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. Author manuscript; available in PMC: 2021 Mar 1.
Published in final edited form as: Kidney Int. 2019 Oct 22;97(3):528–537. doi: 10.1016/j.kint.2019.09.025

Figure 1. Renal dysfunction was present in the hypertensive SS rats, but was abrogated in the SSEts1+/− rats despite similar increases in telemetry blood pressures.

Figure 1

A, SSEts1+/− and the control SS rats were maintained on a 0.3% NaCI diet and then fed a 4% NaCI diet for one week. BP was monitored by radio-telemetry. At baseline, mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) did not differ between SS (Solid line) and SSEts1+/− (Dashed line) rats. One week of high salt intake significantly increased SBP and DBP in both SS and SSEts1+/− rats (*p-value < 0.05, n=6); the increase in SBP and DBP did not differ (p-value >0.05, HT SS vs. HT SSEts1+/−, n=6) between SSEts1+/− and SS rats. B, With the development of hypertension, mean serum creatinine concentrations of the HT SS and HT SSEts1+/− groups were higher than both Pre-HT groups; however, mean serum creatinine levels were less in the HT SSEts1+/− group, compared with HT SS (#p-value <0.05, n=8). C, After one week of high salt intake, HT SS rats also showed a significant increase in the urinary excretion of albumin as compared with the other three groups of rats (#p-value < 0.05, n=8).