We examined the consequences of
genetic susceptibility or resistance to NaCl-induced
hypertension and of prior
salt loading (high or low NaCl intake) on the responses of isolated perfused Dahl
salt-sensitive (DS) and Dahl
salt-resistant rat (DR) kidneys to
atriopeptin II.
Atriopeptin II increased the glomerular filtration rate only in kidneys from high NaCl-fed rats, irrespective of their DS or DR status. Superimposition of
norepinephrine on
atriopeptin II further increased the glomerular filtration rate only in kidneys from low NaCl-fed rats (which had not reacted to
atriopeptin II alone), irrespective of their DS or DR status, and did not change the glomerular filtration rate of high NaCl-fed rats.
Norepinephrine alone, without
atriopeptin II, uniformly decreased the glomerular filtration rate by about 80%.
Atriopeptin II increased
sodium excretion of high NaCl and low NaCl DR kidneys by more than five times as much as in the corresponding DS kidneys. Therefore, the glomerular filtration rate response to
atriopeptin II varied globally with dietary NaCl, independently of
genetic predisposition or resistance to NaCl-induced
hypertension. The natriuretic response to
atriopeptin II was blunted in kidneys from rats genetically susceptible to NaCl-induced
hypertension, independently of their NaCl consumption.
Atriopeptin II also ameliorated or reversed the adverse effect of
norepinephrine on the glomerular filtration rate.