Arterial and renal venous active and inactive renin were studied in 5 patients with long established moderate hypertension following unilateral acute reductions of renal perfusion pressure (15% and 70% of control) by inflating a balloon catheter introduced into the right renal artery. This procedure failed to induce the expected release of active renin; total and inactive renin levels were also unchanged. On the contrary in a single normotensive patient smaller reductions of the renal perfusion pressure (-15% and -30%) were able to acutely increase the release of active renin with a concurrent conversion of inactive renin but without inducing blood pressure changes. These findings show that the renin pattern typical of unilateral renovascular hypertension, including the intrarenal activation of inactive renin, could be reproduced acutely in a normotensive subject. Moreover, a complete reversal of the above mentioned active and inactive renin pattern was observed in a recent onset renovascular hypertensive patient within 30 min from successful percutaneous transluminal dilation. The negative results observed in our hypertensive patients suggest that structural changes induced by the long duration of hypertension might have reduced the sensitivity of the baroceptors involved in renin release.
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http://dx.doi.org/10.3109/10641968209062391 | DOI Listing |
Am J Ther
January 2025
Department of Interventional Cardiology, Queen Elizabeth Hospital, Birmingham, United Kingdom.
Front Endocrinol (Lausanne)
January 2025
Endocrinology and Diabetes Center, Yokohama Rosai Hospital, Yokohama, Japan.
Several decades have passed since the description of the first patient with primary aldosteronism (PA). PA was initially classified in two main forms: aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA). However, the pathogenesis of PA has now been shown to be far more complex.
View Article and Find Full Text PDFObjectives: This clinical study assessed the three-year, long-term effects of esaxerenone, a non-steroidal aldosterone receptor blocker, on Japanese patients with type 2 diabetes, diabetic kidney disease, and hypertension who were receiving renin-angiotensin system inhibitors.
Materials And Methods: Data from a computerized diabetic care database were used to retrospectively compare esaxerenone users (Group A) with non-esaxerenone users (Group B). Propensity score weighting was applied to Group B.
Front Cardiovasc Med
January 2025
School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Cardiometabolic diseases (CMD) are leading causes of death and disability worldwide, with complex pathophysiological mechanisms in which inflammation plays a crucial role. This review aims to elucidate the molecular and cellular mechanisms within the inflammatory microenvironment of atherosclerosis, hypertension and diabetic cardiomyopathy. In atherosclerosis, oxidized low-density lipoprotein (ox-LDL) and pro-inflammatory cytokines such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α) activate immune cells contributing to foam cell formation and arterial wall thickening.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Cardiology, the 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Oxidative stress-associated proximal tubular cells (PTCs) damage is an important pathogenesis of hypertensive renal injury. We previously reported the protective effect of VEGFR3 in salt-sensitive hypertension. However, the specific mechanism underlying the role of VEGFR3 in kidney during the overactivation of the renin-angiotensin-aldosterone system remains unclear.
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