The influence of increased lability of blood pressure on the development of aortic atherosclerosis was examined. Because sinoaortic denervation (SAD) produced increased lability of blood pressure without blood pressure elevation, the development of atheromatous plaque was examined in SAD rats. These rats were fed a high-cholesterol diet and were denuded of endothelium so that development of atherosclerosis was accelerated. Five groups of male Wistar rats were used: A) controls, B) high-cholesterol diet (HC), C) HC+denudation (DN), D) HC+DN+renal artery clipping (2K1C), and E) HC+DN+sinoaortic denervation (SAD). Denudation was accomplished by scraping the aortic lumen with a balloon catheter, and hypertension was induced by clipping the left renal artery. After recording blood pressure and heart rate for 6 weeks, the rats were killed, blood samples were collected, and thoracic aortas were removed for pathologic examination. All the groups of rats fed a high-cholesterol diet developed marked hypercholesterolemia and hypotriglyceridemia. High-cholesterol diet alone could not induce aortic atherosclerosis, whereas aorta of HC+DN rats showed slight intimal thickening with smooth muscle cell proliferation. On the other hand, aorta of HC+DN + 2K1C rats showed marked atheromatous plaque with prominent cellular proliferation, and aorta of SAD rats also showed mild to moderate atheromatous plaque. Accordingly, we concluded that increased variability in circadian blood pressure per se, as well as hypertension, could induce aortic atherosclerosis in the hypercholesterolemic and endothelium-denuded rats.
We report a normomagnesemic patient with low normal blood pressure, hypokalemic alkalosis, hyperreninemia, hyperaldosteronism, and hypocalciuria. In renal clearance studies, distal delivery increased well and fractional distal solute reabsorption was dramatically diminished after the administration of furosemide, whereas thiazide produced no change in distal delivery and a moderate decrease in fractional distal solute reabsorption. These findings suggested that there may have been a defective locus in some part of the thiazide-sensitive segment of the distal convoluted tubule. As the features in this patient appear to be similar to those in Gitelman's syndrome, it is appropriate to designate this case, characterized by lack of hypomagnesemia, as a subgroup of Gitelman's syndrome.
1.To elucidate whether baroreflex could contribute to manifest the diurnal blood pressure variations (DBPV) in normotension and hypertension, DBPV were recorded continuously via a femoral artery in awake normotensive (NT) rats and spontaneously hypertensive rats (SHR) with and without sinoaortic denervation (SAD). To determine the role of central cuz-adrenergic receptor system in DBPV in hypertension, guanabentz (0.5-1.0pg/kg per min) was infused in SHR.2. There were no differences in mean arterial pressure (MAP) variability (SD) of MAP of 24 h (MAP -SD/MAP) and SD of 24 h heart rate (HR -SD/HR) between SHR and NT. SAD did not elevate MAP and HR in both SHR and NT.3. However, in SAD rats, MAP -SD/MAP was significantly greater than those in sham-operated rats in both SHR and NT, while MAP -SD/MAP and HR -SD/HR did not show any difference between the two groups even after SAD.On the other hand, SAD did not augment HR -SD/HR in either strain.4. During guanabentz infusion, MAP was significantly lowered in sham-operated and SAD-SHR. Moreover, MAP -SD/MAP was significantly reduced in sham-operated, but it was not in SAD-SHR.5. These findings suggest that baroreflex could suppress tonically the diurnal change of blood pressure in NT and SHR. The regulation of diurnal blood pressure by baroreflex via a central a-adrenergic receptor system may be altered in SHR.
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