https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(05)17741-1.pdf

Global burden of hypertension: analysis of worldwide data

PurposeTo examine the prevalence and the level of awareness, treatment and control of hypertension in different world regions.Study selectionA literature search of the MEDLINE database, using the Medical Subject Headings prevalence, hypertension, blood pressure and cross-sectional studies, was condu

Worldwide prevalence of hypertension: a systematic review.

Adenosine is a key endogenous molecule that regulates tissue function by activating four G-protein-coupled adenosine receptors: A1, A2A, A2B and A3. Cells of the immune system express these receptors and are responsive to the modulatory effects of adenosine in an inflammatory environment. Animal models of asthma, ischaemia, arthritis, sepsis, inflammatory bowel disease and wound healing have helped to elucidate the regulatory roles of the various adenosine receptors in dictating the development and progression of disease. This recent heightened awareness of the role of adenosine in the control of immune and inflammatory systems has generated excitement regarding the potential use of adenosine-receptor-based therapies in the treatment of infection, autoimmunity, ischaemia and degenerative diseases.

/pdf/adenosine-receptors-therapeutic-aspects-for-inflammatory-and-3bo18pvzz6.pdf

Adenosine receptors: therapeutic aspects for inflammatory and immune diseases

Article de synthese traitant de la pharmacologie de l'oxyde nitrique, du facteur EDRF et du GMP cyclique dans les vaisseaux sanguins et les thrombocytes, de l'isolation et de l'identification du facteur EDRF comme de l'oxyde nitrique, et de la formation, de la liberation et du metabolisme de l'endothelium derived NO (EDNO)

Biological actions and properties of endothelium-derived nitric oxide formed and released from artery and vein.

There is a large market for blood pressure measuring devices not only in clinical medicine but also among the public where the demand for self measurement of blood pressure is growing rapidly. For consumers, whether medical or lay, accuracy should be of prime importance when selecting a device to measure blood pressure. However, most devices have not been evaluated for accuracy independently using the two most widely used protocols: the British Hypertension Society (BHS) protocol and the standard set by the US Association for the Advancement of Medical Instrumentation (AAMI). 1 2 The Working Group on Blood Pressure Monitoring of the European Society of Hypertension has decided to review blood pressure measuring devices regularly to guide purchasers.3 For this first report devices for which there is published evidence of independent validation using these protocols have been surveyed. Because most blood pressure devices have not been independently validated, only a fraction of the many devices available have been surveyed. Devices that have been validated recently for which results have not yet been published were not included, but this shortcoming should be addressed in future.

#### Summary points

Two manual sphygmomanometers have been validated, one is recommended

Five devices for clinical use in hospitals have been validated, two are recommended

23 devices for self measurement of blood pressure have been validated, five are recommended

24 devices for ambulatory measurement of blood pressure have been validated, 16 are recommended

Validations and recommendations will be updated on the BMJ 's website

### Validation standards

In 1987, the American Association for the Advancement of Medical Instrumentation published a standard for sphygmomanometers which included a protocol for evaluating the accuracy of devices.4 In 1990 a protocol was devised by the British Hypertension Society.5 Both protocols have since been revised. 1 2 Since the two protocols can be reconciled the …

https://www.bmj.com/content/bmj/322/7285/531.1.full.pdf

Blood pressure measuring devices: recommendations of the European Society of Hypertension

We think that the available data on adenosine formation suggest the two signals are responsible for adenosine release from cardiac myocytes: (1) the ratio of oxygen supply to demand and (2) agonist-triggered release of extracellular adenine nucleotides. We do not believe that the available data support the oxygen consumption hypothesis. The few studies which allow us to judge the relative importance of these two signals suggest that both hypoxia and sympathetic nerve stimulation release adenosine primarily by decreasing O2 supply:demand. Agonist triggered nucleotide release may be quantitatively important in situations in which decreased O2 supply/demand cannot explain increased release, i.e., isoproterenol and acetylcholine administration.

Regulation of adenosine formation by the heart.

