SODIUM INTAKE MODULATES RENAL VASCULAR REACTIVITY TO ENDOTHELIN‐1 IN DAHL RATS

1. The systemic and renal haemodynamic responses to endothelin‐1 (ET1) were evaluated and compared to Angiotensin II (AII) in anaesthetized Dahl salt‐sensitive (DS) and salt‐resistant (DR) rats on either low (0.1% NaCl in diet) or high (8% NaCl in diet) salt intake. 2. Baseline mean arterial pressure on low salt diet was similar in both strains, while on high salt diet it was 73 ± 4 mmHg in DR rats and 119 ± 8 mmHg in DS rats (P<0.05). Baseline renal blood flow (RBF) and renal vascular resistance (RVR) were similar in all groups. 3. AII in bolus injection induced a short, dose‐dependent increase in blood pressure and renal vascular resistance and a fall in renal blood flow. The maximal pressure increase was significantly greater in DS rats on high salt diet than that in each of the other groups (P<0.05). The fall in renal blood flow and the increase in renal vascular resistance were attenuated in both strains on low salt diet. 4. ET1 induced an initial decrease followed by a prolonged increase in blood pressure; both phases were similar in all groups. However, renal vascular reactivity to ET1 was markedly modulated by salt intake. On low salt diet, following a bolus injection of ET1 (1 nmol/kg), RBF decreased by 34% in DR and by 20% in DS rats, while on high salt diet RBF decreased by 34% in DR and by 80% in DS rats (P<0.05 high vs low salt). RVR increased only by 98% and 72% on low salt diet in DR and DS rats, respectively (P<0.05 vs baseline), whereas on high salt diet RVR increased by 584% and 554% in DR and DS rats respectively (P<0.05 high vs low salt). 5. It is concluded that DS rats are not hypersensitive to ET1 as they are to other pressor agents, and that salt intake, rather than blood pressure, modulates substantially the renal vascular reactivity to ET1.