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1

Sparks, H. V. "Learning the regulation of peripheral blood flow." Advances in Physiology Education 277, no. 6 (December 1999): S164. http://dx.doi.org/10.1152/advances.1999.277.6.s164.

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Анотація:
Students can learn a great deal about the peripheral circulation when teaching is based on five building blocks: hemodynamic principles, neurohumoral control, and three elements of local control of blood flow (metabolic, myogenic, and paracrine). Study of a particular special circulation starts with the application of these building blocks in the context of the function of that tissue. For example, control of skin blood flow is largely concerned with regulation of body temperature (neurohumoral control) and the response to injury (paracrine control). Regulation of coronary blood flow is almost entirely a matter of meeting the metabolic needs of the myocardium (metabolic control). By mixing and matching the five building blocks and keeping in mind the special functions of a particular tissue, students can master the peripheral circulation efficiently.
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2

Al-Shammari Mohammed Jasim Ismael, Hayder Yousif Falih, and Sagalaeva Irina Vladimirovna. "Hemodynamic criteria of the circulatory system in ethnic groups of students with different types of autonomic regulation of the heart rate." journal of the college of basic education 25, no. 104 (September 25, 2019): 312–20. http://dx.doi.org/10.35950/cbej.v25i104.4651.

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Under physiological conditions, the first years of university studies of the students of Arabic and African subgroups with moderate parasympathetic autonomous regulation) MPAR( and self-regulation )SR( were characterized by toughness, low effectiveness of the system of blood circulation, increased peripheral vascular resistance, vascular type of self-regulation of blood circulation )TSC (; Indian and Latino-American subgroups with MPAR SR revealed the weakness and low efficiency of the circulatory system, the optimal general peripheral blood circulation )GPBC( and cardiovascular type of self-regulation of blood circulation )TSC( were revealed in Indian and Latino-American subgroups with moderate parasympathetic autonomous regulation self-regulation )MPAR SR (and subgroups with prounonced parasympathetic autonomous regulation self-regulation)PPAR SR( showed high endurance of the circulatory system. The Russian subgroup with moderate parasympathetic autonomous regulation self-regulation) MPAR SR (has the highest endurance of the circulatory system and current functional fatigue, the most marked in the subgroup with prounonced parasympathetic autonomous regulation )PPAR (increased general peripheral blood circulation and cardiovascular type of self-regulation of blood circulation.
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3

Upchurch, Gilbert R. "Nitric oxide and the regulation of the peripheral circulation." Journal of Vascular Surgery 34, no. 2 (August 2001): 379. http://dx.doi.org/10.1067/mva.2001.115818.

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4

&NA;. "NITRIC OXIDE AND THE REGULATION OF THE PERIPHERAL CIRCULATION." Shock 14, no. 2 (August 2000): 246. http://dx.doi.org/10.1097/00024382-200014020-00031.

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5

Slavnoe, N. V., V. V. Markov, N. A. Kovpan, V. M. Rudichenko, and G. N. Terekhova. "Peripheral circulation regulation in patients with the hypothalamic syndrome neuroendocrine metabolic form." Problems of Endocrinology 39, no. 6 (December 15, 1993): 17–20. http://dx.doi.org/10.14341/probl11928.

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Peripheral circulation and regulating hormonal (renin- angiotensin-aldosterone system) and electrolytic (plasma sodium and potassium) factors were studied in 102 patients with the hypothalamic syndrome neuroendocrine metabolic form administered pathogenetic therapy with antiserotonin and dopaminergic drugs as well as routine therapy. Blood plasma sodium vasopressin and aldosterone levels were found increased, arterial vessel reactivity in the forearm reduced, and venous circulation disordered in these patients. Routine therapy failed to normalize electrolytes and hormonal parameters and was conducive to a still more marked reduction of arterial vessel reactivity. Peritol therapy resulted in a reduction of vasopressin concentration and normalization of blood plasma sodium and aldosterone, as well as in improvement of the myogenic mechanisms of vascular tone regulation and normalization of venous circulation parameters. A course of parlodel therapy lead to normalization of blood plasma levels of vasopressin, aldosterone, and sodium but no changes in the regional vessels were observed.
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6

Manasyan, S. G., S. Yu Ermolov, A. G. Apresyan, and A. V. Arutyunyan. "Modified methods of polygepatography and peripheral arterial tonometry in the assessment of peripheral circulation regulation." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 27, no. 6 (March 18, 2022): 683–95. http://dx.doi.org/10.18705/1607-419x-2021-27-6-683-695.

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Objective. The purpose of the work was to assess the application of modified ways of polyhepatography (PHG) and peripheral arterial tonometry (PAT) in the evaluation of regulation of peripheral circulation (capillary blood flow).Design and methods. We included 150 people, divided into four groups. The first group (n = 40) includes patients with stage II hypertension, moderate and high risk of cardiovascular complications. The second group (n = 40) includes patients with stable forms of coronary heart disease in combination with hypertension. The third group (n = 40) includes patients with chronic liver diseases. The fourth group (n = 30) consisted of subjects without anamnestic and objective data of pathology. All subjects underwent a comprehensive clinical and laboratory examination, an assessment of intrahepatic hemodynamics by the PGG method, an assessment of the endothelial function by the PAT method. A modified method of PAT was used to evaluate the central reaction of the peripheral blood flow regulation system (endothelium-independent vasodilation).Results. Endothelial dysfunction was found in patients with cardiovascular pathology and in patients with chronic liver diseases. A modified method of PAT showed a multidirectional reaction of peripheral blood flow to the test with local ischemia. A number of features were identified in the study groups when assessing disorders of intrahepatic microcirculation. Patients of group I had multidirectional disorders of arteriovenous inflow (45% cases, confidence interval (CI) from 27 % to 63 %) and outflow (37,5 %, CI from 22 % to 56 %) in the liver, while in patients of group II and group III, disorders of arteriovenous inflow were more common, 85 % (CI from 70 % to 95%) and 90% (82 % to 94%), respectively. Rheographic signs of bile passage disorders were more common in groups II and III. A significant negative relationship was established between endothelial dysfunction and the severity of intrahepatic microcirculation disorders (r = –0,35, p < 0,001).Conclusions. Modified methods of peripheral arterial tone and PHG enable assessment of local and central mechanisms of blood flow regulation at the microvascular level in patients with hypertension, coronary heart disease and chronic liver diseases. The relationship between impaired endothelial function and intrahepatic microcirculation allows us to consider the liver as a target organ in cardiovascular pathology.
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7

Andersson, Rune, and Per Bjerle. "Peripheral Circulation, Particularly Heat Regulation Reactions, in Patients with Amyloidosis and Polyneuropathy." Acta Medica Scandinavica 199, no. 1-6 (April 24, 2009): 191–96. http://dx.doi.org/10.1111/j.0954-6820.1976.tb06715.x.

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8

Zadorozhnia, V., O. Kuchkovsky, and O. Kovaleva. "Vegetative status and adaptation peculiarities possibilities in student youth depending on blood circulation self-regulation type." Visnyk of Lviv University. Biological series, no. 83 (December 25, 2020): 83–97. http://dx.doi.org/10.30970/vlubs.2020.83.10.

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Vegetative status and adaptive capabilities peculiarities of aged 19 to 21 girls depending on their blood circulation self-regulation type were studied in this work. The study was conducted at the Biology Faculty of Zaporizhzhia National University, Zaporizhzhia. Such primary indices as heart rate and blood pressure were studied in all test individuals. Based on the obtained data, the blood circulation self-regulation type in each subject was determined separately, which allowed to form three groups (individuals with cardiovascular, vascular and mixed blood circulation self-regulation types). The assessment scheme included cardiovascular system indices calculation such as average dynamic arterial pressure, specific peripheral resistance, cardiac output, cardiac index, stroke volume, external myocardial function, myocardial stress index, myocardial efficiency criterion, autonomic regulation index (vegetative Kerdo’s index) and adaptive potential. The results were processed by variation statistics methods, and the obtained data were subjected to correlation analysis. Deviations from the reference values were revealed in systemic hemodynamics ave­rage group parameters analysis in female students with different blood circulation regulation types. It was recorded that the average dynamic pressure exceeded the normal upper limit by 2.5 % and 6.2 %, respectively, in persons with mixed and vascular regulation type. Specific peripheral resistance indices obtained from data analysis in girls with different blood circulation self-regulation types revealed that this index did not exceed the normal in the groups with mixed and vascular type, in contrast to the group with the cardiac type. The specific peripheral resistance was lower by 5.2 % than the lower limit of the reference value for this index in the latter group. Statistically significant differences were identified in cardiac output, cardiac index and stroke volume parameters in girls with different self-regulation circulatory types. Specific trends were identified in the average group and individual myocardial function indices in girls depending on the self-regulation type. Statistical significance was found between myocardial stress indices in girls with different self-regulation types. Both the average group and individual vegetative Kerdo’s index indices fluctuated within eytony in the mixed type persons group. The mean group autonomic index values in girls with vascular type indicated pronounced vagotonia. We found that the largest percentage of all respondents had satisfactory adaptation. The largest number of girls with satisfactory adaptation had a vascular self-regulation type (83.33 %) and a mixed type (81.82 %), a smaller percentage of girls from these groups (16.68 % and 18.18 %, respectively) had adaptation mechanisms functional stress. In the group with the cardiac type, almost half (46.15 %) had adaptation mechanisms functional stress, and the rest (53.85 %) had satisfactory adaptation. Thus, the differences in cardiovascular system indices, the autonomic nervous system sympathetic and parasympathetic parts influences ratio on the cardiovascular system were determined, as well as the adaptive potential in 19-21 years old girls can be attributed to blood circulation compensatory-adaptive reactions.
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9

Sheriff, D. D. "PASSIVE REGULATION OF CARDIAC OUTPUT BY THE ELASTIC CHARACTERISTICS OF THE PERIPHERAL CIRCULATION." Medicine & Science in Sports & Exercise 30, Supplement (May 1998): 217. http://dx.doi.org/10.1097/00005768-199805001-01240.

