| 1. |
- Charkoudian, N., et al.
(författare)
-
Sympathetic neural activity to the cardiovascular system: Integrator of systemic physiology and interindividual characteristics
- 2014
-
Ingår i: Comprehensive Physiology. - : Wiley. - 2040-4603. ; 4:2, s. 825-850
-
Tidskriftsartikel (refereegranskat)abstract
- The sympathetic nervous system is a ubiquitous, integrating controller of myriad physiological functions. In the present article, we review the physiology of sympathetic neural control of cardiovascular function with a focus on integrative mechanisms in humans. Direct measurement of sympathetic neural activity (SNA) in humans can be accomplished using microneurography, most commonly performed in the peroneal (fibular) nerve. In humans, muscle SNA (MSNA) is composed of vasoconstrictor fibers; its best-recognized characteristic is its participation in transient, moment-to-moment control of arterial blood pressure via the arterial baroreflex. This property of MSNA contributes to its typical "bursting" pattern which is strongly linked to the cardiac cycle. Recent evidence suggests that sympathetic neural mechanisms and the baroreflex have important roles in the long term control of blood pressure as well. One of the striking characteristics of MSNA is its large interindividual variability. However, in young, normotensive humans, higher MSNA is not linked to higher blood pressure due to balancing influences of other cardiovascular variables. In men, an inverse relationship between MSNA and cardiac output is a major factor in this balance, whereas in women, beta-adrenergic vasodilation offsets the vasoconstrictor/pressor effects of higher MSNA. As people get older (and in people with hypertension) higher MSNA is more likely to be linked to higher blood pressure. Skin SNA (SSNA) can also be measured in humans, although interpretation of SSNA signals is complicated by multiple types of neurons involved (vasoconstrictor, vasodilator, sudomotor and pilomotor). In addition to blood pressure regulation, the sympathetic nervous system contributes to cardiovascular regulation during numerous other reflexes, including those involved in exercise, thermoregulation, chemoreflex regulation, and responses to mental stress.
|
|
| 2. |
- Crossley, Dane A, et al.
(författare)
-
Mass Transport : Circulatory System with Emphasis on Nonendothermic Species.
- 2017
-
Ingår i: Comprehensive Physiology. - : John Wiley & Sons. - 2040-4603. ; 7:1, s. 17-66
-
Tidskriftsartikel (refereegranskat)abstract
- Mass transport can be generally defined as movement of material matter. The circulatory system then is a biological example given its role in the movement in transporting gases, nutrients, wastes, and chemical signals. Comparative physiology has a long history of providing new insights and advancing our understanding of circulatory mass transport across a wide array of circulatory systems. Here we focus on circulatory function of nonmodel species. Invertebrates possess diverse convection systems; that at the most complex generate pressures and perform at a level comparable to vertebrates. Many invertebrates actively modulate cardiovascular function using neuronal, neurohormonal, and skeletal muscle activity. In vertebrates, our understanding of cardiac morphology, cardiomyocyte function, and contractile protein regulation by Ca2+ highlights a high degree of conservation, but differences between species exist and are coupled to variable environments and body temperatures. Key regulators of vertebrate cardiac function and systemic blood pressure include the autonomic nervous system, hormones, and ventricular filling. Further chemical factors regulating cardiovascular function include adenosine, natriuretic peptides, arginine vasotocin, endothelin 1, bradykinin, histamine, nitric oxide, and hydrogen sulfide, to name but a few. Diverse vascular morphologies and the regulation of blood flow in the coronary and cerebral circulations are also apparent in nonmammalian species. Dynamic adjustments of cardiovascular function are associated with exercise on land, flying at high altitude, prolonged dives by marine mammals, and unique morphology, such as the giraffe. Future studies should address limits of gas exchange and convective transport, the evolution of high arterial pressure across diverse taxa, and the importance of the cardiovascular system adaptations to extreme environments. © 2017 American Physiological Society. Compr Physiol 7:17-66, 2017.
|
|
| 3. |
- Granger, D. Neil, et al.
