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. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: Hypertension. 2018 Nov;72(5):1172–1179. doi: 10.1161/HYPERTENSIONAHA.118.11694

Figure 4. RMIC COX-2 deficiency caused salt-sensitive hypertension and papillary damage in response to chronic salt loading Both COX-2f/f and RMIC COX-2−/− mice were fed with a high salt diet (8% NaCl) after tamoxifen administration for 2 weeks.

Figure 4

A: Systolic blood pressure (SBP) was monitored with tail cuff microphonic manometer following initiation of high salt treatment (8% NaCl). High salt administration had no apparent effect on blood pressure in COX-2f/f mice throughout experiment period, but increased blood pressure in RMIC COX-2 deficient mice for the first 5 weeks, and then led to progressively decreased blood pressure. N= 7 in COX-2f/f mice and n = 6 RMIC COX-2−/− mice. All values are means ± SEM.

B: Diastolic blood perssure (SBP), systolic blood pressure (SBP) and mean arterial pressure (MAP) measured by carotid catheterization after a high salt diet for 4–5 weeks was markedly higher in RMIC COX-2−/− mice than in COX-2f/f mice. **P < 0.01; n = 8 in COX-2f/f mice and n = 6 in RMIC COX-2−/− mice.

C and D: Both COX-2f/f and RMIC COX-2−/− mice were fed with a high salt diet (8% NaCl) for 9 weeks, and then fed with normal chow for 3 weeks. C: Blood pressure was markedly lower in RMIC COX-2−/− mice than in COX-2f/f mice. ***P < 0.001; n= 7 in COX-2f/f mice and n = 6 RMIC COX-2−/− mice.

D: Urine osmolality was markedly lower in RMIC COX-2−/− mice than in COX-2f/f mice after 16 hours of water deprivation. **P < 0.01; n= 6 in COX-2f/f mice and n = 5 RMIC COX-2−/− mice.

All values are shown as mean ± SEM. P values were calculated by Student’s t test.