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10

Thomas, Gail D. "Neural control of the circulation." Advances in Physiology Education 35, no. 1 (March 2011): 28–32. http://dx.doi.org/10.1152/advan.00114.2010.

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The purpose of this brief review is to highlight key concepts about the neural control of the circulation that graduate and medical students should be expected to incorporate into their general knowledge of human physiology. The focus is largely on the sympathetic nerves, which have a dominant role in cardiovascular control due to their effects to increase cardiac rate and contractility, cause constriction of arteries and veins, cause release of adrenal catecholamines, and activate the renin-angiotensin-aldosterone system. These effects, as well as the control of sympathetic outflow by the vasomotor center in the medulla and the importance of sensory feedback in the form of peripheral reflexes, especially the baroreflexes, are discussed in the context of cardiovascular regulation.
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11

Cianci, T., G. Zoccoli, P. Lenzi, and C. Franzini. "Loss of integrative control of peripheral circulation during desynchronized sleep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 2 (August 1, 1991): R373—R377. http://dx.doi.org/10.1152/ajpregu.1991.261.2.r373.

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Regional blood flow (BF) changes during sleep were measured in rabbits at low, neutral, and high ambient temperatures (Ta) with radioactive microspheres. At both low and high Ta, peripheral vasomotor changes at the onset of desynchronized sleep (DS) were incompatible with thermoregulatory homeostasis. At low Ta, BF decreased in muscle (with the disappearance of shivering), whereas it increased in the arteriovenous anastomoses (AVA) and in the splanchnic bed. At high Ta, BF decreased in muscle (with the disappearance of panting) and in the AVA, whereas it increased in the splanchnic bed. An impaired central nervous regulation underlies the disruption of peripheral circulation patterns in this sleep stage. The lack of adaptive vasomotor adjustments in DS, which has little consequence in normal conditions, may become relevant in cardiovascular pathophysiology when BF redistribution through increased neurogenic vasomotor activity becomes a major compensating mechanism.
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12

Sabiryanov, A., E. Sabiryanova, S. Sashenkov, and I. Izarovskaia. "MECHANISMS OF THE EFFECT OF TRADITIONAL MASSAGE ON CENTRAL AND PERIPHERAL CIRCULATION IN ADOLESCENT FEMALES INVOLVED IN RUNNING SPORTS." Human Sport Medicine 20, no. 3 (November 25, 2020): 64–69. http://dx.doi.org/10.14529/hsm200307.

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Aim. The paper aims to analyze the effect of traditional massage on functional recovery of the cardiovascular system in adolescent females involved in running sports. Materials and methods. A 10-day traditional back and neck massage program was used as a recovery technique. The indicators of the central and peripheral circulation, the time and frequency characteristics of the heart rate, as well as finger pulse amplitude were obtained before and after the program. Results. After traditional massage, adolescent females involved in running sports demonstrate a decrease in heart rate, which is associated with a decrease in sympathoadrenal regulation of chronotropic heart function (a decrease in VLF, a decrease in the amplitude of dominant VLF and LF harmonics). Regression and canonical analysis shows that heart rate dependence of the activity of regulation levels changes. There is an increase in peripheral blood circulation and a decrease in blood pressure associated with both humoral and metabolic factors and a decrease in sympathoadrenal influences, which is confirmed by an analysis of pulse amplitude variability. It is shown that the dynamics of the time and frequency characteristics of VLF range is a marker of physiological changes in blood circulation after massage therapy. Conclusion. The effect of traditional massage on the blood circulation of adolescent females involved in running sports is associated with adaptation to massage effects and is manifested by changes in the neurohumoral regulation of hemodynamics.
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13

Cowley, AWJ, C. Hinojosa-Laborde, BJ Barber, DR Harder, JH Lombard, and AS Greene. "Short-Term Autoregulation of Systemic Blood Flow and Cardiac Output." Physiology 4, no. 6 (December 1, 1989): 219–25. http://dx.doi.org/10.1152/physiologyonline.1989.4.6.219.

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The contribution of local autoregulatory mechanisms to the overall control of the systemic circulation has been analyzed using theoretical and experimental approaches. Mechanisms that regulate regional vascular resistance and contribute importantly to the overall moment-to-moment regulation of cardiac output and total peripheral resistance are reviewed.
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14

Mattos, João D., Monique O. Campos, Marcos P. Rocha, Daniel E. Mansur, Helena N. M. Rocha, Vinicius P. Garcia, Natalia G. Rocha, et al. "Differential vasomotor responses to isocapnic hyperoxia: cerebral versus peripheral circulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 1 (January 1, 2020): R182—R187. http://dx.doi.org/10.1152/ajpregu.00248.2019.

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Isocapnic hyperoxia (IH) evokes cerebral and peripheral hypoperfusion via both disturbance of redox homeostasis and reduction in nitric oxide (NO) bioavailability. However, it is not clear whether the magnitude of the vasomotor responses depends on the vessel network exposed to IH. To test the hypothesis that the magnitude of IH-induced reduction in peripheral blood flow (BF) may differ from the hypoperfusion response observed in the cerebral vascular network under oxygen-enriched conditions, nine healthy men (25 ± 3 yr, mean ± SD) underwent 10 min of IH during either saline or vitamin C (3 g) infusion, separately. Femoral artery (FA), internal carotid artery (ICA), and vertebral artery (VA) BF (Doppler ultrasound), as well as arterial oxidant (8-isoprostane), antioxidant [ascorbic acid (AA)], and NO bioavailability (nitrite) markers were simultaneously measured. IH increased 8-isoprostane levels and reduced nitrite levels; these responses were followed by a reduction in both FA BF and ICA BF, whereas VA BF did not change. Absolute and relative reductions in FA BF were greater than IH-induced changes in ICA and VA perfusion. Vitamin C infusion increased arterial AA levels and abolished the IH-induced increase in 8-isoprostane levels and reduction in nitrite levels. Whereas ICA and VA BF did not change during the vitamin C-IH trial, FA perfusion increased and reached similar levels to those observed during normoxia with saline infusion. Therefore, the magnitude of IH-induced reduction in femoral blood flow is greater than that observed in the vessel network of the brain, which might involve the determinant contribution that NO has in the regulation of peripheral vascular perfusion.
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15

Shumilova, T. E., V. I. Shereshkov, and A. D. Nozdrachev. "Regulation of peripheral and systemic blood circulation in rats in conditions of acute nitrite hypoxia." Biology Bulletin 39, no. 6 (November 2012): 547–55. http://dx.doi.org/10.1134/s106235901206012x.

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16

Sheriff, Don D., and Jennifer R. Mendoza. "Passive Regulation of Cardiac Output During Exercise by the Elastic Characteristics of the Peripheral Circulation." Exercise and Sport Sciences Reviews 32, no. 1 (January 2004): 31–35. http://dx.doi.org/10.1097/00003677-200401000-00007.

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17

Onizuka, Masataka, Shigemi Ishikawa, Osamu Ishibashi, Michiharu Suga, Kiyofumi Mitsui, and Toshio Mitsui. "Suppression of prostanoid formation and regulation of peripheral circulation after surgery using thrombin inhibitor (MD805)." Surgery Today 28, no. 6 (June 1998): 618–25. http://dx.doi.org/10.1007/s005950050194.

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18

Goralski, Kerry B., Dalya Abdulla, Christopher J. Sinal, Andre Arsenault, and Kenneth W. Renton. "Toll-like receptor-4 regulation of hepaticCyp3a11metabolism in a mouse model of LPS-induced CNS inflammation." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 3 (September 2005): G434—G443. http://dx.doi.org/10.1152/ajpgi.00562.2004.

