure (8,9). In addition to the decrease in blood pressure, Krum H et al. also observed improved LVH and heart function after RSD (10). However, although the roles of RSD in decreasing blood pressure and suppressing sympathetic pressure have been clarified, the potential mechanism affecting LVH remains to be elucidated in further studies.