Atrial and arterial baroreceptor influences on the circulatory response to acute changes in renal perfusion

We have recently reported a neurally mediated reflex increase in hindlimb vascular resistance associated with an acute decrease in renal perfusion pressure in the chloralose-urethane-anesthetized rabbit. The present study was designed to investigate the influence of this reflex in the body's integrated response to circulatory disturbances by investigating the influence of carotid baroreceptor and left atrial receptors on this reflex and assessing the effect of acute changes in renal perfusion on the heart. Interaction of the renal-generated reflex with carotid baroreceptors was investigated by independent perfusion of the carotid sinus region. Responses in hindlimb perfusion pressure, at constant flow, to changes in renal perfusion were greatest with the carotid sinus perfusion pressure (CSP) low (27 +/- 4 mmHg (1 mmHg = 133.3 Pa) increase in hindlimb pressure at low CSP vs. 19 +/- 3 mmHg increase at normal CSP) and were inhibited with maximum carotid stimulation. Partial mitral obstruction, resulting in left atrial distension and atrial receptor stimulation, attenuated the hindlimb vascular response. The increase in hindlimb pressure under control conditions was 34 +/- 10 mmHg compared with 20 +/- 5 mmHg during atrial receptor stimulation. However, acute reduction of renal perfusion pressure did not result in any changes in heart rate, cardiac output, or inotropic state. It appears that both atrial and arterial baroreflexes modify the reflex change in hindlimb vascular resistance associated with acute alterations of renal perfusion.