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Central nervous system (CNS) infection and inflammation severely reduce the capacity of cytochrome P-450 metabolism in the liver. We developed a mouse model to examine the effects of CNS inflammation on hepatic cytochrome P-450 metabolism. FVB, C57BL/6, and C3H/HeouJ mice were given Escherichia coli LPS (2.5 μg) by intracerebroventricular (ICV) injection. The CNS inflammatory response was confirmed by the elevation of TNF-α and/or IL-1β proteins in the brain. In all mouse strains, LPS produced a 60–70% loss in hepatic Cyp3a11 expression and activity compared with saline-injected controls. Adrenalectomy did not prevent the loss in Cyp3a11 expression or activity, thereby precluding the involvement of the hypothalamic-adrenal-pituitary axis. Endotoxin was detectable (1–10 ng/ml) in serum between 15 and 120 min after ICV dosing of 2.5 μg LPS. Peripheral administration of 2.5 μg LPS by intraperitoneal injection produced similar serum endotoxin levels and a similar loss (60%) in Cyp3a11 expression and activity in the liver. The loss of Cyp3a11 in response to centrally or peripherally administered LPS could not be evoked in Toll-like receptor-4 (TLR4)-mutant (C3H/HeJ) mice, indicating that TLR4 signaling pathways are directly involved in the enzyme loss. In summary, we conclude that LPS is transferred from the brain to the circulation in significant quantities in a model of CNS infection or inflammation. Subsequently, LPS that has reached the circulation stimulates a TLR4-dependent mechanism in the periphery, evoking a reduction in Cyp3a11 expression and metabolism in the liver.
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19

Hoggard, N., L. Hunter, JS Duncan, and DV Rayner. "Regulation of adipose tissue leptin secretion by alpha-melanocyte-stimulating hormone and agouti-related protein: further evidence of an interaction between leptin and the melanocortin signalling system." Journal of Molecular Endocrinology 32, no. 1 (February 1, 2004): 145–53. http://dx.doi.org/10.1677/jme.0.0320145.

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The central role of the melanocortin system in the regulation of energy balance has been studied in great detail. However, the functions of circulating melanocortins and the roles of their peripheral receptors remain to be elucidated. There is increasing evidence of a peripheral action of melanocortins in the regulation of leptin production by adipocytes. Here we investigate the interaction of alpha-melanocyte stimulating hormone (alpha-MSH) and agouti-related protein (AgRP) in the regulation of leptin secretion from cultured rat adipocytes and examine the changes in circulating alpha-MSH and AgRP in lean and obese rodents after hormonal and energetic challenge. Leptin secretion (measured by ELISA) and gene expression (by real-time quantitative PCR) of differentiated rat adipocytes cultured in vitro were inhibited by the administration of alpha-MSH (EC50=0.24 nM), and this effect was antagonised by antagonists of the melanocortin receptors MC4R and MC3R (AgRP and SHU9119). The presence of MC4R in rat adipocytes (RT-PCR and restriction digest) supports the involvement of this receptor subtype in this interaction. Leptin administered to ob/ob mice in turn increases the release of alpha-MSH into the circulation, suggesting a possible feedback loop between the site of alpha-MSH release and the release of leptin from the adipose tissue. However, the physiological significance of this putative feedback probably depends upon the underlying state of energy balance, since in the fasting state low plasma alpha-MSH is paralleled by low plasma leptin.
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20

Ebert, T. J., B. J. Morgan, J. A. Barney, T. Denahan, and J. J. Smith. "Effects of aging on baroreflex regulation of sympathetic activity in humans." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 3 (September 1, 1992): H798—H803. http://dx.doi.org/10.1152/ajpheart.1992.263.3.h798.

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Arterial baroreflexes contribute importantly to blood pressure regulation through their influence on parasympathetic outflow to the sinus node and sympathetic outflow to the peripheral circulation. Baroreflex control of heart rate is known to be diminished in older individuals. Whether advancing age is associated with a parallel attenuation in baroreflex control of sympathetic outflow to the peripheral circulation has not been studied in humans. To provide such information, we made direct measurements of muscle sympathetic nerve activity (MSNA) in healthy males who ranged in age from 18 to 71 yr. The subjects were arbitrarily divided into three groups: younger (18–34 yr; n = 35), middle aged (35–50 yr; n = 15), and older (51–71 yr; n = 16). Although basal levels of MSNA were higher in older subjects than in younger and middle-aged subjects, the gains of baroreflex control of MSNA were the same in the older, middle-aged, and younger subjects (-4.6 +/- 0.6, -4.8 +/- 0.9, -5.1 +/- 0.5 U/mmHg, P greater than 0.10). In contrast, the gains of baroreflex control of cardiac intervals were attenuated in the older and middle-aged subjects compared with the younger subjects (9.8 +/- 1.2, 13.6 +/- 1.4, 21.7 +/- 1.3 ms/mmHg, P less than 0.05). Our data indicate that although the parasympathetic component of the arterial baroreflex becomes impaired with advancing age, the sympathetic component can be well maintained in healthy individuals even into the seventh decade.
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21

Skinner, Donal C., Neil P. Evans, and BenoÎt Malpaux. "Does a Short Loop Feedback Mechanism for the Control of Luteinizing Hormone Secretion Exist in the Ewe?*." Endocrinology 138, no. 10 (October 1, 1997): 4220–26. http://dx.doi.org/10.1210/endo.138.10.5437.

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Abstract It is not known whether a short loop feedback mechanism for the regulation of LH exists in sheep. This study on ovariectomized ewes investigated whether a bolus injection (10, 1, and 0.1 μg LH or 1μ g BSA; n = 4) or a 3-h continuous infusion of exogenous LH (100 or 1 ng/min; n = 7) into the third ventricle through a permanent indwelling cannula could influence the activity of the GnRH pulse generator, as determined by measurement of endogenous LH secretion. To assess the potential for involvement in a LH short loop feedback system and to estimate the level of LH in the hypothalamic milieu, the concentrations of LH in the peripheral circulation, portal circulation, and third ventricle were measured during an estradiol-induced preovulatory LH surge (n = 4). Neither the bolus nor continuous administration of LH into the third ventricle had any effect on the mean interpulse interval, nadir, pulse amplitude, or circulating level of systemic LH. Furthermore, despite portal LH concentrations being more than 20-fold higher than jugular LH concentrations, LH levels in third ventricular cerebrospinal fluid remained barely detectable and did not reflect dynamic secretory events in the peripheral or hypothalamo-hypophyseal portal blood. These data demonstrate that in ewes, little pituitary LH reaches the third ventricle, and the small amount that does is unable to affect peripheral gonadotropin release. Our study suggests, therefore, that a short loop feedback system for LH does not exist in the ewe.
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22

Potts, J. T., T. Hatanaka, and A. A. Shoukas. "Effect of arterial compliance on carotid sinus baroreceptor reflex control of the circulation." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 3 (March 1, 1996): H988—H1000. http://dx.doi.org/10.1152/ajpheart.1996.270.3.h988.

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Capacitive properties of the arterial and venous segments of the peripheral circulation are important in the regulation of cardiac output and arterial blood pressure. We examined whether an acute increase in arterial compliance C(a) would alter carotid sinus baroreflex control of the circulation. Eight mongrel dogs were anesthetized with pentobarbital sodium, and the carotid sinus regions were isolated and perfused with nonpulsatile pressures. Open-loop baroreflex response curves for systemic arterial pressure (SAP), heart rate (HR), aortic blood flow (ABF), peripheral vascular resistance (PVR), and left ventricular (LV) contractility were obtained when carotid sinus pressure (CSP) was changed in 25-mmHg steps between 50 and 200 mmHg under a control condition and when C(a) was increased by including two hydraulic compliant chambers to the arterial circulation (CS 1.72 ml/mmHg and CL 5.05 ml/mmHg). The compliant chambers significantly increased C(a) and altered the ratio of arterial to venous compliance C(a)/Cv). Changes in C(a)/Cv significantly decreased the maximal open-loop baroreflex gain (Gmax) for SAP (-2.3 +/- 0.5, -1.6 +/- 0.3, and -1.1 +/- 0.2 mmHg/mmHg, control vs. CS vs. CL, P < 0.05). Gmax for ABF was decreased by CS (-0.9 +/- 0.2 vs. -0.3 +/- 0.1 ml.kg-1.min-1, control vs. CS, P < 0.05), and CL reversed the reflex changes in ABF (Gmax: +0.6 +/- 0.3 ml.kg-1.min-1). Gmax for HR, PVR, and LV contractility was not altered when C(a) was increased (P > 0.05). These findings indicate that an increase in C(a) changes C(a)/Cv and alters carotid baroreflex control of SAP by modifying the ABF response. We conclude that a change in C(a)/Cv affects the reflex control of the circulation by altering the distribution of blood volume between the arterial and venous circulations.
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23

Manasyan, A. G., A. L. Dobkes, S. G. Manasyan, S. U. Ermolov, S. V. Serdyukov, S. A. Boldueva, A. S. Lipunova, T. V. Ermolova, O. V. Zaxarova, and D. N. Nikitin. "STUDY THE REGULATION OF PERIPHERAL BLOOD FLOW IN PATIENTSWITH CARDIOVASCULAR DISORDERS." HERALD of North-Western State Medical University named after I.I. Mechnikov 7, no. 2 (June 15, 2015): 52–62. http://dx.doi.org/10.17816/mechnikov20157252-62.

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A new approach to evaluating of the state of cardiovascular system for patients with verified diagnosis of coronary heart disease (CHd), cardiac syndrome X (COAG) and hypertension (GB) by modification of known techniques of the PAT (peripheral arterial tonometry) is represented in the article. The results of studies by the method of us PAT patients with various cardiovascular disease indicate a particular clinical significance is not only the assessment of local «endothelial dysfunction» (the known value of reactive hyperemia index RHI), but also assess the nature of the Central system response regulation of blood circulation. In the article it is shown that more convenient for this relatively simpleCtrlmeasure R(relative change in the amplitude of pulsations in case of occlusion of the blood supplyto the sample identified on the hand are not subjected to occlusion). For patients without evidenceCtrlof cardiovascular disease the index value Rwas close to unity. The hypertensive patients, as a rule,observed values of R<1, and in CHd patients, in contrast, R>1. The differences associated, pre-CtrlCtrlsumably, with the changing balance between the degree of disturbance of peripheral blood circulationand degree of preservation of the reserves of the pumping function of the heart. This allows to consider the index RCtrl as an additional feature, an essential for individual selection of therapy in patients with cardiovascular pathology.
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24

Passino, Claudio, Luciano Bernardi, Giammario Spadacini, Alessandro Calciati, Robert Robergs, Inder Anand, Richard Greene, Emilia Martignoni, and Otto Appenzeller. "Autonomic Regulation of Heart Rate and Peripheral Circulation: Comparison of High Altitude and Sea Level Residents." Clinical Science 91, s1 (December 1, 1996): 81–83. http://dx.doi.org/10.1042/cs0910081supp.

