The interaction between catecholamines (CA) and ANP is not clearly established. The effects of excess endogenous CA on ANP secretion can be investigated in patients with pheochromocytoma. We studied 27 patients with surgically and histologically proven pheochromocytoma (P) aged 19-70 years. In 16 of these patients plasma ANP study was repeated after surgical removal of the tumour. The control group (C) consisted of 20 healthy volunteers aged 21-48 years. Moreover, 42 patients with uncomplicated mild to moderate essential hypertension (EH) aged 18-48 years were also studied. In P higher plasma ANP concentration versus C, EH was found (51.9 +/- 8.1; 25.5 +/- 1.5; 19.3 +/- 1.5 fmol/ml, respectively). In 16 patients with P, increased plasma ANP level (mean 63.3 +/- 12.6 fmol/ml) declined after surgical removal of the tumour (mean 22.4 +/- 2.9 fmol/ml). In the P patients no relationship was found between plasma ANP and hormonal patterns of the tumour or between plasma ANP and plasma catecholamines, whereas significant positive correlations between plasma ANP and both systolic and diastolic blood pressure and heart rate were demonstrated. These results suggest that excess CA produced by the chromaffin tumour induce ANP secretion via stimulation of adrenergic receptors. However, influence of the haemodynamic changes evoked by CA cannot be excluded. It is suggested that increased secretion of ANP may be of some importance in maintaining blood pressure homeostasis in patients with pheochromocytoma.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.3109/08037059209077511 | DOI Listing |
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!