Toward an Integrative Concept of Control of Total Body Sodium

Total body sodium (TBSodium) is a major determinant of body water and arterial pressure. Several observations, in particular that of a “sodium memory,” indicate that TBSodium is a controlled variable. Various regulatory elements are involved, e.g., the renin-angiotensin-aldosterone system, atrial receptors, and renal arterial pressure. Balance studies in dogs provide new insights into their contributions to TBSodium control.

Cardiovascular afferent signals and drinking in response to hypotension in dogs

Arterial hypotension stimulates increases in plasma arginine vasopressin (AVP), plasma renin activity (PRA), and water intake in conscious dogs. We have previously reported that increasing left atrial but not right atrial pressure completely blocks the increase in plasma AVP and PRA induced by hypotension. The goal of the present study was to examine the effect of increasing right or left atrial pressure on water intake induced by arterial hypotension. Dogs were prepared with occluding cuffs on the thoracic inferior vena cava, the pulmonary artery, and the ascending aorta. We reduced mean arterial pressure (MAP) 25% below control by either inferior vena cava constriction (IVCC), pulmonary artery constriction (PAC), or ascending aorta constriction (AAC) and measured water intake over a 2-h period. Cumulative water intake during IVCC ( n = 6) and PAC ( n = 6) was 7.8 ± 2.0 and 6.7 ± 2.6 ml/kg, respectively. There was no difference between either the latency or the volume consumed between the two treatments. In contrast, none of the dogs drank during hypotension induced by AAC ( n = 5). Because the degree of arterial baroreceptor unloading was the same in each treatment by design, we conclude that stimulation of left atrial receptors inhibits drinking in response to arterial hypotension but that stimulation of right atrial receptors has no effect on the response in dogs.

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.Key words: afferent renal nerves, baroreceptors, atrial receptors, vascular resistance.