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25

Wecht, Jill M., Noam Y. Harel, James Guest, Steven C. Kirshblum, Gail F. Forrest, Ona Bloom, Alexander V. Ovechkin, and Susan Harkema. "Cardiovascular Autonomic Dysfunction in Spinal Cord Injury: Epidemiology, Diagnosis, and Management." Seminars in Neurology 40, no. 05 (September 9, 2020): 550–59. http://dx.doi.org/10.1055/s-0040-1713885.

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AbstractSpinal cord injury (SCI) disrupts autonomic circuits and impairs synchronistic functioning of the autonomic nervous system, leading to inadequate cardiovascular regulation. Individuals with SCI, particularly at or above the sixth thoracic vertebral level (T6), often have impaired regulation of sympathetic vasoconstriction of the peripheral vasculature and the splanchnic circulation, and diminished control of heart rate and cardiac output. In addition, impaired descending sympathetic control results in changes in circulating levels of plasma catecholamines, which can have a profound effect on cardiovascular function. Although individuals with lesions below T6 often have normal resting blood pressures, there is evidence of increases in resting heart rate and inadequate cardiovascular response to autonomic provocations such as the head-up tilt and cold face tests. This manuscript reviews the prevalence of cardiovascular disorders given the level, duration and severity of SCI, the clinical presentation, diagnostic workup, short- and long-term consequences, and empirical evidence supporting management strategies to treat cardiovascular dysfunction following a SCI.
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26

Nikishina, Yu O., A. Ya Sapronova, and M. V. Ugrumov. "The Effect of Dopamine Secreted by the Brain into the Systemic Circulation on Prolactin Synthesis by the Pituitary gland in Ontogenesis." Acta Naturae 8, no. 3 (September 15, 2016): 111–17. http://dx.doi.org/10.32607/20758251-2016-8-3-111-117.

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This research was aimed at studying the brains endocrine function in ontogenesis. It has been previously shown in our laboratory that the brain serves as the source of dopamine in the systemic circulation of rats prior to the formation of the blood-brain barrier. This paper provides direct evidence that dopamine secreted by the brain directly into the systemic circulation in this period of ontogenesis has an inhibitory effect on prolactin secretion by pituitary cells. These results provide the basis for a fundamentally new understanding of the brains role in the neuroendocrine regulation of the development and function of peripheral target organs and, particularly in this study, the pituitary gland.
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27

Fang, Jennifer S., and Karen K. Hirschi. "Molecular regulation of arteriovenous endothelial cell specification." F1000Research 8 (July 29, 2019): 1208. http://dx.doi.org/10.12688/f1000research.16701.1.

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Анотація:
The systemic circulation depends upon a highly organized, hierarchal blood vascular network that requires the successful specification of arterial and venous endothelial cells during development. This process is driven by a cascade of signaling events (including Hedgehog, vascular endothelial growth factor (VEGF), Notch, connexin (Cx), transforming growth factor-beta (TGF- β), and COUP transcription factor 2 (COUP-TFII)) to influence endothelial cell cycle status and expression of arterial or venous genes and is further regulated by hemodynamic flow. Failure of endothelial cells to properly undergo arteriovenous specification may contribute to vascular malformation and dysfunction, such as in hereditary hemorrhagic telangiectasia (HHT) and capillary malformation-arteriovenous malformation (CM-AVM) where abnormal vessel structures, such as large shunts lacking clear arteriovenous identity and function, form and compromise peripheral blood flow. This review provides an overview of recent findings in the field of arteriovenous specification and highlights key regulators of this process.
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28

Weinmann, Pamela, Karin Scharffetter-Kochanek, S. Bradley Forlow, Thorsten Peters, and Barbara Walzog. "A role for apoptosis in the control of neutrophil homeostasis in the circulation: insights from CD18-deficient mice." Blood 101, no. 2 (January 15, 2003): 739–46. http://dx.doi.org/10.1182/blood-2002-01-0239.

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The control of neutrophil turnover in the circulation is a key event in homeostasis and inflammation. Using CD18- deficient (CD18−/−) mice that show a 19-fold increase of blood neutrophil counts when compared with wild-type animals (CD18+/+), we found that apoptosis of peripheral neutrophils was significantly reduced from 27.4% in the wild-type to 4.8% inCD18−/− mice within 4 hours after isolation as measured by analysis of DNA content. This was confirmed by detecting CD16 expression, nuclear morphology, and internucleosomal DNA degradation. In contrast, no difference in apoptosis was observed in neutrophils derived from the bone marrow. Neutrophilia and delayed neutrophil apoptosis were also present inCD18−/−/interleukin 6 (IL-6−/−) double knockout mice. Moreover, plasma ofCD18−/− mice was not able to delay apoptosis of CD18+/+neutrophils and plasma ofCD18+/+ mice did not augment apoptosis of CD18−/−neutrophils. However,CD18−/− neutrophils revealed an up-regulation of the antiapoptotic gene bcl-Xl and a down-regulation of the proapoptotic gene bax-α compared withCD18+/+ neutrophils suggesting that this delayed apoptosis. Accordingly, down-regulation of Bax-α using antisense technique delayed apoptosis and prolonged neutrophil survival. The replacement of the hematopoietic system of CD18+/+ mice by a 1:1 mixture of CD18+/+ andCD18−/− hematopoietic cells abolished the delay of apoptosis in peripheralCD18−/− neutrophils and prevented neutrophilia. Altogether, this suggests that a delay of neutrophil apoptosis inCD18−/− mice causes an alteration of neutrophil homeostasis, which may induce the massive increase of peripheral neutrophil counts. Thus, apoptosis seems to be critically involved in the control of neutrophil turnover in the circulation.
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29

Gibson, Douglas A., Ioannis Simitsidellis, and Philippa T. K. Saunders. "Regulation of androgen action during establishment of pregnancy." Journal of Molecular Endocrinology 57, no. 1 (July 2016): R35—R47. http://dx.doi.org/10.1530/jme-16-0027.

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During the establishment of pregnancy, the ovarian-derived hormones progesterone and oestradiol regulate remodelling of the endometrium to promote an environment that is able to support and maintain a successful pregnancy. Decidualisation is characterised by differentiation of endometrial stromal cells that secrete growth factors and cytokines that regulate vascular remodelling and immune cell influx. This differentiation process is critical for reproduction, and inadequate decidualisation is implicated in the aetiology of pregnancy disorders such as foetal growth restriction and preeclampsia. In contrast to progesterone and oestradiol, the role of androgens in regulating endometrial function is poorly understood. Androgen receptors are expressed in the endometrium, and androgens are reported to regulate both the transcriptome and the secretome of endometrial stromal cells. In androgen-target tissues, circulating precursors are activated to mediate local effects, and recent studies report that steroid concentrations detected in endometrial tissue are distinct to those detected in the peripheral circulation. New evidence suggests that decidualisation results in dynamic changes in the expression of androgen biosynthetic enzymes, highlighting a role for pre-receptor regulation of androgen action during the establishment of pregnancy. These results suggest that such enzymes could be future therapeutic targets for the treatment of infertility associated with endometrial dysfunction. In conclusion, these data support the hypothesis that androgens play a beneficial role in regulating the establishment and maintenance of pregnancy. Future studies should be focussed on investigating the safety and efficacy of androgen supplementation with the potential for utilisation of novel therapeutics, such as selective androgen receptor modulators, to improve reproductive outcomes in women.
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30

Gauna, Carlotta, Piet Uitterlinden, Piet Kramer, Rosalie M. Kiewiet, Joop A. M. J. L. Janssen, Patric J. D. Delhanty, Maarten O. van Aken, et al. "Intravenous Glucose Administration in Fasting Rats Has Differential Effects on Acylated and Unacylated Ghrelin in the Portal and Systemic Circulation: A Comparison between Portal and Peripheral Concentrations in Anesthetized Rats." Endocrinology 148, no. 11 (November 1, 2007): 5278–87. http://dx.doi.org/10.1210/en.2007-0225.

