Dahl S rats have increased natriuretic factor in atria but are markedly hyporesponsive to it.

Abstract

Three experiments were carried out to determine whether atrial natriuretic factor (ANF) plays a part in Dahl hypertension. Results showed that ANF from both atria from 13 Dahl salt-sensitive (S) rats that had been fed a 4% NaCl diet for 12 weeks induced an average peak Na excretion of 23.0 muEq/min/g kidney in 13 Sprague-Dawley (SD) recipients vs 12.6 from atria from 13 salt-resistant (R) rats fed 4% NaCl (-45%, p less than 0.01), possibly indicating greater ANF secretion in S rats in order to enhance a reduced Na excretion. In 13 R rats, the ANF content in both atria increased from 14.0 after a 0.11% NaCl diet to 23.7 after 5 days of 4% NaCl diet (p less than 0.001) and then back to 12.6 after 12 weeks of 4% NaCl (p less than 0.001). Thus, ANF almost doubled after brief Na loading but returned to normal during continued Na loading. In S rats with a tendency to Na retention, ANF was elevated to about 23 in all three periods. ANF produced a 130-fold increase in natriuresis and a renal papillary plasma flow ( RPPF ) of 30.8 ml/min/100 g, 41% above the control level of 21.7, p less than 0.001. The marked increase in RPPF is very likely a partial cause of the natriuresis. A constant amount of ANF was continuously infused intravenously into 10 S rats and nine R rats all on 0.11% NaCl diets. Mean Na excretions in R and S were 5.3 and 4.6 muEq/min/100 g kidney before ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Dual hemodynamic mechanisms for salt-induced hypertension in Dahl salt-sensitive rats.

“…Pitcock et al 14 demonstrated that DS rats have fewer renomedullary interstitial cells than DR rats; whether deficiency of a putative antihypertensive lipid elaborated by these cells is implicated in the hypertension of salt-sensitive rats is unknown. Studies by Hirata et al 15 on the isolated perfused kidney indicated lower renal papillary plasma flow in DS as compared with DR rats; they demonstrated that DS rats had increased natriuretic factor in their atria but that their kidneys were hyporesponsive to this factor. DS rats on a high salt diet have a lower glomerular filtration rate, despite a higher perfusion pressure as compared with DR rats; there is a shift of the arterial pressure-glomerular filtration rate curve so that glomerular filtration rate is less for any given pressure because of exaggerated afferent arteriolar vasoconstriction.…”

Intrarenal Localization of Receptors for α-Rat Atrial Natriuretic Polypeptide: An Autoradiographic Study with [125I]-Labeled Ligand Injected in Vivo into the Rat Aorta

“…Since ANP has been shown to exhibit a marked vasodilating activity (9), it is reasonable to assume that ANP causes the vasodilation of the vasa recta leading to an increase in the renal papillary plasma flow as reported by Borenstein et al (10) and Hirata et al (11). Histotopographical studies in the rat showed that the thin descending limb of the short-loop nephron is located so that it is in close contact with the vasa recta (12).…”

Proposition of a Feasible Protocol to Evaluate Salt Sensitivity in a Population-Based Setting.

“…Second, salt-sensitive subjects may have impaired natriuretic responses to ANP, which could cause sodium-water retention in the body and lead to suppression of PRA. In this regard, it is worth noting that hypo-responsiveness to ANP has been suggested to be etiologically related to blunted natriuresis and other hemodynamic abnormalities in the Dahl salt-sensitive rat (22). Nonetheless, it remains to be clarified whether hypo-responsiveness to ANP occurs in salt-sensitive subjects, and if so, whether it contributes to the development of salt-induced hypertension.…”