Obesity may compound the increased risk of hypertension and cardiovascular disease in individuals born prematurely by further augmenting the prematurity-associated imbalance in the renin-angiotensin system.
The most commonly used drugs were agents acting on the renin-angiotensin system (67.9%), statins (62.3%), antithrombotic agents (48.4%), and biguanides (37.1%) for the treatment of hypertension (76.7%), dyslipidemia (54.1%), and diabetes (47.8%).
Budget impact analysis of increasing prescription of renin-angiotensin system inhibitors drugs to standard anti-hypertensive treatments in patients with diabetes and hypertension in a hypothetical cohort of Malaysian population.
Previously, we reported that global genetic deletion of 2 pore-domain TWIK-relative acid-sensitive potassium channels, TASK-1 and TASK-3, from mice produces striking aldosterone excess, low renin, and hypertension.
We investigated the pharmacology of aprocitentan (<i>N</i>-[5-(4-bromophenyl)-6-[2-[(5-bromo-2-pyrimidinyl)oxy]ethoxy]-4-pyrimidinyl]-sulfamide), a potent dual ET<sub>A</sub>/ET<sub>B</sub> receptor antagonist, on blood pressure (BP) in two models of experimental hypertension: deoxycorticosterone acetate (DOCA)-salt rats (low-renin model) and spontaneously hypertensive rats [(SHR), normal renin model].
Recent reports have shown that ORS may suppress hypertension by controlling the renin-angiotensin-aldosterone system (RAAS) in the kidney, but its action mechanism has not been well defined.
To address this, we aimed to determine the effect of deoxycorticosterone acetate (DOCA) -salt (sodium chloride)-induced hypertension on the alterations in renin-angiotensin system, leading to CV and renal dysfunction in uninephrectomized male Sprague Dawley rats.
Low-renin, low-aldosterone hypertension represents a wide spectrum of disorders that includes essential low-reninhypertension, hereditary forms of hypertension, and hypertension secondary to endogenous or exogenous factors.
Chronic treatment of hypertension or heart failure very often includes an angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) as renin-angiotensin system inhibitors (RASi) treatments.
The exact mechanisms of how fetal programming events increase the risk of hypertension and cardiovascular disease are not fully elaborated; however, the focus on alterations in the biochemical components and functional aspects of the renin-angiotensin (Ang) system (RAS) has predominated, particularly activation of the Ang-converting enzyme (ACE)-Ang II-Ang type 1 receptor (AT<sub>1</sub>R) axis.
Decreased level of BDNF is observed in depression and its connection to hypertension has also been demonstrated with affecting the arterial baroreceptors, renin-angiotensin system and endothelial nitric oxide synthase.
Angiotensin II and aldosterone are the main effectors of the renin-angiotensin aldosterone system (RAAS) and have a central role in hypertension as well as cardiovascular and renal disease.
In this review we describe the renin-angiotensin II (AngII) system (RAS) with specific regard to its deleterious contributions to hypertension, facilitation of neuroinflammation and oxidative stress, reduced cerebral blood flow, tissue remodeling, and disruption of memory consolidation and retrieval.
Traditionally, hypertension has been regarded as a disorder of two systems that are involved in the regulation of salt-water balance and cardiovascular function: the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS).
Renin-angiotensin system might play a central role in the direct interaction between hypertension and epilepsy, but other mechanisms may be contemplated.
Novel areas of research in the field of hypertension pharmacology include central nervous system regulators, peripheral noradrenergic inhibitors, gastrointestinal sodium modulators, and a counter-regulatory arm of the renin-angiotensin-aldosterone system.
The development of hypertension in T2DM involves multiple processes, including enhanced sympathetic output, inappropriate activation of renin-angiotensin- aldosterone system, endothelial dysfunction induced through insulin resistance, and abnormal sodium handling by the kidney.