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Ghrelin is produced by the gastrointestinal tract, and its systemic concentrations are mainly regulated by nutritional factors. Our aim was to investigate: 1) endogenous portal and systemic acylated and unacylated ghrelin levels (AG and UAG, respectively); 2) whether an iv glucose tolerance test (IVGTT) modifies AG and UAG; and 3) whether the liver passage plays a role in regulating systemic AG and UAG. To elucidate this, we evaluated the effects of IVGTT or saline injection on endogenous portal and systemic concentrations of glucose, insulin, AG, and UAG in anesthetized fasting rats. Hepatic extraction of insulin, AG, and UAG and the ratio of AG to UAG were also measured. IVGTT suppressed both portal (P &lt; 0.03) and peripheral (P &lt; 0.05) UAG, whereas it only blunted prehepatic, but not peripheral, AG. During fasting, hepatic clearance of UAG was 11%, and it was decreased to 8% by IVGTT. AG was cleared by the liver by 38% but unaffected by glucose. The AG to UAG ratio was higher in the portal than the systemic circulation, both in the saline (P &lt; 0.004) and IVGTT (P &lt; 0.0005) rats. In conclusion, this study shows that: 1) the ratio of AG to UAG is very low in the portal vein and decreases further in the systemic circulation; 2) IVGTT in anesthetized fasting rats inhibits UAG, whereas it only blunts prehepatic, but not systemic, AG; and 3) hepatic clearance of AG is much higher than that of UAG. Thus, our results suggest that peripheral AG metabolic regulation and action are mainly confined within the gastrointestinal tract.
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31

Kumar, Sachin, Jeff Vassallo, Kalpana Nattamai, Jose A. Cancelas, and Hartmut Geiger. "EGFR Signaling in Osteoblasts Regulates Circadian Rhythm of HSPC in Circulation." Blood 126, no. 23 (December 3, 2015): 665. http://dx.doi.org/10.1182/blood.v126.23.665.665.

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Abstract EGFR signaling regulates growth, differentiation, proliferation and migration in multiple organ systems. We previously demonstrated that inhibition of EGFR signaling on hematopoietic stem and progenitor cells (HSPCs) enhances G-CSF induced stem cell mobilization, while preliminary data suggested that inhibition of EGFR signaling in the stem cell niche actually had the opposite effect of inhibiting mobilization (Ryan et al., Nat Med, 2010). We thus tested the novel hypothesis that there is a role for EGFR signaling in the bone marrow (BM) niche with respect to regulating hematopoiesis. We utilized a set of mouse strains that express the recombinase Cre under distinct promoters to specifically delete EGFR in various types of stroma cells including Col-Cre; EGFRf/f (deletion in osteoprogenitor/osteoblasts (OBs)), Dermo-Cre; EGFRf/f (mesenchymal stem cells (MSCs) including chondrocytes and OB), Tie2-Cre; EGFRf/f (Endothelial cells) and Nestin-Cre; EGFRf/f (Schwann/neural cells) and compared them to no Cre-EGFRf/f mice as control wild type for EGFR. Basic parameters of steady-state hematopoiesis were not altered in mice devoid of EGFR signaling in the various types of stroma cells listed above. We further investigated HSPC mobilization in EGFRf/f mice and interestingly, Col-cre and Dermo-cre EGFRf/f mice exhibited a lower number of circulating HSPC in blood in comparison to wild type mice, as determined by colony forming units (CFUs) or flow cytometry. Deletion of the EGFR in endothelial (Tie2-Cre) and neuronal (Nestin-Cre) compartments did not result in a decline in the number of circulating HSPCs. Upon G-CSF challenge, Col-cre and Dermo-cre EGFRf/f mice mobilized HSPCs similar to controls, suggesting that EGFR signaling in OBs/MSCs is dispensable for G-CSF induced mobilization. HSPCs circulation under steady state follows a circadian rhythm. We next tested whether EGFR signaling in OBs might play a role in circadian rhythm driven HSPC circulation. After 5 hours of light cycle i.e. Zeitgeber time-5 (ZT-5), when the number of circulating HSPCs is high, Col-Cre EGFRf/f and Dermo-Cre EGFRf/f mice presented with low numbers of circulating HSPCs. After 13 hours of light cycle (ZT-13) (low number of circulating HSPCs), the number of HSPCs in blood in Col-Cre EGFRf/f and Dermo-Cre EGFRf/f mice were similar to controls. Together, this suggests that EGFR signaling in OBs is essential for the rhythmic increase in circulating HSPC in blood at ZT5. Currently, we are investigating molecular mechanisms driven by EGFR signaling in OBs that regulate HSPC retention in BM and circadian regulation of EGFR signaling. In summary, our data suggest an important and also very specific (no other phenotype altered) role of EGFR signaling for regulating the circadian rhythm of HSPC circulation in peripheral blood. Disclosures No relevant conflicts of interest to declare.
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32

Lapko, Inna V., Alla V. Zheglova, Kristina V. Klimkina, and Inessa A. Bogatyreva. "Neurohumoral regulation under exposure to vibration and physical overloads." Hygiene and sanitation 101, no. 10 (October 23, 2022): 1200–1205. http://dx.doi.org/10.47470/0016-9900-2022-101-10-1200-1205.

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Introduction. In response to the action of various occupational factors, central regulatory mechanisms, including the hypothalamus, are involved. Clarification of the influence of the hypothalamus on the indicators of peripheral blood circulation, peripheral innervation and bone metabolism under the influence of vibration and physical overloads is relevant for the diagnosis and treatment of occupational diseases of a neurological profile. The aim of the study. To establish the relationship between hypothalamic disorders and functional indicators of occupational diseases of the peripheral nervous system under the influence of vibration and physical overloads. Material and methods. One hundred fifteen tunnellers and machinists of the drilling rig of JSC “KMAruda Combine”, 26 tunnellers of the drainage mine of JSC “Stoilensky Mining and Processing Plant”, 65 workers of auxiliary occupations were examined. Depending on the influencing factor, they were divided into four groups with occupational neurological pathology, the fifth group was control Examined cases were divided into subgroups: A - without hypothalamic disorders and B - with hypothalamic syndrome. The criteria for the diagnosis of hypothalamic syndrome are clinical. All the examined patients underwent rheovasography, stimulation electroneuromyography of the extremities, ultrasound densitometry. Results. It was found that in patients with vibration disease from the effects of local or general vibration, especially when combined with lumbosacral radiculopathy during rheovasography, there are decrements in pulse blood filling, changes in vascular tone in vessels of various calibers and venous dysfunction, which are aggravated against the background of hypothalamic disorders. Hypothalamic disorders contribute to the aggravation of peripheral nerve indices: a decrease in the amplitude of the M-response, the rate of propagation of excitation along sensory axons and an increase in the value of residual latency. Functional assessment of bone tissue revealed the greatest prevalence of osteopenia syndrome in patients with vibration disease and its combined forms with lumbosacral radiculopathy in subgroups with hypothalamic-pituitary dysfunction (up to 33.6%). The frequency of detected functional disorders was established to increase with the progression of occupational diseases. Limitations. The study was conducted in workers with neurological occupational diseases exposed to vibration and physical overloads. Conclusions. Neurohumoral disorders, manifested by hypothalamic syndrome caused by exposure to general and local vibration in combination with physical overloads, contribute to the development or aggravation of functional changes in the body of workers, aggravating the course of occupational diseases of the peripheral nervous system, which can be used to develop diagnostic and treatment methods, and study the pathogenesis of diseases.
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33

Ratner, Cecilia, Louise J. Skov, Zindy Raida, Thomas Bächler, Kathrin Bellmann-Sickert, Christelle Le Foll, Bjørn Sivertsen, et al. "Effects of Peripheral Neurotensin on Appetite Regulation and Its Role in Gastric Bypass Surgery." Endocrinology 157, no. 9 (July 20, 2016): 3482–92. http://dx.doi.org/10.1210/en.2016-1329.

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Neurotensin (NT) is a peptide expressed in the brain and in the gastrointestinal tract. Brain NT inhibits food intake, but the effects of peripheral NT are less investigated. In this study, peripheral NT decreased food intake in both mice and rats, which was abolished by a NT antagonist. Using c-Fos immunohistochemistry, we found that peripheral NT activated brainstem and hypothalamic regions. The anorexigenic effect of NT was preserved in vagotomized mice but lasted shorter than in sham-operated mice. This in combination with a strong increase in c-Fos activation in area postrema after ip administration indicates that NT acts both through the blood circulation and the vagus. To improve the pharmacokinetics of NT, we developed a pegylated NT peptide, which presumably prolonged the half-life, and thus, the effect on feeding was extended compared with native NT. On a molecular level, the pegylated NT peptide increased proopiomelanocortin mRNA in the arcuate nucleus. We also investigated the importance of NT for the decreased food intake after gastric bypass surgery in a rat model of Roux-en-Y gastric bypass (RYGB). NT was increased in plasma and in the gastrointestinal tract in RYGB rats, and pharmacological antagonism of NT increased food intake transiently in RYGB rats. Taken together, our data suggest that NT is a metabolically active hormone, which contributes to the regulation of food intake.
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34

Gao, Haoyang, Lingli Zhang, Zhikun Wang, Kai Yan, Linlin Zhao, and Weihua Xiao. "Research Progress on Transorgan Regulation of the Cardiovascular and Motor System through Cardiogenic Exosomes." International Journal of Molecular Sciences 23, no. 10 (May 21, 2022): 5765. http://dx.doi.org/10.3390/ijms23105765.

