A Possible Interaction Between Systemic and Renal Angiotensinogen in the Control of Blood Pressure
Por: Nirupama Ramkumar, Deborah Stuart, Jian Ying y Donald E. Kohan. American Journal of Hypertension, Volume 26, Issue 4, Pp. 473-480.
Angiotensinogen (AGT) is synthesized in the liver and proximal tubule. AGT overexpression at either site might increase blood pressure (BP). We used transgenic mice with AGT overexpression in proximal tubule (K), liver (L), or both sites (KL) to determine the relative contributions of hepatic- and proximal tubule–derived AGT in modulating BP. Mice with liver AGT overexpression manifest salt-sensitive hypertension, whereas mice with renal AGT overexpression are hypertensive regardless of salt intake. Systemic AGT may stimulate endogenous renal AGT synthesis during high sodium intake, leading to hypertension in L mice. [Actualizado: 3 de junio 2013]
Esta sección expone trabajos actuales, de carácter investigativo sobre la hipertensión arterial.
How important is it to control nocturnal hypertension with angiotensin II type 1 receptor blockers?
Por: Shin-ichiro Miura y Keijiro Saku. Hypertension Research (2013) 36, 194–195.
Better blood pressure (BP) control is associated with remarkable clinical benefits with regard to cardiovascular (CV) and renal protection. Patients with chronic kidney disease (CKD) are at significantly higher risk of CV disease (CVD),1 and patients with overt proteinuria as well as albuminuria without a reduction in the estimated glomerular filtration rate (eGFR) are also at significantly higher risk.1 In addition, proteinuria or albuminuria itself should be a target for reducing hard end points. Angiotensin II (Ang II) type 1 (AT1) receptor blockers (ARBs) are highly selective for the AT1 receptor and block the deleterious effects of Ang II.2 ARBs clearly decrease proteinuria and protect the kidneys.3 A nocturnal increase in BP on ambulatory monitoring is superior to office BP for predicting a worsening of albuminuria in elderly individuals with type 2 diabetes. [Actualizado: 11 de marzo 2013]
Esta sección expone trabajos actuales, de carácter investigativo sobre la hipertensión arterial.
Hypertension and the J-curve phenomenon: implications for tight blood pressure control
Por: Fabio Angeli, Gianpaolo Reboldi y Paolo Verdecchia. Hypertension Research (2013) 36, 109–111.
The term J-curve is used in several fields of science to refer to a variety of J-shaped diagrams where a curve initially falls, but then rises to higher levels. In cardiovascular (CV) medicine, the J-curve phenomenon arises when a risk factor becomes inversely related to risk below a certain point, whereas the more widely accepted positive risk association exists across most of the observed risk factor distribution. In simpler terms, when elevated blood pressure (BP) is lowered, the risk of CV events decreases, but lowering BP below a critical ‘nadir’ is no longer beneficial and possibly deleterious, thus shaping a J-curve. [Actualizado: 8 de febrero de 2013]
Esta sección mostrará algunos trabajos que puedan ser útiles a nuestros facultativos por su interés práctico o teórico.
Blood pressure control and favourable pleiotropic effects of aliskiren
Por: Graziano Riccioni. Hypertension Research (2013) 36, 102–103.
Hypertension and its acute and chronic complications are one of the most important risk factors associated with significant morbidity and mortality worldwide and will increase in importance as a public health problem by 2020.1 The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC7) establishes that the goal of antihypertensive therapy is to reduce cardiovascular and renal morbidity and mortality. Despite the wide range of antihypertensive agents available, less than one third of patients with hypertension have their blood pressure (BP) controlled. The mechanism of primary (essential) hypertension includes genetic predisposition, endothelial cell dysfunction, sympathetic nervous system (SNS) hyperactivity, abnormalities in renin angiotensin aldosterone system (RAAS) function, hyperinsulinism and insulin resistance. [Actualizado: 8 de febrero de 2013]
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