H. Yoneda et al., BLUNTED NATRIURETIC RESPONSE TO ENDOGENOUS ATRIAL-NATRIURETIC-PEPTIDEDURING RAPID CARDIAC PACING IN ANESTHETIZED DOGS, Clinical and experimental pharmacology and physiology, 25(5), 1998, pp. 341-346
1. We investigated whether diuresis and natriuresis induced by endogen
ous atrial natriuretic peptide (ANP) were blunted during rapid cardiac
pacing. 2. Changes in plasma ANP renal function and haemodynamics dur
ing rapid cardiac pacing were studied in anaesthetized closed-chest do
gs. Dogs were paced via the right ventricle at a rate of 200 b.p.m. (m
oderate pacing) or 250 b.p.m. (severe pacing) for 180 min. 3. The maxi
mal increases in plasma ANP and urinary excretion of cGMP during sever
e pacing were four-and three-fold higher, respectively, than those dur
ing moderate pacing. Despite the higher concentration of plasma ANP, t
he maximal increases in urine volume, urinary excretion of sodium and
fractional excretion of sodium during severe pacing were similar to th
ose during moderate pacing. Mean arterial pressure and renal vascular
resistance were decreased only by severe pacing. The increase in total
peripheral resistance during severe pacing was significantly smaller
than that during moderate pacing. However, the glomerular filtration r
ate was kept at basal levels by both moderate and severe pacing. 4. Th
ese results suggest that there are certain mechanisms that counteract
renal tubular sodium reabsorption induced by endogenous ANP under cond
itions of severe pacing. The suppression occurs at tubular sites but n
ot at glomerular sites. One of the possibilities for the suppression i
s the decrease in renal perfusion pressure accompanied by decreases in
peritubular capillary hydrostatic pressure.