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The heart is the core organ of the circulatory system. Through the blood circulation system, it has close contact with all tissues and cells in the body. An exosome is an extracellular vesicle enclosed by a phospholipid bilayer. A variety of heart tissue cells can secrete and release exosomes, which transfer RNAs, lipids, proteins, and other biomolecules to adjacent or remote cells, mediate intercellular communication, and regulate the physiological and pathological activities of target cells. Cardiogenic exosomes play an important role in regulating almost all pathological and physiological processes of the heart. In addition, they can also reach distant tissues and organs through the peripheral circulation, exerting profound influence on their functional status. In this paper, the composition and function of cardiogenic exosomes, the factors affecting cardiogenic exosomes and their roles in cardiovascular physiology and pathophysiology are discussed, and the close relationship between cardiovascular system and motor system is innovatively explored from the perspective of exosomes. This study provides a reference for the development and application of exosomes in regenerative medicine and sports health, and also provides a new idea for revealing the close relationship between the heart and other organ systems.
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35

Bernát, Sándor Iván. "The efficacy of the bio-electro-magnetic-regulation therapy and pentoxifylline treatment in peripheral arterial stenosis." Orvosi Hetilap 154, no. 42 (October 2013): 1674–79. http://dx.doi.org/10.1556/oh.2013.29693.

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Introduction: There are limited therapeutic options to improve microcirculation. Aim: The question of the study was to investigate any potential beneficial effect of bio-electro-magnetic-regulation therapy on microcirculation in patients suffering from peripheral arterial stenosis including the circulation of lower extremities, as well as intermittent claudication. Method: Thirty patients suffering from peripheral arterial stenosis (Fontaine IIa and IIb) were recruited. The first step of the study was to determine the pain free and maximal walking distance with a treadmill unit. After the placebo period patients received 8 and 20 minutes bio-electro-magnetic-regulation treatment 16 times. After the treatment the pain free and maximal walking distance were measured again. In the second stage of the study the patients were treated by pentoxifylline infusions. Results: bio-electro-magnetic-regulation treatment increased the pain free period by 57.4% (p = 0.005) and the maximal walking distance by 36.6% (p = 0.042). The two forms of therapy together increased the pain free and maximal walking distance by 81.9% and by 84.0%, respectively. The combined therapy was very effective in contrast to placebo and bio-electro-magnetic-regulation treatment (p = 0.000373 and p = 0.00741, respectively). Conclusions: The bio-electro-magnetic-regulation therapy mainly affected the microvessels and pentoxifylline therapy rather had beneficial effects on hemoreology. The clinical effectiveness of combined therapy was good or excellent in 70% of patients. Orv. Hetil., 154 (42), 1674–1679.
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36

Liu, Wenhao, Xin-Zhuang Yang, Dingding Zhang, Xin He, Qianlan Yu, Xinquan Liu, and Yi Dai. "Differential Regulation of the Immune System in Peripheral Blood Following Ischemic Stroke." BioMed Research International 2022 (June 8, 2022): 1–15. http://dx.doi.org/10.1155/2022/2747043.

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AIM. Previous studies have provided insights into complex immune system changes caused by ischemic stroke (IS), while detailed reports are lacking especially in peripheral blood. Here, we sought to identify genetic biomarkers in immune system which significantly associated with the occurrence of IS and explore candidate drugs that can regulate the process. We also investigated whether gene expression alternation of immune genes contributed to differential distribution of immune cells in peripheral blood following IS. Method. 108 IS samples and 47 matched controls were obtained from the GEO database. Immune-related genes (IRGs) and their associated drugs were collected from the ImmPort and PharmGBK databases, respectively. Random forest (RF) regression and least absolute shrinkage and selection operator (LASSO) logistic regression were applied to identify immune-related genetic biomarkers (IRGBs) of IS, and accuracy was verified using neural network models. Finally, proportion changes of various immune cells in peripheral blood of IS patients were evaluated using CIBERSORT and xCell and correlation analyses were performed between IRGBs and differentially distributed immune cells. Results. A total of 537 genes were differentially expressed between IS and control samples. Four immune-related differential expressed genes identified by regression analysis presented strong predictive power ( AUC = 0.909 ) which we suggeseted them as immune-related genetic biomarkers (IRGBs). We also demonstrated six immune-related genes targeted by known drugs. In addition, post-IS immune system presented an increase in the proportion of innate immune cells and a decrease in adaptive immune cells in the peripheral circulation, and IRGBs showing significance were associated with this process.Conclusion. The study identified CARD11, ICAM2, VIM, and CD19 as immune-related genetic biomarkers of IS. Six immune-related DEGs targeted by known drugs were found and provide new candidate drug targets for modulating the post-IS immune system. The innate immune cells and adaptive immune cells are diversified in the post-IS immune system, and IRGBs might play important role during this process.
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37

McMillen, I. C., B. S. Muhlhausler, J. A. Duffield, and B. S. J. Yuen. "Prenatal programming of postnatal obesity: fetal nutrition and the regulation of leptin synthesis and secretion before birth." Proceedings of the Nutrition Society 63, no. 3 (August 2004): 405–12. http://dx.doi.org/10.1079/pns2004370.

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Exposure to either an increased or decreased level of intrauterine nutrition can result in an increase in adiposity and in circulating leptin concentrations in later life. In animals such as the sheep and pig in which fat is deposited before birth, leptin is synthesised in fetal adipose tissue and is present in the fetal circulation throughout late gestation. In the sheep a moderate increase or decrease in the level of maternal nutrition does not alter fetal plasma leptin concentrations, but there is evidence that chronic fetal hyperglycaemia and hyperinsulinaemia increase fetal fat mass and leptin synthesis within fetal fat depots. Importantly, there is a positive relationship between the relative mass of the ‘unilocular’ component of fetal perirenal and interscapular adipose tissue and circulating fetal leptin concentrations in the sheep. Thus, as in the neonate and adult, circulating leptin concentrations may be a signal of fat mass in fetal life. There is also evidence that leptin can act to regulate the lipid storage, leptin synthetic capacity and potential thermogenic functions of fat before birth. Thus, leptin may act as a signal of energy supply and have a ‘lipostatic’ role before birth. Future studies are clearly required to determine whether the intrauterine and early postnatal nutrient environment programme the endocrine feedback loop between adipose tissue and the central and peripheral neuroendocrine systems that regulate energy balance, resulting in an enhanced risk of obesity in adult life.
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38

Tsyrlin, V. A. "The pharmacology of antihypertensive medicines." Regional blood circulation and microcirculation 19, no. 2 (June 27, 2020): 75–88. http://dx.doi.org/10.24884/1682-6655-2020-19-2-75-88.

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Анотація:
The lecture presents contemporary view on the human cardiovascular system organization. The mechanisms determining the systemic blood pressure level are shown; the factors regulating minute volume of blood circulation and peripheral resistance to blood flow are described. The mechanisms of neurogenic and basal vascular tone are noted, the role of humoral and endothelial regulation mechanisms of the artery lumen s is indicated. Based on the recent evidences of the circulatory system functioning, we gave a description of the main medicinal compounds used in clinical practice to decrease blood pressure. The pharmacological drugs decreasing neurogenic vascular tone and inhibiting basal vascular tone are indicated. The data of drug action, its pharmacodynamics and basic principles of combined use for the rational treatment of hypertension are presented. The lecture may be interesting to physiologists, pharmacologists, cardiologists, therapists, medical students and clinical residents.
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39

Meddows-Taylor, Stephen, Desmond J. Martin, and Caroline T. Tiemessen. "Dysregulated Production of Interleukin-8 in Individuals Infected with Human Immunodeficiency Virus Type 1 andMycobacterium tuberculosis." Infection and Immunity 67, no. 3 (March 1, 1999): 1251–60. http://dx.doi.org/10.1128/iai.67.3.1251-1260.1999.

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ABSTRACT Interleukin-8 (IL-8) production in vivo was monitored in four study groups: normal blood donors, patients with pulmonary tuberculosis (TB), patients with human immunodeficiency virus type 1 (HIV-1) infection, and dually infected (HIV/TB) patients. We show that whereas there was evidence of detectable levels of cell-associated IL-8 (mRNA and protein) in peripheral cells of healthy individuals, this was largely lost in the disease states studied. Coupled with this finding was significantly increased circulating levels of IL-8 in HIV-1-infected individuals with or without concomitant pulmonary TB (P < 0.001). On the other hand, the capacity of peripheral mononuclear cells to produce IL-8 spontaneously ex vivo was enhanced in HIV-1 and TB patients (P < 0.05) and many of the HIV/TB group, but their corresponding capacities to respond to various stimuli, in particular phytohemagglutinin, were significantly diminished compared to those of normal donors (P < 0.05). Circulating levels of IL-8 in a group of HIV/TB patients were significantly positively correlated with the percentage of polymorphonuclear leukocytes (PMN) in the peripheral circulation (r = 0.65; P = 0.01), the proportions of IL-8 receptor A (IL-8RA)-expressing (r = 0.86;P < 0.01) and IL-8RB-expressing (r = 0.77; P < 0.01) PMN, and the capacity of PMN to migrate in response to IL-8 as chemoattractant (r = 0.68; P < 0.01). IL-8RB fluorescence intensity, however, was negatively correlated with plasma IL-8 levels (r = −0.73; P < 0.01). Our results suggest that altered regulation of IL-8 in HIV-1 may have important implications for antimicrobial defenses and for normal immune processes.
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40

Sheares, Karen K. K., Trina K. Jeffery, Lu Long, Xudong Yang та Nicholas W. Morrell. "Differential effects of TGF-β1 and BMP-4 on the hypoxic induction of cyclooxygenase-2 in human pulmonary artery smooth muscle cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 287, № 5 (листопад 2004): L919—L927. http://dx.doi.org/10.1152/ajplung.00012.2004.

