The aim of this study is to determine whether red blood cell K + content (RBC Ki ) is associated with blood pressure levels and, if so, could RBC Ki be a marker of potassium changes in other cells involved in blood pressure regulation. The study was performed on 50 untreated hypertensives, 32 of their offspring and 50 age-and sex-matched controls. Systolic (SBP) and diastolic (DBP) blood pressures, height, weight, plasma, urine and red blood cell electrolytes were measured in all subjects. RBC Ki was significantly lower in hypertensives than in offspring of hypertensives and normotensive controls. Offspring of hypertensives had significantly lower RBC Ki than normotensive controls. Plasma K + was significantly lower both in hypertensives and offspring of hypertensives when compared to normotensive controls. A significant negative correlation was found in hypertensives between RBC Ki and DBP (r ¼ À0.27, P ¼ 0.04) and in offspring of hypertensives between RBC Ki and DBP (r ¼ À0.43, P ¼ 0.02). A significant correlation was found in hypertensives between RBC Ki and plasma K + (r ¼ 0.3, P ¼ 0.02). A positive correlation with borderline significance was found in hypertensives between RBC Ki and ionized Ca 2+ (r ¼ 0.2, P ¼ 0.1). In conclusion, our results support the hypothesis that RBC Ki is associated with blood pressure levels and that the measurement of RBC Ki levels may represent a biochemical marker for K + changes in other cells involved in blood pressure regulation. Further studies are necessary to explain the exact mechanisms of reduced RBC Ki levels in hypertensive patients and their offspring.

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Coronary heart disease (CHD) is the leading cause of morbidity and mortality across the entire world. In effect, reversion of angina or improvement of ECG remains an unrealistic therapeutic option for most patients. Unfortunately, most research clinical trials in these patients have focused on coronary atherosclerosis, even decades after the first observation that angina, and myocardial infarction may occur in the presence of normal coronary arteries. Further, there has been little attention from academic and pharmaceutical institutions on comparative therapeutic research as it has been recently addressed by the Institute of Medicine of the National Academies in USA, and by a similar statement from the World Medical Association in the year 2000. This review, thus, has tried to present the best of our knowledge on the pathophysiology and management of CHD, along with other striking relevant but neglected findings with some recent patents. Four sections were included from the physiological principles of myocardial oxygen delivery, with emphasis on RBC sensing O(2) demand and delivery in myocardial ischemia, up to the recent advances on approaches intended to reverse angina and the ECG alteration in coronary heart disease. Finally, this review presents the principles, design and results of the first New Drug Application to address improvement in RBC K uptake, and consequently the chain of simultaneous tissue H/K and O(2)/CO(2) exchanges, and NO-generation, along with their promising therapeutic effect on reversion of angina, and ST-T alterations in coronary artery disease patients.

The assessment of potassium (K) effects in hypertension involves a history of complex research in cell K function and body K homeostasis. These studies provide evidence for the role of K ions in vascular and renal function, insulin resistance, glucose uptake, and the renin-angiotensin-aldosterone system; and there have been an impressive number of clinical and epidemiologic research relating dietary intake K and regulation of blood pressure. However, the usual technique by which K metabolism is assessed in clinical practice (plasma or serum K) provides no useful data for estimating disorders in cell K transport that occurs in hypertensive patients or that may follow the administration of diuretics, beta-blockers, or nonsteroidal anti-inflammatory drugs. This fact becomes more crucial if associated with the physiologic decline in body K stores occurring after the age of 30 years, which may impair the long-term treatment of hypertensive individuals. In this context, this article presents a review of the clinical and research methods that can be used to assess more accurately K metabolism and cell K physiology in hypertensive patients, including a heritable defect in red blood cell K transport.

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