Static contraction causes a reflex-induced release of arginine vasopressin in anesthetized cats
Lea R. Liviakisa and Charles L. StebbinsCorresponding Author Contact Information, a
a Department of Internal Medicine, Division of Cardiovascular Medicine, and Department of Human Physiology, University of California, Davis, Davis, CA, USA
Received 27 March 2000;
accepted 8 June 2000.
Available online 19 October 2000.
We tested the hypothesis that brief static contraction of the triceps surae muscle causes reflex-induced increases in plasma arginine vasopressin (AVP) in anesthetized cats. Arterial blood samples, for measurement of plasma AVP, were taken before and after 30 s of electrically stimulated static contraction performed at a low intensity (<20% of maximal; n = 5), a high intensity (>70% of maximal; n = 7), and a high intensity after denervation of the triceps surae (n = 5). The low intensity contraction protocol was repeated during α-adrenergic blockade (n = 7) to minimize potential baroreflex-induced inhibition of AVP release. Passive stretch of the triceps surae was conducted (n = 5) to determine effects of muscle mechanoreceptor stimulation on the release of AVP. Low intensity contraction had no effect on plasma AVP. During α-adrenergic blockade, this same contraction intensity caused this peptide to increase from12.8 ± 2.1 to 17.7 ± 2.6 pg/ml. High intensity contraction caused an increase in AVP (13.2 ± 3.5 to 26.1 ± 6.6 pg/ml) that was abolished by denervation (14.4 ± 3.7 vs. 17.1 ± 6.6 pg/ml). Passive stretch had no effect on plasma AVP. These findings suggest that brief static contraction causes increases in plasma AVP that are reflex in nature, intensity dependent, opposed by the arterial baroreflex, and probably unrelated to muscle mechanoreceptor activation.
Author Keywords: Arterial baroreflex; α-Adrenergic receptor antagonism; Muscle mechanoreceptors