Abstract
The role of inflammation in afferent arteriole (AA) function in DOCA‐salt hypertension was studied using the blood‐perfused juxtamedullary nephron technique. DOCA rats receiving the anti‐inflammatory agent, pentosan polysulfate (PPS) for 3 weeks developed hypertension similarly to DOCA alone (181±5 vs. 180±7mmHg) and basal AA diameters were also similar (15.2±0.9 vs. 16.2±0.4μm, n=9‐11). AA autoregulation was normal in sham rats (uninephrectomy). Step (15mmHg) increases in perfusion pressure from 65‐170mmHg caused pressure‐dependent AA constriction to 68±3% of control at 170mmHg. Pressure‐mediated AA responses were markedly attenuated in DOCA rats. Diameter remained between 90 and 101% of control over the range of PP studied, indicating a loss of autoregulation. PPS partially restored autoregulation in DOCA rats. Diameters were 110±2 and 76±3% of control at 65 and 170mmHg, respectively. AA responses to a P2X1 receptor agonist, ?,γ ‐methylene ATP (0.01 to 100μM) were assessed in separate groups. PPS improved the attenuated AA constriction to ?,γ ‐methylene ATP in DOCA rats. The maximal vasoconstriction was 81±6% of control compared to 70±2% in sham and 90±1% in DOCA (p<0.05). In conclusion, inflammatory processes contribute to AA dysfunction in DOCA‐salt hypertension by impairing autoregulation and AA reactivity to P2X1 receptor activation.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
