The major characteristic of renal hemodynamics in hypertension is abnormally high resistance of the preglomerular vessel, most likely the afferent arteriole (Af-Art). Although endothelium-derived relaxing factor (EDRF)/nitric oxide (NO) has been studied extensively in large vessels, little is known about its role in Af-Art reactivity. Using isolated microperfused Af-Arts of 12- to 13-week-old spontaneously hypertensive rats (SHRs) and their normotensive control, Wistar-Kyoto (WKY) rats, we examined the effect of acetylcholine (ACh) or N(ω)-nitro-L-arginine (L-NAME), which stimulates or blocks endothelium-derived NO, respectively. Af-Arts were preconstricted with norepinephrine to 70 ± 5 and 62 ± 4% of the control diameter in SHRs and WKY rats, respectively; the intraluminal pressure was kept at either 100 or 70 mm Hg. In SHRs, ACh (1 nM-0.1 mM) added to the Af- Art perfusate caused no vasodilation but tended to decrease the diameter further to 59 ± 6% of control (N = 8). In contrast, in WKY rats, ACh reversed the luminal diameter to 90 ± 4% of control (N = 6, p < 0.01 compared with SHRs). Contrary to the responses to ACh, blockade of endothelium-derived NO with L-NAME decreased the basal diameter by 31 ± 8 and 14 ± 5% in SHRs and WKY rats, respectively. We conclude that ACh- induced vasodilation is impaired in SHR Af-Art. The impaired response to ACh may be due to factors other than endothelium-derived NO such as endothelium- derived contracting factor (EDCF).
- Glomerular hemodynamics
- N(ω)- nitro-L-arginine
- Renal microcirculation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine