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The Role of Flaxseed Micronutrients and Nitric Oxide (NO) in Blood Vessel and Heart Function
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
In brief, the renin-angiotensin-aldosterone system of the kidneys regulates blood volume. In response to rising blood pressure, the kidneys secrete renin into the blood. Renin converts the plasma protein angiotensinogen into angiotensin I, which in turn is converted into angiotensin II by enzymes from the lungs. Angiotensin II activates two mechanisms that raise blood pressure:
Physiologic Changes
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Hemodynamic changes in pregnancy that have been well established include an increase in cardiac output and a decrease in both systemic and pulmonary vascular resistance. There is an overall increase in heart rate and a decrease in blood pressure. Blood volume, plasma volume, and erythrocyte volume all increase, with a greater relative increase in plasma volume, resulting in a dilutional lowering of hematocrit and other blood indices. There is also a redistribution of cardiac output with an increase in flow to the uterus, kidneys, skin, and breasts [1]. The renin–angiotensin–aldosterone system is activated in step with estrogen increases and assists in maintaining blood pressure and retaining water and salt despite increased renal excretion [7].The increase in stroke volume and cardiac output creates a more audible physiologic flow murmur and splitting of the S2 sound during pregnancy, which may be striking upon physical exam.
Applied Physiology: Renal Failure
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Major endocrine functions of the kidney include the control of red cell formation via erythropoietin synthesized in the peritubular cells and the control of arterial blood pressure via the renin–angiotensin system. Renal failure can lead to anaemia and hypertension. In early renal failure, renin is secreted from the juxtaglomerular cells in the ischaemic areas of the kidney. Renin activates the renin–angiotensin–aldosterone system. Angiotensin II causes vasoconstriction and stimulates the aldosterone (which increases Na+ and water retention) release from the adrenal cortex. This would account for hypertension in early renal failure.
Soyasaponin I alleviates hypertensive intracerebral hemorrhage by inhibiting the renin–angiotensin–aldosterone system
Published in Clinical and Experimental Hypertension, 2023
Wei Li, Shao-Guang Li, Lan Li, Li-Jian Yang, Zeng-Shi Li, Xi Li, An-Yuan Ye, Yang Xiong, Yi Zhang, Yuan-Yuan Xiong
The pathological mechanism of neurological impairment caused by HICH mainly includes the occupying effect of the hematoma, as well as cerebral edema, intracranial hypertension, altered local cerebral blood flow, and abnormalities of the coagulation and fibrinolytic system induced by hematoma breakdown products and vasoactive substances released from damaged brain tissues (14). Hematoma compression alone is not sufficient to cause severe damage to the brain tissues, whereas impaired cerebral circulation and metabolism caused by secondary cerebral edema are thought to be critical factors triggering brain damage after HICH (15,16). Overactivated RAAS is an important contributor to the development of hypertension and HICH. Renin, an aspartic protease synthesized and secreted by paraglomerular cells, initiates RAAS activation by converting angiotensinogen into angiotensin I. The catalytic hydrolysis of angiotensin I by ACE generates angiotensin II, which then acts on the adrenal cortex and leads to aldosterone release (17). Overactivation of RAAS can cause vasoconstriction and water and sodium retention, increase blood pressure, and myocardial contractility, thereby increasing the effective circulating blood volume and exacerbating hypertension (18). It has been clearly demonstrated clinically that the application of RAAS inhibitors such as ACEIs and ARBs significantly improved the prognosis of HICH (6). Therefore, inhibition of RAAS activation is an effective way to mitigate HICH.
The relationship between circadian rhythm of blood pressure and vascular dysfunction in essential hypertension
Published in Clinical and Experimental Hypertension, 2023
Yancui Sun, Ying Zhang, Fei Liu, Xiaojie Liu, Tesfaldet H. Hidru, Xiaolei Yang, Yinong Jiang
The main mechanisms of an abnormal nighttime BP dip aggravating blood vessel damage may involve dysregulation of the sympathetic nervous system and renin-angiotensin-aldosterone system (25–27). Cuspidi et al (26). investigated the association between nocturnal BP patterns and sympathetic drive in essential hypertensive patients and found that a stepwise increase in sympathetic nerve activation occurred from normotensive controls to extreme dipper, dipper, non-dipper, and reverse dipper hypertensive patients. Another study reported that non-dippers were characterized by reduced nighttime decreases in norepinephrine and epinephrine and heightened alpha 1-adrenergic receptor responsiveness compared with dippers. Arterial compliance is also influenced by sympathetic neural activity; therefore, sympathetic nervous system activity may represent a link between vessel damage and nighttime BP dipping (28). Second, increasing nocturnal natriuresis plays an essential role in the elevation of nocturnal BP (29,30). This condition activates the renin-angiotensin-aldosterone system, leading to impaired blood vessels.
Extensive Keloid and Hypertrophic Mixed Scarring Pattern in Ear Lobes of a 14-Year-Old African Female: A Case Report
Published in Fetal and Pediatric Pathology, 2023
Javier Arredondo Montero, Mónica Bronte Anaut, Carlos Bardají Pascual
Keloids are abnormal scarring patterns of complex etiopathogenesis, mediated by alterations in fibroblastic differentiation and migration [1]. African populations have a greater tendency to abnormal scarring patterns, mainly of the keloid type [2]. Although the underlying pathophysiological mechanism has not been elucidated, it may be related to the renin-angiotensin aldosterone system, which is supported by the higher prevalence of arterial hypertension in these populations [3, 4]. In relation to the immunohistochemical study of keloids, the literature is scarce, with some articles suggesting that cyclooxygenase-1 [5] and Krox20 [6] may be interesting markers for diagnosis. To date, there are no specific studies on this subject in the African population. There are previously published reports of aberrant and disfiguring scarring earlobe patterns in the African population, although they are scarce [7, 8]. To the best of our knowledge, the largest earlobe keloids documented to date measured 10 × 8 and 12 × 7 cm, respectively [7]. In all, histology revealed a keloid pattern. The case presented below is noteworthy for the massive size of the lesions.