No abstract

Blood pressure (BP) variability is calculated as the standard deviation of ambulatory BP. Blood pressure variability is associated with the cardiovascular morbidity; however whether it is related to target organ damage is controversial. In this study we examined a possible relationship between the BP variability and left ventricular hypertrophy (LVH), and between BP variability and brachial-ankle pulse wave velocity (baPWV). The present study was conducted on 111 consecutive Japanese hypertensive patients who were hospitalized for the educational program in our hospital under stable sodium chloride intake (6 g/day). Blood pressure measurements were at 30-minute intervals all day. In a multivariable analysis adjusted with confounding factor, LVH was associated with 24-hour systolic BP (SBP), 24 hour diastolic BP (DBP), daytime SBP, daytime DBP, nighttime SBP, and nighttime DBP. Additionally, nighttime DBP variability was related to LVH. By the same method, baPWV as a dependent variable was related to 24-hour SBP and nighttime SBP. Furthermore, nighttime SBP variability was concerned with baPWV. The LVH was associated with not only BP level but also with nighttime DBP variability. The baPWV was also related not only to BP level but also to nighttime SBP variability.

The purpose of this study was to examine the possible difference in the 24-hr BP profile--including short-term BP variability, assessed as the standard deviation--between diabetic and non-diabetic hypertensives. We measured 24-hr ambulatory BP in 11 diabetic hypertensives (diabetic HT) and 10 non-diabetic hypertensives (non-diabetic HT) who were hospitalized for the educational program in our hospital and were under stable salt intake. Renal function and sleep apnea were also estimated. There were no significant differences in 24-hr systolic BP (141 mmHg vs. 135 mmHg, ns), daytime systolic BP (143 mmHg vs. 138 mmHg, ns), and nighttime systolic BP (135 mmHg vs. 130 mmHg, ns) between diabetic HT and non-diabetic HT. The values of 24-hr HR (69.7 beats/min vs. 65.2 beats/min, ns) and 24-hr HR variability (9.9 beats/min vs. 10.1 beats/min, ns) were also similar between the groups. Interestingly, diabetic HT had a significantly greater 24-hr systolic and diastolic BP variability than non-diabetic HT (18.2 mmHg vs. 14.5 mmHg, p < 0.05; 11.5 mmHg vs. 9.6 mmHg, p < 0.05, respectively). The values for creatinine clearance, urinary protein excretion, and apnea-hypopnea index were similar between the groups. Bivariate linear regression analysis demonstrated that fasting blood glucose was the primary determinant of 24-hr diastolic BP variability (r = 0.661, p < 0.01). Multiple stepwise regression analysis revealed that fasting blood glucose was a significant and independent contributor to 24-hr systolic BP variability (r = 0.501, p < 0.05). Taken together, these results demonstrate that BP variability is increased in diabetic hypertensives. Furthermore, it is possible that an elevation of fasting blood glucose may contribute to the enhanced BP variability in hypertensives.

Abstract-We previously cloned a novel molecule interacting with angiotensin II (Ang II) type 1 receptor protein (ATRAP) and showed it to be an endogenous inhibitor of Ang II type 1 receptor signaling in cardiovascular cells.In this study, we tested a hypothesis that the balance of tissue expression of ATRAP and Ang II type 1 receptor is regulated in a tissue-specific manner during the development of hypertension and related cardiac hypertrophy. T he renin-angiotensin system has been implicated in the pathogenesis of hypertension and cardiovascular remodeling based on the generation of angiotensin II (Ang II), a key regulator of cardiovascular homeostasis. The pathophysiological actions of Ang II are mediated by the Ang II type 1 receptor (AT1R). AT1R activates G proteins through the third intracellular loop and the intracellular carboxyl-terminal tail of the receptor. 1 The carboxyl-terminal end of AT1R is involved in the control of AT1R internalization independently of G protein coupling and plays an important role in linking receptor-mediated signal transduction to the specific biological response to Ang II such as cardiovascular remodeling. 2 We previously cloned a novel AT1R-associated protein (ATRAP) that specifically interacts with the carboxylterminal domain of AT1R. 3,4 We showed that ATRAP is expressed in many tissues such as the kidney, heart, and liver. 5 Previous studies showed that ATRAP exerts its inhibitory action on AT1R signaling by promoting a constitutive internalization of AT1R and decreasing the cell surface AT1R number. 6,7 In this study, we examined whether the expression of ATRAP is regulated in a tissue-specific manner in spontaneously hypertensive rats (SHR). We further investigated whether the balance of tissue expression of ATRAP and AT1R in SHR is modulated during the development of hypertension and by the treatment with the AT1R-specific blocker olmesartan at either a depressor or subdepressor dose.