(författare)
-
The Gastrointestinal Circulation : Physiology and Pathophysiology
- 2015
-
Ingår i: COMPREHENSIVE PHYSIOLOGY. - : Wiley. - 2040-4603. ; 5:3, s. 1541-1583
-
Tidskriftsartikel (refereegranskat)abstract
- The gastrointestinal (GI) circulation receives a large fraction of cardiac output and this increases following ingestion of a meal. While blood flow regulation is not the intense phenomenon noted in other vascular beds, the combined responses of blood flow, and capillary oxygen exchange help ensure a level of tissue oxygenation that is commensurate with organ metabolism and function. This is evidenced in the vascular responses of the stomach to increased acid production and in intestine during periods of enhanced nutrient absorption. Complimenting the metabolic vasoregulation is a strong myogenic response that contributes to basal vascular tone and to the responses elicited by changes in intravascular pressure. The GI circulation also contributes to a mucosal defense mechanism that protects against excessive damage to the epithelial lining following ingestion of toxins and/or noxious agents. Profound reductions in GI blood flow are evidenced in certain physiological (strenuous exercise) and pathological (hemorrhage) conditions, while some disease states (e.g., chronic portal hypertension) are associated with a hyperdynamic circulation. The sacrificial nature of GI blood flow is essential for ensuring adequate perfusion of vital organs during periods of whole body stress. The restoration of blood flow (reperfusion) to GI organs following ischemia elicits an exaggerated tissue injury response that reflects the potential of this organ system to generate reactive oxygen species and to mount an inflammatory response. Human and animal studies of inflammatory bowel disease have also revealed a contribution of the vasculature to the initiation and perpetuation of the tissue inflammation and associated injury response. (C) 2015 American Physiological Society.
|
|
| 4. |
- Grillner, Sten, et al.
(författare)
-
Basal Ganglia-A Motion Perspective
- 2020
-
Ingår i: Comprehensive Physiology. - : Wiley. - 2040-4603. ; 10:4, s. 1241-1275
-
Tidskriftsartikel (refereegranskat)abstract
- The basal ganglia represent an ancient part of the nervous system that have remained organized in a similar way over the last 500 million years and are of importance for our ability to determine which actions to choose at any given moment in time. Salient or reward stimuli act via the dopamine system and contribute to motor or procedural learning (reinforcement learning). The input stage of the basal ganglia, the striatum, is shaped by glutamatergic input from the cortex and thalamus and by the dopamine system. All intrinsic neurons of the striatum are GABAergic and inhibitory except for the cholinergic interneurons. Too little dopamine and all vertebrates show symptoms similar to that of a Parkinsonian patient, whereas too much dopamine results in hyperkinesia with involuntary movements. In this article, we discuss the detailed organization of the basal ganglia, with the different cell types, their properties, and contributions to basal ganglia functions. The striatal projection neurons represent 95% of all neurons in the striatum and are subdivided into two types, one that projects directly to the output stage, referred to as the "direct" pathway that promotes action, and the other subtype that targets the output nuclei via intercalated basal ganglia nuclei. This "indirect" pathway has an opposite effect. The striatal projection neurons express a set of ion channels that give them a high threshold for activation, whereas neurons in all other parts of the basal ganglia have a resting discharge that allows for modulation in both an increased and decreased direction.
|
|
| 5. |
- Hedenstierna, Göran, et al.
(författare)
-
Respiratory Function During Anesthesia : Effects on Gas Exchange
- 2012
-
Ingår i: COMPREHENSIVE PHYSIOLOGY. - : Wiley. - 2040-4603. ; 2:1, s. 69-96
-
Tidskriftsartikel (refereegranskat)abstract
- Anaesthesia causes a respiratory impairment, whether the patient is breathing spontaneously or is ventilated mechanically. This impairment impedes the matching of alveolar ventilation and perfusion and thus the oxygenation of arterial blood. A triggering factor is loss of muscle tone that causes a fall in the resting lung volume, functional residual capacity. This fall promotes airway closure and gas adsorption, leading eventually to alveolar collapse, that is, atelectasis. The higher the oxygen concentration, the faster will the gas be adsorbed and the aleveoli collapse. Preoxygenation is a major cause of atelectasis and continuing use of high oxygen concentration maintains or increases the lung collapse, that typically is 10% or more of the lung tissue. It can exceed 25% to 40%. Perfusion of the atelectasis causes shunt and cyclic airway closure causes regions with low ventilation/perfusion ratios, that add to impaired oxygenation. Ventilation with positive end-expiratory pressure reduces the atelectasis but oxygenation need not improve, because of shift of blood flow down the lung to any remaining atelectatic tissue. Inflation of the lung to an airway pressure of 40 cmH(2)O recruits almost all collapsed lung and the lung remains open if ventilation is with moderate oxygen concentration (< 40%) but recollapses within a few minutes if ventilation is with 100% oxygen. Severe obesity increases the lung collapse and obstructive lung disease and one-lung anesthesia increase the mismatch of ventilation and perfusion. CO2 pneumoperitoneum increases atelectasis formation but not shunt, likely explained by enhanced hypoxic pulmonary vasoconstriction by CO2. Atelectasis may persist in the postoperative period and contribute to pneumonia.
|
|
| 6. |
- Jansson, Leif, et al.