SUMMARY. Under certain conditions, a progressive increase in vascular resistance occurs within ischemic myocardium during the first 3 hours after coronary artery stenosis. We tested the hypothesis that the increased resistance is due to local release of a vasoconstrictor substance in the ischemic region. Relative ischemia was produced in anesthetized dogs by a combination of acute coronary arterial stenosis and increased myocardial metabolism. A hydraulic occluder on the left anterior descending coronary artery was adjusted to maintain distal left anterior descending coronary artery pressure at 50 mm Hg during atrial pacing at 180 beats/min. Myocardial blood flows were measured with 15 fim microspheres after 30 and 180 minutes of relative ischemia. During this time, transmural left anterior descending coronary artery flow decreased by an average of 30%. Infusion of adenosine into the ischemic region after 180 minutes produced a 74 ± 17% increase in flow, indicating the presence of substantial vasodilator reserve. Stimulation of metabolism in the ischemic area by norepinephrine infusion increased flow by 54 ± 17%. Indomethacin treatment after 180 minutes of ischemia, however, caused left anterior descending coronary artery flow to decrease by 22 ± 8%. a-Receptor blockade (phenoxybenzamine) in the left anterior descending coronary artery bed prior to ischemia prevented the flow decrease between 30 and 180 minutes. Phentolamine administration after 180 minutes also resulted in increased left anterior descending coronary artery flow. However, the addition of propranolol to phenoxybenzamine-treated hearts reversed the vasodilatory influence of phenoxybenzamine, resulting in a flow decrease within the ischemic region similar to that seen without any pharmacological intervention. We conclude that during 3 hours of relative ischemia in this preparation, blood vessels in the ischemic area (1) are not maximally dilated, and (2) undergo a progressive vasoconstriction via an unknown mechanism. Phenoxybenzamine prevents the progressive vasoconstriction, apparently by increasing norepinephrine release. (Circ Res 51: 411-420, 1982)

Progressive Coronary Vasoconstriction during Relative Ischemia in Canine Myocardium

We have characterized the dilation response to increased blood flow in the canine femoral and saphenous arteries. An arteriovenous shunt was created and changes in arterial diameter measured by sonomi

Endothelium-dependent flow-induced dilation of canine femoral and saphenous arteries.

• This summary provides an overview of some of the new information about the metabolic and regulatory functions of vascular endothelial cells and discusses possible important consequences of endothelial abnormalities in disease. (Arch Intern Med1987;147:569-573)

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=intemed&articleId=608015&pdfFileName=archinte_147_3_034.pdf

Endothelial cells. Not just a cellophane wrapper.

If adenosine is the major factor responsible for myocardial metabolic vasodilation, its release should be sustained as long as oxygen consumption and coronary flow are augmented. To see if adenosine meets this criterion, we examined the time course of its release during norepinephrine infusion in isolated, non-working guinea pig hearts (n = 8). During an 11-minute infusion period (steady state perfusate concentration = 6 X 10(-8) M), the coronary effluent was collected over 30-second intervals for measurements of coronary flow (ml/min per g), and adenosine and inosine release (pmol/min per g). Myocardial oxygen consumption (MVO2 = microliter O2/min per g) was measured at 1, 4, 6.5, and 11 minutes. Control values of coronary flow, myocardial oxygen consumption, and adenosine and inosine release were 7.5 +/- 0.4, 85 +/- 5, 22 +/- 5, and 431 +/- 39, respectively. During norepinephrine infusion, coronary flow, myocardial oxygen consumption, and adenosine release attained maximal levels within one minute (inosine within 2 minutes). These values were 10.6 +/- 0.4, 125 +/- 9, 849 +/- 110, and 2595 +/- 581, respectively. Thereafter, coronary flow and myocardial oxygen consumption values were sustained. In contrast, adenosine and inosine release significantly declined to nadirs by 9.5 minutes. Thereafter, steady state levels were maintained at 117 +/- 24 and 960 +/- 294, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Harvey V. Sparks

Papers

Regulation of adenosine formation by the heart.

Progressive Coronary Vasoconstriction during Relative Ischemia in Canine Myocardium

Endothelium-dependent flow-induced dilation of canine femoral and saphenous arteries.

Endothelial cells. Not just a cellophane wrapper.

Phasic release of adenosine during steady state metabolic stimulation in the isolated guinea pig heart.