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Анотація:
Chronic hypoxia-induced pulmonary hypertension results partly from proliferation of smooth muscle cells in small peripheral pulmonary arteries. Previously, we demonstrated that hypoxia modulates the proliferation of human peripheral pulmonary artery smooth muscle cells (PASMCs) by induction of cyclooxygenase-2 (COX-2) and production of antiproliferative prostaglandins ( 55 ). The transforming growth factor (TGF)-β superfamily plays a critical role in the regulation of pulmonary vascular remodeling, although to date an interaction with hypoxia has not been examined. We therefore investigated the pathways involved in the hypoxic induction of COX-2 in peripheral PASMCs and the contribution of TGF-β1 and bone morphogenetic protein (BMP)-4 in this response. In the present study, we demonstrate that hypoxia induces activation of p38MAPK, ERK1/2, and Akt in PASMCs and that these pathways are involved in the hypoxic regulation of COX-2. Whereas inhibition of p38MAPK or ERK1/2 activity suppressed hypoxic induction of COX-2, inhibition of the phosphoinositide 3-kinase pathway enhanced hypoxic induction of COX-2. Furthermore, exogenous TGF-β1 induced COX-2 mRNA and protein expression, and our findings demonstrate that release of TGF-β1 by PASMCs during hypoxia contributes to the hypoxic induction of COX-2 via the p38MAPK pathway. In contrast, BMP-4 inhibited the hypoxic induction of COX-2 by an MAPK-independent pathway. Together, these findings suggest that the TGF-β superfamily is part of an autocrine/paracrine system involved in the regulation of COX-2 expression in the distal pulmonary circulation, and this modulates hypoxia-induced pulmonary vascular cell proliferation.
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41

Ishikawa-Sekigami, Tomomi, Yoriaki Kaneko, Hideki Okazawa, Takeshi Tomizawa, Jun Okajo, Yasuyuki Saito, Chie Okuzawa, et al. "SHPS-1 promotes the survival of circulating erythrocytes through inhibition of phagocytosis by splenic macrophages." Blood 107, no. 1 (January 1, 2006): 341–48. http://dx.doi.org/10.1182/blood-2005-05-1896.

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Анотація:
Abstract The lifespan of circulating red blood cells (RBCs) produced in bone marrow is determined by their elimination through phagocytosis by splenic macrophages. The mechanism by which RBC elimination is regulated has remained unclear, however. The surface glycoprotein SHPS-1, a member of the immunoglobulin superfamily, is abundant in macrophages. We have now examined the regulation of RBC turnover with the use of mice that express a mutant form of SHPS-1 lacking most of its cytoplasmic region. The mutant mice manifested mild anemia as well as splenomegaly characterized by expansion of the red pulp. The numbers of erythroid precursor cells in the spleen and of circulating reticulocytes were also increased in the mutant mice. In contrast, the half-life of circulating RBCs was reduced in these animals, and the rate of clearance of injected opsonized RBCs from the peripheral circulation was increased in association with their incorporation into splenic macrophages. Phagocytosis of opsonized RBCs by splenic macrophages from mutant mice in vitro was also increased compared with that observed with wild-type macrophages. These results suggest that SHPS-1 negatively regulates the phagocytosis of RBCs by splenic macrophages, thereby determining both the lifespan of individual RBCs and the number of circulating erythrocytes.
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42

Kjekshus, Harald, Otto A. Smiseth, Randi Klinge, Erik Øie, Marit E. Hystad, and Håvard Attramadal. "Regulation of ET: pulmonary release of ET contributes to increased plasma ET levels and vasoconstriction in CHF." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 4 (April 1, 2000): H1299—H1310. http://dx.doi.org/10.1152/ajpheart.2000.278.4.h1299.

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Анотація:
Endothelin (ET) contributes to the increased systemic vascular resistance and elevated cardiac filling pressures seen in congestive heart failure (CHF). We investigated to what extent ET-mediated vasoconstriction in CHF occurs through an endocrine action of elevated plasma ET or by an autocrine/paracrine mechanism related to induction of vascular ET gene expression. Three weeks of pacing (225 beats/min) induced a marked release of ET-1 from the pulmonary circulation with a sixfold elevation of arterial plasma ET in CHF pigs compared with sham-operated pigs. Arterial plasma ET was the strongest and only independent predictor of systemic vascular resistance. In contrast, vascular preproET-1 and ET-receptor mRNA expression were unaltered or decreased in CHF pigs and did not correlate with indexes of vascular tone. However, myocardial preproET-1 mRNA expression increased twofold in CHF pigs. PreproET-2 and preproET-3 mRNAs were not detectable in cardiovascular tissues. In conclusion, plasma ET was markedly increased because of an augmented release from the pulmonary circulation during CHF, and arterial plasma ET correlated with systemic vascular resistance. The absence of ET induction in the peripheral vasculature suggests that ET increases vascular tone during CHF by an endocrine, not an autocrine/paracrine, mechanism.
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43

Connolly, C. C., K. E. Steiner, R. W. Stevenson, D. W. Neal, P. E. Williams, K. G. Alberti, and A. D. Cherrington. "Regulation of glucose metabolism by norepinephrine in conscious dogs." American Journal of Physiology-Endocrinology and Metabolism 261, no. 6 (December 1, 1991): E764—E772. http://dx.doi.org/10.1152/ajpendo.1991.261.6.e764.

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Анотація:
The effects of norepinephrine (NE) at levels present in the circulation and synaptic cleft during stress on glucose metabolism were examined in overnight-fasted conscious dogs with fixed basal levels of insulin and glucagon. Plasma NE rose from 132 +/- 14 to 442 +/- 85 pg/ml and 100 +/- 20 to 3,244 +/- 807 pg/ml during 3 h of low (n = 6) and high (n = 5) NE infusion, respectively. Plasma glucose and glucose production rose only with high NE infusion (from 108 +/- 4 to 159 +/- 15 mg/dl and 2.78 +/- 0.24 to 3.41 +/- 0.38 mg.kg-1.min-1, respectively). NE infusion caused dose-dependent net hepatic lactate consumption, but net hepatic alanine uptake fell only with high NE infusion (31%). Alanine conversion to glucose rose by 67 +/- 13, 136 +/- 20, and 412 +/- 104%, and intrahepatic gluconeogenic efficiency rose by 42 +/- 27, 299 +/- 144, and 212 +/- 21% with saline and with low and high NE infusion, respectively. In conclusion, NE enhances gluconeogenesis by stimulating peripheral precursor release, by increasing substrate movement into the hepatocyte, and by increasing intrahepatic gluconeogenic efficiency. However, only the higher NE levels affected glucose metabolism profoundly enough to stimulate glucose production and to elevate the glucose level.
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44

Murphy, Michelle, and Francis J. P. Ebling. "The Role of Hypothalamic Tri-Iodothyronine Availability in Seasonal Regulation of Energy Balance and Body Weight." Journal of Thyroid Research 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/387562.

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Анотація:
Seasonal cycles of body weight provide a natural model system to understand the central control of energy balance. Studies of such cycles in Siberian hamsters suggest that a change in the hypothalamic availability of thyroid hormone is the key determinant of annual weight regulation. Uptake of thyroid hormone into the hypothalamus from the peripheral circulation occurs largely through a specific monocarboxylate transporter expressed by tanycyte cells lining the third ventricle. Tanycytes are the principal brain cell type expressing type II and type III deiodinases, so they control the local concentrations of T4, T3, and inactive metabolites. Type III deiodinase mRNA in tanycytes is photoperiodically upregulated in short photoperiod. This would be expected to reduce the availability of T3 in the hypothalamus by promoting the production of inactive metabolites such as rT3. Experimental microimplantation of T3 directly into the hypothalamus during short-days promotes a long-day phenotype by increasing food intake and body weight without affecting the peripheral thyroid axis. Thus, thyroid hormone exerts anabolic actions within the brain that play a key role in the seasonal regulation of body weight. Understanding the precise actions of thyroid hormone in the brain may identify novel targets for long-term pharmacological manipulation of body weight.
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45

Kim, Hyun Kyung, Maria De La Luz Sierra, Cassin Kimmel Williams, A. Virginia Gulino, and Giovanna Tosato. "G-CSF down-regulation of CXCR4 expression identified as a mechanism for mobilization of myeloid cells." Blood 108, no. 3 (August 1, 2006): 812–20. http://dx.doi.org/10.1182/blood-2005-10-4162.

