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: The Lancet Commission on Hypertension identified that a key action to address the worldwide burden of high blood pressure (BP) was to improve the quality of BP measurements by using BP devices that have been validated for accuracy. Currently, there are over 3000 commercially available BP devices, but many do not have published data on accuracy testing according to established scientific standards. This problem is enabled through weak or absent regulations that allow clearance of devices for commercial use without formal validation. In addition, new BP technologies have emerged (e.g. cuffless sensors) for which there is no scientific consensus regarding BP measurement accuracy standards. Altogether, these issues contribute to the widespread availability of clinic and home BP devices with limited or uncertain accuracy, leading to inappropriate hypertension diagnosis, management and drug treatment on a global scale. The most significant problems relating to the accuracy of BP devices can be resolved by the regulatory requirement for mandatory independent validation of BP devices according to the universally-accepted International Organisation for Standardization Standard. This is a primary recommendation for which there is an urgent international need. Other key recommendations are development of validation standards specifically for new BP technologies and online lists of accurate devices that are accessible to consumers and health professionals. Recommendations are aligned with WHO policies on medical devices and universal healthcare. Adherence to recommendations would increase the global availability of accurate BP devices and result in better diagnosis and treatment of hypertension, thus decreasing the worldwide burden from high BP.

The effects of intrarenal bolus injections of equal molar doses of angiotensin II and angiotensin III on renal blood flow were examined in seven pentobarbital anaesthetized dogs. Renal blood flow was measured with an electromagnetic flow probe. Angiotensin II produced a greater decrease in renal blood flow than angiotensin III at all bolus doses tested when the integral of the renal blood flow response was examined. In 10 other dogs, we compared the molar dose of intrarenal constant infusions of angiotensin II and angiotensin III required to decrease total renal blood flow by approximately 25%. The effect these peptides had on the distribution of renal cortical blood flow was determined with radioactive microspheres. In the constant infusion experiments, more moles of angiotensin III than angiotensin II were required to produce a given decrease in renal blood flow in each experiment. The average percent decrease in blood flow to each of the four cortical zones produced by angiotensin II was not different from that produced by angiotensin III. Our data demonstrate that angiotensin II is more potent than angiotensin III as a vasoconstrictor in the renal vasculature.

The function of the renin-angiotensin system (RAS) is influenced by changes in sodium balance and angiotensin II (ANG II) levels. In previous studies it has been difficult to assess the physiological effects on blood pressure homeostasis of different rates of ANG II infusion and of different levels of sodium in the diet. The present study examined the quantitative effects of ANG II in conscious dogs on low, normal and high sodium intake with the endogenous RAS blocked by continuous intravenous infusion of enalapril [MK-421,N-(1(S)-carbethoxy-3-phenyl propyl)-L-alanyl-L-proline maleate]. Conscious dogs on three different sodium diets, low, normal and high (5, 30 and 250 mmol/day), were infused continuously with enalapril, 4 mg/kg/day, and studied with superinfused ANG II at rates of 0, 1, 3, 6 and 12 ng/kg/min, each period lasting 1 week. Converting enzyme inhibitor (CEI) decreased mean arterial blood pressure (MAP) equally in dogs on low and normal sodium intake by 20 mmHg, but did not have a significant effect in dogs on high sodium intake. The initial infusion of ANG II at the lowest rate had a pronounced effect on MAP in dogs on normal and high sodium, but had no effect in the sodium depleted dogs. However, at the higher rates of infusion, the angiotensin increased the pressure equally at all levels of sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

The lung is thought to be the major site for conversion of angiotensin I (AI) to angiotensin II (AII), although a significant amount of AI conversion is also known to occur in the peripheral circulation. Reports suggest that pulmonary conversion of AI to AII is more sensitive to inhibition by specific kininase II inhibitors than extrapulmonary conversion. This latter observation prompted us to seek for a dose of SQ20881 and/or captopril that would suppress the conversion of AI to AII in the lung without affecting extrapulmonary conversion of AI and thereby peripheral pressor responses to intravenously administered AI. Experiments were performed on 15 pentobarbital anaesthetized dogs. The AII arterial-venous difference across the lung was measured during an intravenous (i.v.) infusion of AI which produced a steady-state rise in blood pressure of 20 mmHg. This protocol was repeated with the same dose of AI following three graded doses of either SQ20881, captopril or vehicle. Results showed that the systemic pressor response to AI cannot be dissociated from pulmonary AI conversion.