Abstract-Accurate measurement of blood pressure is essential to classify individuals, to ascertain blood pressure-related risk, and to guide management. The auscultatory technique with a trained observer and mercury sphygmomanometer continues to be the method of choice for measurement in the office, using the first and fifth phases of the Korotkoff sounds, including in pregnant women. The use of mercury is declining, and alternatives are needed. Aneroid devices are suitable, but they require frequent calibration. Hybrid devices that use electronic transducers instead of mercury have promise. The oscillometric method can be used for office measurement, but only devices independently validated according to standard protocols should be used, and individual calibration is recommended. They have the advantage of being able to take multiple measurements. Proper training of observers, positioning of the patient, and selection of cuff size are all essential. It is increasingly recognized that office measurements correlate poorly with blood pressure measured in other settings, and that they can be supplemented by self-measured readings taken with validated devices at home. There is increasing evidence that home readings predict cardiovascular events and are particularly useful for monitoring the effects of treatment. Twenty-four-hour ambulatory monitoring gives a better prediction of risk than office measurements and is useful for diagnosing white-coat hypertension. There is increasing evidence that a failure of blood pressure to fall during the night may be associated with increased risk. In obese patients and children, the use of an appropriate cuff size is of paramount importance.
Abstract-Accurate measurement of blood pressure is essential to classify individuals, to ascertain blood pressure-related risk, and to guide management. The auscultatory technique with a trained observer and mercury sphygmomanometer continues to be the method of choice for measurement in the office, using the first and fifth phases of the Korotkoff sounds, including in pregnant women. The use of mercury is declining, and alternatives are needed. Aneroid devices are suitable, but they require frequent calibration. Hybrid devices that use electronic transducers instead of mercury have promise. The oscillometric method can be used for office measurement, but only devices independently validated according to standard protocols should be used, and individual calibration is recommended. They have the advantage of being able to take multiple measurements. Proper training of observers, positioning of the patient, and selection of cuff size are all essential. It is increasingly recognized that office measurements correlate poorly with blood pressure measured in other settings, and that they can be supplemented by self-measured readings taken with validated devices at home. There is increasing evidence that home readings predict cardiovascular events and are particularly useful for monitoring the effects of treatment. Twenty-four-hour ambulatory monitoring gives a better prediction of risk than office measurements and is useful for diagnosing white-coat hypertension. There is increasing evidence that a failure of blood pressure to fall during the night may be associated with increased risk. In obese patients and children, the use of an appropriate cuff size is of paramount importance. (Circulation. 2005;111:697-716.)
Abstract-This paper provides a personal perspective of the role of abnormal renal-pressure natriuresis in the pathogenesis of hypertension. Direct support for a major role of renal-pressure natriuresis in long-term control of arterial pressure and sodium balance comes from studies demonstrating that (1) pressure natriuresis is impaired in all forms of chronic hypertension and (2) prevention of pressure natriuresis from operating, by servo-control of renal perfusion pressure, also prevents the maintenance of sodium balance hypertension. Although the precise mechanisms of impaired pressure natriuresis in essential hypertension have remained elusive, recent evidence suggests that obesity and overweight may play a major role. Obesity increases renal sodium reabsorption and impairs pressure natriuresis by activation of the renin-angiotensin and sympathetic nervous systems and by altered intrarenal physical forces. Chronic obesity also causes marked structural changes in the kidneys that eventually lead to a loss of nephron function, further increases in arterial pressure, and severe renal injury in some cases. Although there are many unanswered questions about the mechanisms of obesity hypertension and renal disease, this is one of the most promising areas for future research, especially in view of the growing, worldwide "epidemic" of obesity.
Abstract-Plasma leptm concentration IS increased m hypertensive obese humans, but whether leptm contributes to the increased arterial pressure m obesity 1s not knownIn this study, we tested whether chronic increases m leptm, to levels comparable to those m obesity, could cause a sustained increase m arterial pressure and also the importance of central nervous system (CNS) versus systemic mechanisms Five male Sprague-Dawley rats were implanted with chronic nonoccludmg catheters m the abdominal aorta and both carotid arteries for CNS mfunon, and five other rats were implanted with an abdominal aorta catheter and femoral vem catheter for intravenous (IV) mfuslon After 7 days of control, leptm was infused mto the carotid arteries or femoral vem at 0 1 pg/kg/mm for 5 days and 1 0 pg/kg/mm for 7 days, followed by a 7-day recovery period. The carotid artery and IV mfuslons of leptm at 1 pg/kg/mm slgmficantly increased plasma leptm levels, from 1.2?0 4 ng/mL to 91f5 ng/mL and from 0 9+-O 1 ng/mL to 9429 ng/mL, respectively, but there was no slgmficant increase m either group at the low dose Food intake also did not change at the low dose but decreased by approximately 65% m the carotid group and 69% m the IV group after 7 days of the 1 pg/kg/mm mfuslon Mean arterial pressure (MAP) Increased slightly at the low dose only m the carotid group, but this was not statlstlcally slgmficant At the higher dose, however, MAP increased significantly from 862 1 mm Hg to 942 1 mm Hg m the carotid group and from 87?1 mm Hg to 9321 mm Hg m the IV group. Heart rate also increased algmficantly m both groups at 1 pg/kg/mm leptm mfuslon Fasting blood glucose and msuhn levels decreased significantly at 1 pg/kg/mm m both the carotid artery group (-10 5% and -82 5%, respectively) and the IV group (-13 6% and -80 4%, respectively) All variables returned to control levels after leptm mfuslon was stopped. These results Indicate that chronic increases m clrculatmg leptm cause sustained increases m arterial pressure and heart rate and are consistent with a possible role for leptm m obesity hypertension.(Hypertension. 1998;31[part 2]:409-414.)Key Words: leptm n hypertension H sympathetic nervous system n blood pressure n heart rate n food intake
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