The evolutionary origins of volition

It appears to be a straightforward implication of distributed cognition principles that there is no integrated executive control system (e.g. Brooks 1991, Clark 1997). If distributed cognition is taken as a credible paradigm for cognitive science this in turn presents a challenge to volition because the concept of volition assumes integrated information processing and action control. For instance the process of forming a goal should integrate information about the available action options. If the goal is acted upon these processes should control motor behavior. If there were no executive system then it would seem that processes of action selection and performance couldn’t be functionally integrated in the right way. The apparently centralized decision and action control processes of volition would be an illusion arising from the competitive and cooperative interaction of many relatively simple cognitive systems. Here I will make a case that this conclusion is not well-founded. Prima facie it is not clear that distributed organization can achieve coherent functional activity when there are many complex interacting systems, there is high potential for interference between systems, and there is a need for focus. Resolving conflict and providing focus are key reasons why executive systems have been proposed (Baddeley 1986, Norman and Shallice 1986, Posner and Raichle 1994). This chapter develops an extended theoretical argument based on this idea, according to which selective pressures operating in the evolution of cognition favor high order control organization with a ‘highest-order’ control system that performs executive functions

Short-term heat acclimation is effective and may be enhanced rather than impaired by dehydration

Most heat acclimation data are from regimes longer than 1 week, and acclimation advice is to prevent dehydration. Objectives: We hypothesized that (i) short-term (5-day) heat acclimation would substantially improve physiological strain and exercise tolerance under heat stress, and (ii) dehydration would provide a thermally independent stimulus for adaptation. Methods: Nine aerobically fit males heat acclimated using controlled-hyperthermia (rectal temperature 38.5°C) for 90 min on 5 days; once euhydrated (EUH) and once dehydrated (DEH) during acclimation bouts. Exercising heat stress tests (HSTs) were completed before and after acclimations (90-min cycling in T a 35°C, 60% RH). Results: During acclimation bouts, [aldosterone] plasma rose more across DEH than EUH (95%CI for difference between regimes: 40-411 pg ml -1 ; P=0.03; n=5) and was positively related to plasma volume expansion (r=0.65; P=0.05), which tended to be larger in DEH (CI: -1 to 10%; P=0.06; n=9). In HSTs, resting forearm perfusion increased more in DEH (by 5.9 ml 100 tissue ml -1 min -1 : -11.5 to -1.0; P=0.04) and end-exercise cardiac frequency fell to a greater extent (by 11 b min -1 : -1 to 22; P=0.05). Hydration-related effects on other endocrine, cardiovascular, and psychophysical responses to HSTs were unclear. Rectal temperature was unchanged at rest but was 0.3°C lower at end exercise (P < 0.01; interaction: P=0.52). Conclusions: Short-term (5-day) heat acclimation induced effective adaptations, some of which were more pronounced after fluid-regulatory strain from permissive dehydration, and not attributable to dehydration effects on body temperature. Am. J. Hum. Biol. 26:311-320, 2014. © 2014 Wiley Periodicals, Inc

Molecular Mechanisms of Kidney Injury and Repair in Arterial Hypertension

The global burden of chronic kidney disease is rising. The etiologies, heterogeneous, and arterial hypertension, are key factors contributing to the development and progression of chronic kidney disease. Arterial hypertension is induced and maintained by a complex network of systemic signaling pathways, such as the hormonal axis of the renin-angiotensin-aldosterone system, hemodynamic alterations affecting blood flow, oxygen supply, and the immune system. This review summarizes the clinical and histopathological features of hypertensive kidney injury and focusses on the interplay of distinct systemic signaling pathways, which drive hypertensive kidney injury in distinct cell types of the kidney. There are several parallels between hypertension-induced molecular signaling cascades in the renal epithelial, endothelial, interstitial, and immune cells. Angiotensin II signaling via the AT1R, hypoxia induced HIFα activation and mechanotransduction are closely interacting and further triggering the adaptions of metabolism, cytoskeletal rearrangement, and profibrotic TGF signaling. The interplay of these, and other cellular pathways, is crucial to balancing the injury and repair of the kidneys and determines the progression of hypertensive kidney disease

