Impaired renal vascular response to a D-1-like receptor agonist but not toan ACE inhibitor in conscious spontaneously hypertensive rats

The natriuretic response to a dopamine 1-like receptor agonist is blunted i n spontaneously hypertensive rats (SHRs). Whether the renal vasodilator res ponse to D-1-like receptor stimulation in SHRs is defective also is unclear . To determine whether the renal hemodynamic response to a D-1-like recepto r is impaired in SHR, we examined the effect of a continuous infusion of th e D-1-like receptor agonist fenoldopam (2 mu g/kg/min) on systemic and rena l hemodynamics in conscious SHRs and Wistar-Kyoto (WKY) rats. As an active control, we used an equivalent antihypertensive dosage of captopril (10 mg/ kg). Fenoldopam significantly increased effective renal plasma flow (ERPF) in WKY rats (+22 +/- 5%; p < 0.01), whereas this response was absent in SHR s (+7 +/- 3%; NS). Mean arterial pressure (MAP) was significantly reduced i n SHRs (-11 +/- 2%; p < 0.001), demonstrating a systemic vasodilator respon se to fenoldopam in SHRs. The reduction in renal vascular resistance (RVR) was more pronounced in WKY rats (-24 +/- 2%) than in SHRs (-13 +/- 4%; p < 0.05). Captopril significantly increased ERPF in SHRs (+16 +/- 3%; p < 0.00 1), demonstrating a preserved renal vasodilatory capacity in SHRs. The blun ting of the renal vasodilatory response to fenoldopam in SHRs is present du ring a high as well as a low sodium intake. In conscious SHRs, the renal va sodilatory response to a D-1-like receptor agonist is impaired, whereas the blood pressure response is more pronounced. The preserved renal vasodilato ry response to captopril indicates that the defective vasodilatory response in SHRs is functional rather than due to altered structural properties of the renal vascular bed.