To clarify the effects of norepinephrine and angiotension II (Ang II) on plasma atrial natriuretic peptide (ANP), both pressor substances were infused into normal volunteers, and plasma ANP levels and venous return were determined. When norepinephrine infusion elevated mean arterial pressure by 15 mm Hg, a transient increase of plasma ANP was observed. However, Ang II infusion showed no effect on plasma ANP levels, even though it also elevated arterial pressure. Superior vena cava flow and left atrial area, which were determined echocardiographically as the index of venous return, increased in the norepinephrine infusion study. However, in the study of Ang II infusion, there was no significant change in either superior vena cava flow or left atrial area. From these results, it was concluded that increased left atrial volume due to increased venous return is the major factor inducing ANP release in norepinephrine infusion.
Download full-text PDF |
Source |
---|
J Cell Mol Med
December 2024
Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE, Université de Lille, Lille, France.
Chronic pressure overload induces adverse cardiac remodelling characterised by left ventricular (LV) hypertrophy and fibrosis, leading to heart failure (HF). Identification of new biomarkers for adverse cardiac remodelling enables us to better understand this process and, consequently, to prevent HF. We recently identified clusterin (CLU) as a biomarker of cardiac remodelling and HF after myocardial infarction.
View Article and Find Full Text PDFCoron Artery Dis
December 2024
Department of Cardiology.
Cardiovasc Toxicol
December 2024
Department of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Sci Adv
October 2024
Institute of Metabolic and Cardiovascular Diseases, INSERM/Paul Sabatier University, UMR1297, Team MetaDiab, Toulouse, France.
Am J Physiol Renal Physiol
December 2024
Tulane Hypertension and Renal Center of Excellence and Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana, United States.
In the proximal tubules of the kidney, angiotensin II (ANG II) binds and activates ANG II type 1 (AT) receptors to stimulate proximal tubule Na reabsorption, whereas atrial natriuretic peptide (ANP) binds and activates natriuretic peptide receptors (NPR) to inhibit ANG II-induced proximal tubule Na reabsorption. These two vasoactive systems play important counteracting roles to control Na reabsorption in the proximal tubules and help maintain blood pressure homeostasis. However, how AT and NPR receptors interact in the proximal tubules and whether natriuretic effects of NPR receptor activation by ANP may be potentiated by deletion of AT (AT) receptors selectively in the proximal tubules have not been studied previously.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!