Vascular smooth muscle contraction in hypertension

Hypertension is a major risk factor for many common chronic diseases, such as heart failure, myocardial infarction, stroke, vascular dementia and chronic kidney disease. Pathophysiological mechanisms contributing to the development of hypertension include increased vascular resistance, determined in large part by reduced vascular diameter due to increased vascular contraction and arterial remodelling. These processes are regulated by complex interacting systems such as the renin angiotensin aldosterone system (RAAS), sympathetic nervous system, immune activation and oxidative stress, which influence vascular smooth muscle function. Vascular smooth muscle cells are highly plastic and in pathological conditions undergo phenotypic changes from a contractile to a proliferative state. Vascular smooth muscle contraction is triggered by an increase in intracellular free calcium concentration ([Ca2+]i), promoting actin-myosin cross-bridge formation. Growing evidence indicates that contraction is also regulated by calcium-independent mechanisms involving RhoA-Rho kinase (ROCK), protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) signaling, reactive oxygen species and reorganization of the actin cytoskeleton. Activation of immune/inflammatory pathways and noncoding RNAs are also emerging as important regulators of vascular function. Vascular smooth muscle cell [Ca2+]i, not only determines the contractile state but also influences activity of many calcium-dependent transcription factors and proteins thereby impacting the cellular phenotype and function. Perturbations in vascular smooth muscle cell signaling and altered function influence vascular reactivity and tone, important determinants of vascular resistance and blood pressure. Here we discuss mechanisms regulating vascular reactivity and contraction in physiological and pathophysiological conditions and highlight some new advances in the field, focusing specifically on hypertension

The spleen: a hub connecting nervous and immune systems in cardiovascular and metabolic diseases

Metabolic disorders have been identified as major health problems affecting a large portion of the world population. In addition, obesity and insulin resistance are principal risk factors for the development of cardiovascular diseases. Altered immune responses are common features of both hypertension and obesity and, moreover, the involvement of the nervous system in the modulation of immune system is gaining even more attention in both pathophysiological contexts. For these reasons, during the last decades, researches focused their efforts on the comprehension of the molecular mechanisms connecting immune system to cardiovascular and metabolic diseases. On the other hand, it has been reported that in these pathological conditions, central neural pathways modulate the activity of the peripheral nervous system, which is strongly involved in onset and progression of the disease. It is interesting to notice that neural reflex can also participate in the modulation of immune functions. In this scenario, the spleen becomes the crucial hub allowing the interaction of different systems differently involved in metabolic and cardiovascular diseases. Here, we summarize the major findings that dissect the role of the immune system in disorders related to metabolic and cardiovascular dysfunctions, and how this could also be influenced by neural reflexes

An Integrated Analysis of the Physiological Effects of Space Flight: Executive Summary

A large array of models were applied in a unified manner to solve problems in space flight physiology. Mathematical simulation was used as an alternative way of looking at physiological systems and maximizing the yield from previous space flight experiments. A medical data analysis system was created which consist of an automated data base, a computerized biostatistical and data analysis system, and a set of simulation models of physiological systems. Five basic models were employed: (1) a pulsatile cardiovascular model; (2) a respiratory model; (3) a thermoregulatory model; (4) a circulatory, fluid, and electrolyte balance model; and (5) an erythropoiesis regulatory model. Algorithms were provided to perform routine statistical tests, multivariate analysis, nonlinear regression analysis, and autocorrelation analysis. Special purpose programs were prepared for rank correlation, factor analysis, and the integration of the metabolic balance data

The key role of nitric oxide in hypoxia: hypoxic vasodilation and energy supply-demand matching

