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Conscious dogs were used to study whether changes in total renal hemodynamics are responsible for diuresis and natriuresis during an experimental increase in left atrial pressure (LAP). To ensure a controlled dietary sodium intake, the dogs ( n=8) were chronically kept on a high or a low sodium intake diet ( HSI; LSI). After the dogs had completely recovered from surgery (carotid loop, thoracotomy, flank incision), LAP was increased by about 10 cm HO for 60 min by tightening a purse string around the mitral annulus (51 expts). Mean urine volume (V) increased in both groups to a comparable degree. Mean sodium excretion increased somewhat more in HSI dogs, but remained elevated in LSI dogs after the LAP increase. Renal blood flow (electromagnetic flow transducer) and inulin clearance did not change. Renal vascular resistance (RVR) increased by about 20% (HSI) and 15% (LSI). - When the induced LAP increase was terminated, V decreased. RVR decreased in HSI dogs by about −11% and in LSI dogs by about −6% below control values.-It is concluded that volume regulatory mechanisms induced by an experimental LAP increase operate independently of changes in total renal blood flow. [ABSTRACT FROM AUTHOR]

10 conscious chronically prepared dogs were used. After recovery from thoracotomy (catheter into the left atrium, nylon purse string around the mitral annulus) they were kept chronically on a low sodium intake (<0.5 meq Na/kg bw daily). On 51 days left atrial pressure (LAP) was increased for 60 min about 10 cm HO once daily by tightening the purse string (distension period: DP). During DP urine volume ( $$\dot V$$ ) increased about threefold, and sodium excretion ( E) about sixfold. The amount of renal sodium loss on the days when LAP was increased exceeded the daily intake considerably. The application of DOCA (15 mg i.m.) did not diminish E during DP and 60 min thereafter. During DP heart rate increased by about 70 b/min and mean arterial blood pressure increased by about 15 mm Hg. The data suggest that stimulation of intrathoracic receptors by a reversible mitral stenosis augments renal sodium excretion even in a state of a highly stimulated tubular sodium resorption. [ABSTRACT FROM AUTHOR]