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.
Magliola
L
L
Department of Physiology, School of Medicine, Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65212, USA. magliolal@missouri.edu
Jones
A W
AW
D000450:Aldosterone; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D017538:Mesenteric Artery, Superior / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D016861:Cyclooxygenase Inhibitors; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D000450:Aldosterone; D011188:Potassium; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine; D007213:Indomethacin