Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1993;21:461-469

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Giannattasio, C.
Right arrow Articles by Grassi, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Giannattasio, C.
Right arrow Articles by Grassi, G.

Hypertension, Vol 21, 461-469, Copyright © 1993 by American Heart Association


ARTICLES

Reflex vasopressin and renin modulation by cardiac receptors in humans

C Giannattasio, A Del Bo, BM Cattaneo, C Cuspidi, E Gronda, M Frigerio, M Mangiavacchi, M Marabini, C De Vita and G Grassi
Istituto di Medicina Interna, Ospedale S. Gerardo, Monza, Italy.

Animal studies have shown that vasopressin secretion is modulated by arterial baroreceptors and cardiopulmonary volume receptors. Whether this is the case also in humans is controversial, however. To determine whether vasopressin is reflexly modulated by cardiac volume receptors, we studied the effect on plasma vasopressin (venous blood, radioimmunoassay) of reducing venous return and left ventricular end- diastolic diameter (echocardiography) by producing a 20-minute lower body negative pressure in 14 healthy subjects (aged 49.3 +/- 3.8 years, mean +/- SEM). The data were compared with those of 14 age-matched heart-transplant recipients, i.e., subjects with cardiac denervation. In healthy subjects, lower body negative pressure at -15 mm Hg caused a modest reduction in left ventricular end-diastolic diameter (-5 +/- 3.4%) and no change in vasopressin, whereas lower body negative pressure at -37.5 mm Hg caused a more marked reduction in left ventricular end-diastolic diameter (-12 +/- 2.5%) and a small, variable, but overall statistically significant (p < 0.05) increase in vasopressin (+145 +/- 46%, p < 0.01). The left ventricular end- diastolic diameter changes induced by the two lower body negative pressure stimuli were similar in heart-transplant recipients, but the vasopressin increase seen with the lower body negative pressure at - 37.5 mm Hg was abolished. The marked increase in plasma renin activity and forearm vascular resistance induced by lower body negative pressure in healthy subjects was also abolished or drastically attenuated in heart-transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
HypertensionHome page
C. Giannattasio, F. Achilli, A. Grappiolo, M. Failla, E. Meles, G. Gentile, I. Calchera, A. Capra, J. Baglivo, A. Vincenzi, et al.
Radial Artery Flow-Mediated Dilatation in Heart Failure Patients: Effects of Pharmacological and Nonpharmacological Treatment
Hypertension, December 1, 2001; 38(6): 1451 - 1455.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
G. Jacob, A. C. Ertl, J. R. Shannon, R. Furlan, R. M. Robertson, and D. Robertson
Effect of standing on neurohumoral responses and plasma volume in healthy subjects
J Appl Physiol, March 1, 1998; 84(3): 914 - 921.
[Abstract] [Full Text] [PDF]