The loss of endothelium-dependent vascular relaxation in hypertension.
We investigated endothelium-dependent relaxation in rat aortae, using three models of experimental hypertension: deoxycorticosterone and salt; one-kidney, one clip renovascular hypertension; and coarctation. Isolated aortae were contracted with phenylephrine, and relaxation was subsequently induced with acetylcholine or calcium ionophore A23187. Blood vessels denuded of endothelium did not relax in response to acetylcholine or A23187. Blood vessels from animals with high blood pressure had decreased relaxation responses to acetylcholine and A23187, and also to the endothelium-independent vasodilator sodium nitroprusside. Unlike acetylcholine and A23187, however, nitroprusside completely relaxed the blood vessels from the hypertensive animals, though the sensitivity to nitroprusside was much lower in these vessels. Subsequent reversal of hypertension caused a return of endothelium-dependent relaxation. Loss of endothelium-dependent relaxation occurs readily in the aortae with the development of hypertension; this phenomenon appears to be related to elevated pressure.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D003900:Desoxycorticosterone; D006973:Hypertension / Q000503:physiopathology*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide; D051381:Rats; D011919:Rats, Inbred Strains; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000378:metabolism*
D001095:Arachidonic Acids; D014665:Vasodilator Agents; D016718:Arachidonic Acid; D009569:Nitric Oxide; D000001:Calcimycin; D003900:Desoxycorticosterone; D000109:Acetylcholine; D007213:Indomethacin