Significance: a mismatch between energy supply and demand induces tissue hypoxia with the potential to cause cell death and organ failure. Whenever arterial oxygen concentration is reduced, increases in blood flow - 'hypoxic vasodilation' - occur in an attempt to restore oxygen supply. Nitric oxide is a major signalling and effector molecule mediating the body's response to hypoxia, given its unique characteristics of vasodilation (improving blood flow and oxygen supply) and modulation of energetic metabolism (reducing oxygen consumption and promoting utilization of alternative pathways). Recent advances: this review covers the role of oxygen in metabolism and responses to hypoxia, the hemodynamic and metabolic effects of nitric oxide, and mechanisms underlying the involvement of nitric oxide in hypoxic vasodilation. Recent insights into nitric oxide metabolism will be discussed, including the role for dietary intake of nitrate, endogenous nitrite reductases, and release of nitric oxide from storage pools. The processes through which nitric oxide levels are elevated during hypoxia are presented, namely (i) increased synthesis from nitric oxide synthases, increased reduction of nitrite to nitric oxide by heme- or pterin-based enzymes and increased release from nitric oxide stores, and (ii) reduced deactivation by mitochondrial cytochrome c oxidase. Critical issues: several reviews covered modulation of energetic metabolism by nitric oxide, while here we highlight the crucial role NO plays in achieving cardiocirculatory homeostasis during acute hypoxia through both vasodilation and metabolic suppression Future directions: we identify a key position for nitric oxide in the body's adaptation to an acute energy supply-demand mismatc

Arterial hypertension prevention as an actual medical and social problem

Social changes, technological re-equipment, intensive formation of urban infrastructure have led to a constant increase in stress factors and an excessive growth of the nervous and psychological population burden. As a result of these processes in economically developed countries, acute diseases are becoming less and less significant, unlike the group of chronic disorders, such as arterial hypertension. Data from the review of the literature and the data we have received indicate that there is an increase in the level of cortisol in the blood in the phase of anxiety, which reduces in the resistance phase. A significant role is played by another hormone - insulin, which plays a key role in the development of the general adaptive syndrome. Through it the body implements numerous counter-defects in relation to the regulatory influence of catecholamines and cortisol. In conditions of prolonged stress, the level of insulin in the blood decreases and diabetes develops. The effect of cortisol and catecholamines in the resistance phase persists. The level of oxidative modification of blood plasma proteins indices depends on the behavior of the individual and changes in his psycho-emotional state, while a prolonged increase in the levels of catecholamines and cortisol in peripheral blood causes the development of psychosomatic pathology. It is proved that under the influence of complex action of risk factors there are significant changes in the psycho-emotional state that cause hypertension. This is confirmed by the presence of the highest level of reactive anxiety in patients with hypertension of the 1st stage on the background of the lowest personal anxiety which is the basis for the occurrence of the disease. With the progression of hypertension there are more profound changes in the personality of the patient, which is accompanied by the accumulation of personal anxiety, which can lead to a depressive state of neurotic genesis, which we observed with its complication. On the basis of a comprehensive study, the effect of stress on the occurrence of a syndrome of psychoemotional stress is shown, which leads to a steady increase in blood pressure - hypertension, and with its subsequent action complicates its course

Aerospace Medicine and Biology: A continuing bibliography with indexes, supplement 165, March 1977

This bibliography lists 198 reports, articles, and other documents introduced into the NASA scientific and technical information system in February 1977

Are Large Physiological Reactions to Acute Psychological Stress Always Bad for Health?

How we react physiologically to stress has long been considered to have implications for our health. There is now persuasive evidence that individuals who show large cardiovascular reactions to stress are at increased risk of developing cardiovascular disease, particularly hypertension. By implication, low reactivity is protective or benign. However, there is recent evidence that low reactivity may predict elevated risk for a range of adverse health outcomes, such as depression, obesity, poor self-reported health, and compromised immunity. In addition, low cortisol and cardiovascular reactivity may be a characteristic of individuals with addictions to tobacco and alcohol, as well as those at risk of addiction and those who relapse from abstinence. Our ideas about reactivity may have to be revised in the light of such findings