Blood Pressure In Stroke-prone Research Articles

Inhibition of Rac1-Derived Reactive Oxygen Species in Nucleus Tractus Solitarius Decreases Blood Pressure and Heart Rate in Stroke-Prone Spontaneously Hypertensive Rats

Reactive oxygen species (ROS) in the brain are thought to contribute to the neuropathogenesis of hypertension by enhancing sympathetic nervous system activity. The nucleus tractus solitarius (NTS), which receives afferent input from baroreceptors, has an important role in cardiovascular regulation. reduced nicotinamide-adenine dinucleotide phosphate oxidase is thought to be a major source of ROS in the NTS. Rac1 is a small G protein and a key component of reduced nicotinamide-adenine dinucleotide phosphate oxidase. The role of Rac1-derived ROS in the NTS in cardiovascular regulation of hypertension is unknown. Therefore, we examined whether inhibition of Rac1 in the NTS decreases ROS generation, thereby reducing blood pressure in stroke-prone spontaneously hypertensive rats (SHRSPs). The basal Rac1 activity level in the NTS was greater in SHRSPs than in Wistar-Kyoto rats. Inhibition of Rac1, induced by transfecting adenovirus vectors encoding dominant-negative Rac1 into the NTS, decreased blood pressure, heart rate, and urinary norepinephrine excretion in SHRSPs but not in Wistar-Kyoto rats. Inhibition of Rac1 also reduced nicotinamide-adenine dinucleotide phosphate oxidase activity and ROS generation. In addition, Cu/Zn-superoxide dismutase activity in the NTS of SHRSPs was decreased compared with that of Wistar-Kyoto rats, despite the increased ROS generation. Overexpression of Cu/Zn-superoxide dismutase in the NTS decreased blood pressure and heart rate in SHRSPs. These results indicate that the activation of Rac1 in the NTS generates ROS via reduced nicotinamide-adenine dinucleotide phosphate oxidase in SHRSPs, and this mechanism might be important for the neuropathogenesis of hypertension in SHRSPs.

The effects of maternal mild protein restriction on stroke incidence and blood pressure in stroke-prone spontaneously hypertensive rats (SHRSP).

The effect of maternal protein restriction during pregnancy on the offspring's blood pressure was assessed in stroke-prone spontaneously hypertensive rats (SHRSP) which are genetically predisposed to hypertension and stroke. After the confirmation of pregnancy, the control group was given a 20% casein diet, and the low-protein group was fed a 9% casein diet. After the confirmation of delivery, commercial feed was given to both of the groups. No differences were seen between the control and low-protein offspring in regard to body weight, blood pressure elevation, or life span. One percent saline solution was put in the control and low-protein groups after the age of 11 weeks. Blood pressure increased markedly in the low-protein group, on the blood pressure level in the low-protein group on week 2 after salt loading (242+/-6 mmHg) was significantly higher than that in the control group (223+/-9 mmHg; p<0.05). The survival duration was significantly shorter in the low-protein group (113+/-4 days) than in the control group (135+/-22 days; p<0.05). These results suggest that maternal protein malnutrition in SHRSP exerted a high salt sensitivity and a malignant influence on stroke incidence on offspring.

Effects of long term oral administration of ketanserin and trichlormethiazide on blood pressure in stroke-prone spontaneously hypertensive rats.

Effects of long term oral administration of ketanserin and trichlormethiazide on blood pressure in stroke-prone spontaneously hypertensive rats.

Angiotensin Converting Enzyme (ACE) in the Kidney

With regard to the concept of the local action of the renin angiotensin system (RAS) involved in blood pressure regulation, the presence of angiotensin converting enzyme (ACE) in a variety of organs suggests that locally produced angiotensin II (ANG II) shares, at least to some extent, the actions of this peptide on respective target organs of ANG II. However, renal ACE is less well understood for its relationship between blood pressure and enzyme activity. In our present studies, with a single oral administration of enalapril to spontaneously hypertensive rats, the inhibition of renal cortical and aortic ACE, but not plasma ACE, coincided with a reduction in blood pressure. Development of high blood pressure in stroke-prone, spontaneously hypertensive rats (SHRSP) from 7 to 22 weeks of age was accompanied by an increase in ACE activity in the renal cortex. Aortic and pulmonary ACE also tended to increase with age, but was less prominent. Isolated brush-border membranes contained abundant ACE, both in Wistar-Kyoto rats and SHRSP, and the levels of ACE in renal cortical homogenates closely correlated to the levels of brush-border ACE. Thus, changes in renal cortical ACE activity in response to the ACE inhibition and in cases of SHRSP in relation to aging are apparently associated with changes in blood pressure. It is likely that renal cortical ACE activity reflects the enzyme activity in the brush borders. Thus, brush-border ACE should probably be taken into account when discussing possible roles of renal ACE.

Partial Replacement of Sodium by Potassium in the Diet Restores Impaired Noradrenaline Inactivation and Lowers Blood Pressure in Stroke-Prone Spontaneously Hypertensive Rats

1. Partial replacement of sodium by potassium in the diet attenuates the rise in blood pressure in stroke-prone spontaneously hypertensive rats (SHR-SP). 2. The blood pressure-lowering effect of potassium cannot be ascribed to a reduction in intravascular volume. 3. The increased dietary intake of potassium leads to a reduced stimulation of the sympathoneuronal and sympathoadrenal system by cold compared with the response of sodium-loaded rats. 4. The impaired inactivation of noradrenaline observed in sodium-loaded SHR-SP is improved in SHR-SP on a potassium-substituted diet. 5. It is concluded that changes in dietary intake of sodium and potassium modulate sympathetic activity and the metabolism of noradrenaline, both of which are related to the development of hypertension in SHR-SP.