DITHIOTHREITOL-INDUCED ALTERATIONS OF BLOOD-PRESSURE, VASCULAR REACTIVITY AND AORTIC MICROSOMAL CALCIUM-UPTAKE IN SPONTANEOUSLY HYPERTENSIVE RATS

Abstract

Dithiothreitol, a potent sulfhydryl reducing agent, depressed systolic blood pressure to a greater extent in genetically hypertensive rats (SHR) than in normotensive Wistar-Kyoto rats (WKY). Dithiothreitol depressed the contractile response to norepinephrine and KCl of isolated aortic strips from both SHR and WKY. Dithio-bis-2-nitrobenzoid acid, a sulfhydryl oxidizing agent, restored the responsiveness of rat aortic strips to these contractile agents. Microsomes isolated from rat aortae sequester Ca in the presence of ATP. This activity, generally referred to as Ca-pump activity, was postulated to function in smooth muscle relaxation and is significantly depressed in aortic microsomes of the SHR. Dithiothreitol (10 mM) greatly increased and dithio-bis-2-nitrobenzoic acid (100 mM) decreased the ATP-dependent Ca pump activity of microsomes isolated from both SHR and WKY aortae. Sulfhydryl groups may influence systems involved in vascular reactivity and blood pressure regulation.