Size dependence of functional alterations in mesenteric arteries from the aldosterone-salt hypertensive rat

We tested the hypothesis that an elevated potassium-42 ((42)K(+)) efflux (highly dependent on Ca(2+)) and an increase in the sensitivity of contraction and (42)K(+) efflux to norepinephrine (NE) in conduit arteries of aldosterone-salt hypertensive rats (AHR) extended to smaller, distributing arteries. Functional endpoints were compared in two sizes of arteries from the mesenteric bed: second-order branches of the superior mesenteric artery (SMA branches) and the SMA. Contraction and free cytosolic Ca(2+) concentration ([Ca(2+)](c); fura-2 microfluorometry) were measured simultaneously and (42)K(+) efflux was measured separately in SMA branches. Contraction and (42)K(+) efflux were measured separately in SMA. Basal tone, [Ca(2+)](c), and (42)K(+) efflux were similar in SMA branches from AHR and control-salt rats (CSR). However, basal (42)K(+) efflux was elevated in SMA from AHR compared to CSR. The sensitivity of the contractile, [Ca(2+)](c), and (42)K(+) efflux responses to NE was similar in SMA branches. In contrast, the sensitivity of the contractile and (42)K(+) efflux responses to NE was enhanced in SMA from AHR compared to CSR. Inhibiton of endothelium-derived vasoactive substances by pretreatment with N(omega)-nitro-L-arginine methyl ester and indomethacin significantly shifted the NE concentration-response relationships to the left for contraction, [Ca(2+)](c), and (42)K(+) efflux in both SMA branches and SMA from CSR. A similar shift to the left was observed in AHR for contraction but not consistently for [Ca(2+)](c) and (42)K(+) efflux. We conclude that SMA branches from AHR demonstrate neither the elevated basal (42)K(+) efflux, nor the NE supersensitivity exhibited by SMA. Endothelial function was not impaired both in SMA and SMA branches.