(författare)
-
Pancreatic Blood Flow with Special Emphasis on Blood Perfusion of the Islets of Langerhans
- 2019
-
Ingår i: COMPREHENSIVE PHYSIOLOGY. - : WILEY. - 2040-4603. ; 9:2, s. 799-837
-
Tidskriftsartikel (refereegranskat)abstract
- The pancreatic islets are more richly vascularized than the exocrine pancreas, and possess a 5- to 10-fold higher basal and stimulated blood flow, which is separately regulated. This is reflected in the vascular anatomy of the pancreas where islets have separate arterioles. There is also an insulo-acinar portal system, where numerous venules connect each islet to the acinar capillaries. Both islets and acini possess strong metabolic regulation of their blood perfusion. Of particular importance, especially in the islets, is adenosine and ATP/ADP. Basal and stimulated blood flow is modified by local endothelial mediators, the nervous system as well as gastrointestinal hormones. Normally the responses to the nervous system, especially the parasympathetic and sympathetic nerves, are fairly similar in endocrine and exocrine parts. The islets seem to be more sensitive to the effects of endothelial mediators, especially nitric oxide, which is a permissive factor to maintain the high basal islet blood flow. The gastrointestinal hormones with pancreatic effects mainly influence the exocrine pancreatic blood flow, whereas islets are less affected. A notable exception is incretin hormones and adipokines, which preferentially affect islet vasculature. Islet hormones can influence both exocrine and endocrine blood vessels, and these complex effects are discussed. Secondary changes in pancreatic and islet blood flow occur during several conditions. To what extent changes in blood perfusion may affect the pathogenesis of pancreatic diseases is discussed. Both type 2 diabetes mellitus and acute pancreatitis are conditions where we think there is evidence that blood flow may contribute to disease manifestations.
|
|
| 7. |
- Joyner, M. J., et al.
(författare)
-
Neural Control of the Circulation: How Sex and Age Differences Interact in Humans
- 2015
-
Ingår i: Comprehensive Physiology. - : Wiley. - 2040-4603. ; 5:1, s. 193-215
-
Tidskriftsartikel (refereegranskat)abstract
- The autonomic nervous system is a key regulator of the cardiovascular system. In this review, we focus on how sex and aging influence autonomic regulation of blood pressure in humans in an effort to understand general issues related to the cardiovascular system as a whole. Younger women generally have lower blood pressure and sympathetic activity than younger men. However, both sexes show marked interindividual variability across age groups with significant overlap seen. Additionally, while men across the lifespan show a clear relationship between markers of whole body sympathetic activity and vascular resistance, such a relationship is not seen in young women. In this context, the ability of the sympathetic nerves to evoke vasoconstriction is lower in young women likely as a result of concurrent beta(2)-mediated vasodilation that offsets alpha-adrenergic vasoconstriction. These differences reflect both central sympatho-inhibitory effects of estrogen and also its influence on peripheral vasodilation at the level of the vascular smooth muscle and endothelium. By contrast postmenopausal women show a clear relationship between markers of whole body sympathetic traffic and vascular resistance, and sympathetic activity rises progressively in both sexes with aging. These major findings in humans are discussed in the context of differences in population-based trends in blood pressure and orthostatic intolerance. The many areas where there is little sex-specific data on how the autonomic nervous system participates in the regulation of the human cardiovascular system are highlighted. (C) 2015 American Physiological Society.
|
|
| 8. |
|
|
| 9. |
- Liu, Ruisheng, et al.
(författare)
-
The Role of Macula Densa Nitric Oxide Synthase 1 Beta Splice Variant in Modulating Tubuloglomerular Feedback
- 2023
-
Ingår i: COMPREHENSIVE PHYSIOLOGY. - : John Wiley & Sons. - 2040-4603. ; 13:1, s. 4215-4229
-
Tidskriftsartikel (refereegranskat)abstract
- Abnormalities in renal electrolyte and water excretion may result in inappropriate salt and water retention, which facilitates the development and maintenance of hypertension, as well as acid-base and electrolyte disorders. A key mechanism by which the kidney regulates renal hemodynamics and electrolyte excretion is via tubuloglomerular feedback (TGF), an intrarenal negative feedback between tubules and arterioles. TGF is initiated by an increase of NaCl delivery at the macula densa cells. The increased NaCl activates luminal Na-K-2Cl cotransporter (NKCC2) of the macula densa cells, which leads to activation of several intracellular processes followed by the production of paracrine signals that ultimately result in a constriction of the afferent arteriole and a tonic inhibition of single nephron glomerular filtration rate. Neuronal nitric oxide (NOS1) is highly expressed in the macula densa. NOS1 beta is the major splice variant and accounts for most of NO generation by the macula densa, which inhibits TGF response. Macula densa NOS1 beta-mediated modulation of TGF responses plays an essential role in control of sodium excretion, volume and electrolyte hemostasis, and blood pressure. In this article, we describe the mechanisms that regulate macula densa-derived NO and their effect on TGF response in physiologic and pathologic conditions. (c) 2023 American Physiological Society.
|
|
