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Concerted regulation of renal plasma flow and glomerular filtration rate by renal
dopamine and NOS I in rats on high salt intake
#MMPMID28351967
Ibarra ME
; Albertoni Borghese MF
; Majowicz MP
; Ortiz MC
; Loidl F
; Rey-Funes M
; Di Ciano LA
; Ibarra FR
Physiol Rep
2017[Mar]; 5
(6
): ? PMID28351967
show ga
Under high sodium intake renal dopamine (DA) increases while NOS I expression in
macula densa cells (MD) decreases. To explore whether renal DA and NOS I, linked
to natriuresis and to the stability of the tubuloglomerular feedback,
respectively, act in concert to regulate renal plasma flow (RPF) and glomerular
filtration rate (GFR). Male Wistar rats were studied under a normal sodium intake
(NS, NaCl 0.24%) or a high sodium intake (HS, NaCl 1% in drinking water) during
the 5 days of the study. For the last two days, the specific D(1)-like receptor
antagonist SCH 23390 (1 mg kg bwt(-1) day(-1), sc) or a vehicle was administered.
HS intake increased natriuresis, diuresis, and urinary DA while it decreased
cortical NOS I expression (P < 0.05 vs. NS), Nicotinamide adenine dinucleotide
phosphate diaphorase (NADPH-d) activity in MD (P < 0.001 vs. NS) and cortical
nitrates+nitrites (NOx) production (NS 2.04 ± 0.22 vs. HS 1.28 ±
0.10 nmol mg protein(-1), P < 0.01). Treatment with SCH 23390 to rats on HS
sharply decreased hydroelectrolyte excretion (P < 0.001 vs. HS) while NOS I
expression, NADPH-d activity and NOx production increased (P < 0.05 vs. HS for
NOS I and P < 0.001 vs. HS for NADPH-d and NOx). SCH 23390 increased RPF and GFR
in HS rats (P < 0.01 HS+SCH vs. HS). It did not cause variations in NS rats.
Results indicate that when NS intake is shifted to a prolonged high sodium
intake, renal DA through the D(1)R, and NOS I in MD cells act in concert to
regulate RPF and GFR to stabilize the delivery of NaCl to the distal nephron.
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