0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Diabetes-Induced Vascular Hypertrophy Is Accompanied by Activation of Na + -H + Exchange and Prevented by Na + -H + Exchange Inhibition

      Read this article at

      ScienceOpenPublisher
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Related collections

          Most cited references 23

          • Record: found
          • Abstract: found
          • Article: not found

          Pathogenesis, prevention, and treatment of diabetic nephropathy.

           M. J. Cooper (1998)
          It is likely that the pathophysiology of diabetic nephropathy involves an interaction of metabolic and haemodynamic factors. Relevant metabolic factors include glucose-dependent pathways such as advanced glycation, increased formation of polyols, and activation of the enzyme, protein kinase C. Specific inhibitors of the various pathways are now available, enabling investigation of the role of these processes in the pathogenesis of diabetic nephropathy and potentially to provide new therapeutic approaches for the prevention and treatment of diabetic nephropathy. Haemodynamic factors to consider include systemic hypertension, intraglomerular hypertension, and the role of vasoactive hormones, such as angiotensin II. The mainstay of therapy remains attaining optimum glycaemic control. Antihypertensive therapy has a major role in slowing the progression of diabetic nephropathy. Agents that interrupt the renin-angiotensin system such as angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists may be particularly useful as renoprotective agents in both the hypertensive and normotensive context.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Small artery structure in hypertension. Dual processes of remodeling and growth.

              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Hoe 694, a new Na+/H+ exchange inhibitor and its effects in cardiac ischaemia.

              1. The benzoylguanidine derivative Hoe 694 ((3-methylsulphonyl-4- piperidino-benzoyl) guanidine methanesulphonate) was characterized as an inhibitor of Na+/H+ exchange in rabbit erythrocytes, rat platelets and bovine endothelial cells. The potency of the compound was slightly lower or comparable to ethylisopropyl amiloride (EIPA). 2. To investigate a possible cardioprotective role of the Na+/H+ exchange inhibitor Hoe 694, rat isolated working hearts were subjected to ischaemia and reperfusion. In these experiments all untreated hearts suffered ventricular fibrillation on reperfusion. Addition of 10(-7) M Hoe 694 to the perfusate almost abolished reperfusion arrhythmias in the rat isolated working hearts. 3. Hoe 694 reduced the release of lactate dehydrogenase (LDH) and creatine kinase (CK), which are indicators of cellular damage during ischaemia, into the venous effluent of the hearts by 60% and 54%, respectively. 4. The tissue content of glycogen at the end of the experiments was increased by 60% and the high energy phosphates ATP and creatine phosphate were increased by 240% and 270% respectively in the treated hearts as compared to control hearts. 5. Antiischaemic effects of the Na+/H+ exchange inhibitor, Hoe 694, were investigated in a second experiment in anaesthetized rats undergoing coronary artery ligation. In these animals, pretreatment with Hoe 694 caused a dose-dependent reduction of ventricular premature beats and ventricular tachycardia as well as a complete suppression of ventricular fibrillation down to doses of 0.1 mg kg-1, i.v. Blood pressure and heart rate remained unchanged. 6. We conclude that the new Na+/H+ exchange inhibitor, Hoe 694, shows cardioprotective and antiarrhythmic effects in ischaemia and reperfusion in rat isolated hearts and in anaesthetized rats. In view of the role which Na+/H+ exchange seems to play in the pathophysiology of cardiac ischaemia these effects could probably be attributed to Na+/H+ exchange inhibition.
                Bookmark

                Author and article information

                Journal
                Circulation Research
                Circulation Research
                Ovid Technologies (Wolters Kluwer Health)
                0009-7330
                1524-4571
                December 08 2000
                December 08 2000
                : 87
                : 12
                : 1133-1140
                Affiliations
                [1 ]From the Department of Medicine (K.J.-D., T.J.A., J.R.R., R.E.G., M.E.C.), University of Melbourne, Austin and Repatriation Medical Centre–Repatriation Campus, West Heidelberg, and Cell Biology of Diabetes Laboratory (K.M.H., C.A.F., P.J.L.), Baker Medical Research Institute, Melbourne, Victoria, Australia.
                Article
                10.1161/01.RES.87.12.1133
                704a8893-4be8-4674-a531-e23e59563ec7
                © 2000

                Comments

                Comment on this article