Literature DB >> 1717629

Increased plasma level of substance P in patients with severe congestive heart failure treated with ACE inhibitors.

S Valdemarsson1, L Edvinsson, R Ekman, P Hedner, A Sjöholm.   

Abstract

The effects of angiotensin-converting-enzyme (ACE) inhibitors on circulatory regulating mechanisms in congestive heart failure (CHF) were studied by comparison of plasma levels of catecholamines, neuropeptide Y-like immunoreactivity (NPY-LI), substance P (SP-LI), calcitonin gene-related peptide (CGRP-LI), vasopressin (ADH-LI), atrial natriuretic peptide (ANP-LI) and renin activity (PRA) in patients with severe CHF (NYHA III-IV) with (n = 15) or without (n = 17) ACE inhibitors in addition to digoxin and diuretic therapy. Data were also compared with those for healthy subjects (n = 31) and patients with moderate CHF (NYHA I-II). Catecholamines and NPY-LI were increased to the same extent in both groups with severe CHF. CGRP-LI showed no changes relative to controls in any of the patient groups, and was not affected by ACE inhibitors. The SP-LI level was significantly increased in all patient groups. Patients with severe CHF on ACE inhibition had a SP-LI level of 4.05 +/- 0.79 pmol l-1, compared to a concentration of 2.28 +/- 0.30 pmol l-1 (P less than 0.05) in the patient group with a comparable degree of CHF but without ACE inhibition. In the latter group, an inverse relationship appeared between the SP-LI and the serum sodium levels (r = -0.68, P less than 0.05). The patients with severe CHF who received ACE inhibitors had significantly lower ADH-LI levels than the patients with a comparable degree of CHF who were not treated with ACE inhibitors, while the ANP-LI levels was increased to a similar extent in both groups.

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Year:  1991        PMID: 1717629     DOI: 10.1111/j.1365-2796.1991.tb00452.x

Source DB:  PubMed          Journal:  J Intern Med        ISSN: 0954-6820            Impact factor:   8.989


  7 in total

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Authors:  Andrew P Davie; John J V McMurray
Journal:  Br J Clin Pharmacol       Date:  2002-01       Impact factor: 4.335

2.  Attenuation of contractile responses to sympathetic co-transmitters in veins from subjects with essential hypertension.

Authors:  H Lind; D Erilnge; J Brunkwall; L Edvinsson
Journal:  Clin Auton Res       Date:  1997-04       Impact factor: 4.435

3.  Non-human primate and rat cardiac fibroblasts show similar extracellular matrix-related and cellular adhesion gene responses to substance P.

Authors:  Giselle C Meléndez; Edward J Manteufel; Heather M Dehlin; Thomas C Register; Scott P Levick
Journal:  Heart Lung Circ       Date:  2014-12-05       Impact factor: 2.975

Review 4.  Substance P in heart failure: the good and the bad.

Authors:  Heather M Dehlin; Scott P Levick
Journal:  Int J Cardiol       Date:  2013-11-12       Impact factor: 4.164

5.  Substance P acting via the neurokinin-1 receptor regulates adverse myocardial remodeling in a rat model of hypertension.

Authors:  Heather M Dehlin; Edward J Manteufel; Andrew L Monroe; Michael H Reimer; Scott P Levick
Journal:  Int J Cardiol       Date:  2013-07-29       Impact factor: 4.164

Review 6.  The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension.

Authors:  Charmaine C W Lo; Seyed M Moosavi; Kristen J Bubb
Journal:  Front Physiol       Date:  2018-08-23       Impact factor: 4.566

7.  Dipeptidyl Peptidase 4 Inhibition Increases Postprandial Norepinephrine via Substance P (NK1 Receptor) During RAAS Inhibition.

Authors:  Jessica R Wilson; Scott Jafarian Kerman; Scott A Hubers; Chang Yu; Hui Nian; Eric Grouzmann; Philippe J Eugster; Dustin S Mayfield; Nancy J Brown
Journal:  J Endocr Soc       Date:  2019-07-01
  7 in total

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