Genetics and salt modulate renal responses to atrial natriuretic factor.

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.