Mechanisms of impaired excretion of a fluid load after cardiac denervation in dogs

Abstract

The influence of cardiac innervation on the renal response to volume expansion was investigated. Systemic hemodynamic, plasma hormone, and renal clearance measurements were made before, during, and after intravenous administration of 1,000 ml 0.9% saline over 10 min to six control and six cardiac-denervated, chloralose-anesthetized mongrel dogs. Volume expansion resulted in a two- to threefold rise in plasma atrial natriuretic peptide (ANP) concentrations and a 50% rise in glomerular filtration rate (GFR) in both groups. Plasma renin activity (PRA) and plasma arginine vasopressin remained higher throughout in cardiac-denervated compared with control dogs. The marked increases in urine flow rate and sodium and free water clearances seen in the controls were attenuated or abolished after cardiac denervation. These differences were due to the influence of higher PRA and vasopressin in these animals compared with the controls, rather than differences in hemodynamic responses operating via GFR or in direct humoral responses via ANP secretion.

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

“…The discovery of atrial natriuretic peptide (ANP), an extremely potent natriuretic substance released from atrial myocytes (De Bold, Borenstein, Veress & Sonnenberg, 1981) into the circulation in response to atrial stretch, has suggested a mechanism whereby the heart might exert a direct humoral influence on urine flow. However, in humans (Banner, Williams, Patel, Chalmers, Lightman & Yacoub, 1990) and other mammals (Pitchet, Gutkowska, Cantin & Lavallee, 1988;Williams, Travill, Noble, Drake-Holland t To whom correspondence should be addressed. it has been found previously that, even though ANP responses to atrial expansion are normal following cardiac denervation, natriuresis is attenuated in the absence of cardiac nerves.…”