Fig. 8.

CD161a⁺ immune cell ablation prevents cholinergic hypertension, decreases renal sodium retention, and renal expression of sodium-potassium chloride cotransporter (NKCC2). Young 3- to 4-wk-old spontaneously hypertensive rats underwent intraperitoneal injection of either Isotype Control IGG (n = 5) or anti-CD161a specific antibodies (n = 5) in conjunction with subcutaneous infusion of nicotine (15 mg·kg⁻¹·day⁻¹) for a 2-wk period. A: systolic blood pressure (SBP) was measured throughout the infusion period. Urine, serum, and renal tissues were collected at the end of the infusion period with measurements of sodium, creatinine, and protein. BM, bone marrow. B: spot urinary sodium (left), fractional excretion of sodium (FeNa; middle), and renal function (as measured by urinary protein to creatinine ratio; right) were determined by colorimetric assay. C and D: renal expression of NKCC2 was determined by Western blot analysis on renal homogenates (C) and markers of anti-inflammatory M2 markers (D) were determined by RT-PCR on renal tissue. Student’s t-test was conducted to determine significance between the CD161a ablation and isotype IGG-treated groups. Error bars represent means ± SD. *P < 0.05, **P < 0.01, and ***P < 0.001.