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AJP - Regulatory, Integrative and Comparative Physiology, Vol 252, Issue 4 801-R807, Copyright © 1987 by American Physiological Society
ARTICLES |
M. M. Caverson and J. Ciriello
Experiments were done in alpha-chloralose-anesthetized, paralyzed and artificially ventilated cats with vagus, cervical sympathetic, aortic depressor, and carotid sinus nerves cut bilaterally to investigate the effect of afferent renal nerve (ARN) stimulation on circulating levels of vasopressin (AVP). Electrical stimulation of ARN elicited a pressor response that had two components, a primary (1 degree) component locked in time with the stimulus and a secondary (2 degree) component that had a long onset latency and that outlasted the stimulation period. The 1 degree and 2 degree components of the pressor response were largest at stimulation frequencies of 30 and 40 Hz, respectively. Autonomic blockade with hexamethonium bromide and atropine methylbromide abolished the 1 degree component. Administration of the vasopressin V1-vascular receptor antagonist d(CH2)5VAVP during autonomic blockade abolished the 2 degree component. Plasma concentrations of AVP measured by radioimmunoassay increased from control levels of 5.2 +/- 0.9 to 53.6 +/- 18.6 pg/ml during a 5-min period of stimulation of ARN. Plasma AVP levels measured 20-40 min after stimulation (13.6 +/- 7.0 pg/ml) were not significantly different from control values. Plasma osmolality was not altered during the course of the experiment. These data demonstrate that sensory information originating in the kidney alters the release of vasopressin from the neurohypophysis and suggest that ARN are an important component of the neural circuitry involved in homeostatic mechanisms controlling arterial pressure.
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