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. Author manuscript; available in PMC: 2021 Nov 1.
Published in final edited form as: Hypertension. 2020 Sep 28;76(5):1461–1469. doi: 10.1161/HYPERTENSIONAHA.120.15928

Figure 1. Impact of high dietary sodium intake on blood pressure and NCC activity in Dahl rats.

Figure 1.

(A) Mean arterial pressure (MAP; mmHg), peak ΔMAP (mmHg) in response to i.v. hexamethonium (30 mg/kg), in-vivo NCC activity expressed as peak natriuretic response (ΔUNaV) to intravenous hydrochlorothiazide (HCTZ; 2 mg/kg bolus, 2 mg/kg hour infusion), in-vivo ENaC activity expressed as peak ΔUNaV to intravenous amiloride (2 mg/kg bolus, 2 mg/kg hour infusion), renal NE (pg/mg) and plasma norepinephrine (NE, nmol/L); (B) representative immunoblots for NCC, pNCCT53 and total NCC expression, pNCCT53 expression, pNCC/NCC ratio, and FENa (%) in 3-month old male Dahl Salt-Resistant (DSR) and Dahl Salt-Sensitive (DSS) rats fed a 21-day normal salt (NS; 0.6% NaCl) or high salt (HS; 4% NaCl) diet N=5/6 per group mean ± SD. Protein expression is shown as fold change with NS target protein expression set to 1 for each group. MAP = mean arterial pressure, UNaV = urinary sodium excretion, NE = norepinephrine, FENa = Fractional Excretion of Sodium. Differences in peak natriuretic responses, MAP, plasma and renal NE, and protein expression within each group between NS and HS diets were determined using a student’s t test. *P < 0.05 vs. respective NS group.