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Abstract CXCR4 receptor expression is required for the retention of granulocyte precursors and mature neutrophils within the bone marrow, and disruption of the SDF-1/CXCR4 axis in the bone marrow results in the mobilization of myeloid lineage cells to the peripheral circulation. We report that G-CSF down-regulates CXCR4 expression in bone marrow–derived murine and human myeloid lineage cells. When exposed to G-CSF, murine Gr1+ bone marrow myeloid cells display a time-dependent reduction of cell-surface CXCR4 and respond poorly to SDF-1 in attachment and migration assays. Bone marrow–derived cells of nonmyeloid lineage display no change in surface CXCR4 expression upon exposure to G-CSF. Compared with controls, mice treated with G-CSF for mobilization of hematopoietic progenitor cells display reduced levels of CXCR4 selectively in bone marrow Gr1+ myeloid cells. Since bone marrow myeloid cells express G-CSF receptors and G-CSF rapidly reduces CXCR4 expression in purified Gr1+ cells populations, these results provide evidence that G-CSF acts directly on myeloid lineage cells to reduce CXCR4 expression. By down-regulating CXCR4 expression in bone marrow myeloid cells and attenuating their responsiveness to SDF-1, G-CSF promotes their mobilization from the bone marrow to the peripheral blood.
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46

Mamontov, Oleg V., Andrey V. Kozlenok, Alexei A. Kamshilin, and Evgeny V. Shlyakhto. "The Autonomic Regulation of Circulation and Adverse Events in Hypertensive Patients during Follow-Up Study." Cardiology Research and Practice 2019 (December 30, 2019): 1–6. http://dx.doi.org/10.1155/2019/8391924.

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Purpose. Comprehensive study of autonomic regulation assessed during follow-up could provide new detailed information about the risks stratification for hypertensive patients. Therefore, we investigated the associations of these indices with death, stroke, and revascularization during the follow-up observation of 55 patients. Methods. All patients were with target organ damage, and 27 of them had associated clinical conditions (ACC). Mean age of patients with and without ACC was 62.6 ± 4.2 and 51.9 ± 9.9 (mean ± SD) years, respectively. Follow-up was from 66 to 95 months. At entry, autonomic regulation was assessed by the tilt test, Valsalva maneuver, hand-grip test, and cold-stress vasoconstriction. Hemodynamic parameters were measured by continuous blood pressure monitoring, occlusion plethysmography, and electrocardiography. Re-examination of patients was carried out by questioning and physical and laboratory examination. Results. We found that fatal outcomes were associated with a lower Valsalva index (1.34 ± 0.16 vs. 1.69 ± 0.37, P<0.05) and depressed cold vasoconstriction (0.20 ± 0.02 vs. 0.39 ± 0.16%, P<0.05) but with higher peripheral resistance (1.36 ± 0.19 vs. 0.89 ± 0.25, P<0.001) and respiratory-range blood pressure variability (BPV) (18.2 ± 14.2 vs. 6.2 ± 4.2 mmHg, P<0.001). Higher total-range BPV (103 ± 51 vs. 65 ± 45 mmHg, P<0.05) in patients who had a stroke was observed. Initial diastolic orthostatic hypertension (6.6 ± 10.8 vs. 0.4 ± 6.3 mmHg, P<0.05) and lower Valsalva index (1.36 ± 0.11 vs. 1.82 ± 0.37, P<0.05) in patients who suffered a new ACC were important findings as well. Conclusions. This study shows that such autonomic regulation indices as Valsalva index, blood pressure dynamics in the tilt test, cold-stress vasomotor reactivity, and BPV are important for prognosis of hypertension course.
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47

Hamzaoui, K., A. Hamzaoui, L. Zakraoui, and A. Chabbou. "Expression of Bcl-2 in Inflammatory Sites from Patients with Active Behçet's Disease." Mediators of Inflammation 8, no. 2 (1999): 101–6. http://dx.doi.org/10.1080/09629359990595.

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Анотація:
Behçet's disease (BD) is a current systemic vasculitis of unknown aetiology. Eyes, skin, joints, the oral cavity, genital system, blood vessels, central nervous system and lung are usually involved. Defective regulation of programmed cell death (apoptosis) may play a role in the development of (BD), and the protooncogene Bcl-2 is involved in the control of apoptosis in immunocompetent cells. We therefore wished to investigate the expression of Bcl-2 in the peripheral lymphocytes and in two inflammatory sites of patients with active BD: bronchoalveolar lavage (BAL) and cerebrospinal fluid (CSF) lymphocytes. Levels of Bcl-2 expression in the lymphocytes of patients with BD and, for comparison, in the lymphocytes of healthy controls and non-inflammatory neurological diseases (NIND), were studied by two-colour cytofluorography and RNA analysis. In BD patients, a significant proportion of T cells expressed increased amounts of Bcl-2 protein, both in peripheral blood and in inflammatory sites. Mononuclear cells of patients with BD showed increased amount of Bcl-2 messenger RNA. The in vitro incubation of T lymphocytes with IL-10, significantly increased the Bcl-2 expression, specifically in T lymphocytes from inflammatory sites. In active BD, stimulation of HSV-1 T lymphocytes slightly increased Bcl-2 expression, not significantly different from unstimulated HSV-1 T cells. The occurrence of circulating T lymphocytes with abnormally high Bcl-2 expression in peripheral circulation and in inflammatory sites may be explained in part by the increasedin vivoactivation levels, and by aetiopathological agent(s): our findings seem to indicate an important role in the chronic inflammation in BD.
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48

McNeill, J. Robert. "Role of endothelin in regulation of resistance, fluid-exchange, and capacitance functions of the systemic circulation." Canadian Journal of Physiology and Pharmacology 81, no. 6 (June 1, 2003): 522–32. http://dx.doi.org/10.1139/y03-016.

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Анотація:
This article reviews data at the in vivo whole animal and human level. The importance of both flow and pressure recordings and of the methods used to record these variables is emphasized. Exogenous administration of endothelin-1 evokes a transient depressor response mediated by endothelial endothelinB receptors, but the predominate effect of endothelin-1 is a sustained increase in blood pressure resulting from increases in total peripheral resistance. Resistance in the superior mesenteric, renal, and hindquarter vascular beds of animals and forearm resistance in humans is increased. Both endothelinA and, to a lesser extent, endothelinB receptors on vascular smooth muscle mediate the increases in resistance. Endothelin-1 evokes decreases in the precapillary/postcapillary resistance ratio, resulting in increased capillary pressure and net transcapillary filtration. Endothelin-1 evokes increases in mean circulatory filling pressure in animals and in constriction of the human dorsal hand vein. This venoconstrictor activity is mediated primarily through endothelinA and to a lesser extent endothelin B receptors. Endogenously generated endothelin contributes to the hemodynamic effects of angiotensin and vasopressin in certain animal models of hypertension. Antagonists of endothelin evoke modest hemodynamic changes in healthy humans and in some healthy animals, and they decrease vascular resistance dramatically in several salt-sensitive rat models of hypertension and also in some hypertensive human subjects. Thus, endogenously generated ET appears to play a modest role in the healthy organism, but it likely plays a major role in many pathophysiological states as described in companion articles in this issue.Key words: hemodynamics, resistance, fluid exchange, capacitance, endothelin.
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49

Bloemer, Jenna, Priyanka D. Pinky, Manoj Govindarajulu, Hao Hong, Robert Judd, Rajesh H. Amin, Timothy Moore, Muralikrishnan Dhanasekaran, Miranda N. Reed, and Vishnu Suppiramaniam. "Role of Adiponectin in Central Nervous System Disorders." Neural Plasticity 2018 (July 29, 2018): 1–15. http://dx.doi.org/10.1155/2018/4593530.

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Анотація:
Adiponectin, the most abundant plasma adipokine, plays an important role in the regulation of glucose and lipid metabolism. Adiponectin also possesses insulin-sensitizing, anti-inflammatory, angiogenic, and vasodilatory properties which may influence central nervous system (CNS) disorders. Although initially not thought to cross the blood-brain barrier, adiponectin enters the brain through peripheral circulation. In the brain, adiponectin signaling through its receptors, AdipoR1 and AdipoR2, directly influences important brain functions such as energy homeostasis, hippocampal neurogenesis, and synaptic plasticity. Overall, based on its central and peripheral actions, recent evidence indicates that adiponectin has neuroprotective, antiatherogenic, and antidepressant effects. However, these findings are not without controversy as human observational studies report differing correlations between plasma adiponectin levels and incidence of CNS disorders. Despite these controversies, adiponectin is gaining attention as a potential therapeutic target for diverse CNS disorders, such as stroke, Alzheimer’s disease, anxiety, and depression. Evidence regarding the emerging role for adiponectin in these disorders is discussed in the current review.
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50

Dunon, D., N. Allioli, O. Vainio, C. Ody, and B. A. Imhof. "Quantification of T-Cell Progenitors During Ontogeny: Thymus Colonization Depends on Blood Delivery of Progenitors." Blood 93, no. 7 (April 1, 1999): 2234–43. http://dx.doi.org/10.1182/blood.v93.7.2234.

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Abstract An in vivo thymus reconstitution assay based on intrathymic injection of hematopoietic progenitors into irradiated chicks was used to determine the number of T-cell progenitors in peripheral blood, paraaortic foci, bone marrow (BM), and spleen during ontogeny. This study allowed us to analyze the regulation of thymus colonization occurring in three waves during embryogenesis. It confirmed that progenitors of the first wave of thymus colonization originate from the paraaortic foci, whereas progenitors of the second and the third waves originate from the BM. The analysis of the number of T-cell progenitors indicates that each wave of thymus colonization is correlated with a peak number of T-cell progenitors in peripheral blood, whereas they are almost absent during the periods defined as refractory for colonization. Moreover, injection of T-cell progenitors into the blood circulation showed that they homed into the thymus without delay during the refractory periods. Thus, thymus colonization kinetics depend mainly on the blood delivery of T-cell progenitors during embryogenesis.
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