Transtelephonic EKG monitoring increases detection rate of paroxysmal atrial fibrillation in stroke and TIA patients whose 24-hour Holter result was negative, especially if they had frequent premature atrial ectopic beats, recent anterior circulation infarct on MRI, or both.

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Isotonic expansion of extracellular fluids diminishes the reabsorption of sodium in the proximal tubule. If this effect is mediated through some mechanism extrinsic to the kidney, net sodium flux in other epithelial structures, such as the jejunum, should also be influenced. In the rat, expansion of E.C.F. produces in all experiments a diminished reabsorption of sodium and water, which appears during the first period after the infusion of saline is started and becomes statistically significant in the following periods. Because of the experimental conditions, net fluxes are often nverted, giving rise to a secretion. At the same time, the sodium concentration of the solution perfused increases during its transit through the jejunum. Net potassium flux is unchanged. Aldosterone has no influence on the phenomenon whereas angiotensin may have an additive effect. A similar response of two epithelial structures as far apart as the jejunum and the proximal tubule is highly suggestive of a common mechanism extrinsic to the kidney. The experimental model chosen has excluded the role of a suppression of aldosterone and angiotensin. There is lso no support for the involvement of a sodium-potassium exchange system. The present model offers the opportunity to study without any major technical problem the possible role of general, humoral and physical factors, all of which have been proposed as responsible for the diminished reabsorption of sodium in the proximal tubule after E.C.F. expansion.

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Abstract. The haemodynamic and renal effects of synthetic prostaglandin A2 (PGA2) have been studied in 10 hypertensive subjects during a) a short lasting infusion of hypotensive doses of 3–9μg/kg min. of PGA2; b) a continuous infusion starting with subdepressive doses and extended with hypotensive doses.—The rapid hypotensive effect observed with high doses was accompanied by an increase in cardiac output and renal blood flow without significant changes in the peripheral vascular bed. Hepatic blood flow was decreased. These observations show a preferential renal redistribution of cardiac output. During the administration of subdepressive doses of PGA., a marked renal effect was observed, consisting in an increase in free water clearance and diuresis with no significant modifications of general haemodynamics. The natriuretic effect was much less pronounced suggesting that PGA2 is not a specific natriuretic hormone.—The haemodynamic and renal effects of endogenous PGs may play an important role in renal functions and in blood pressure regulation.

1. In basal conditions, plasma arterial prostaglandin (PG) E2 was significantly increased in borderline hypertensive patients (BH) (28.5 ± 6.7 pg/ml) in comparison with sustained essential hypertensive patients (EH) (11.6 ± 3.2 pg/ml) and in comparison with control normotensive subjects (NTS) (5.8 ± 1.4 pg/ml). 2. Plasma arterial PGE2 was positively significantly correlated with cardiac index and negatively significantly correlated with total peripheral resistance in basal conditions. 3. Indomethacin induced more pronounced haemodynamic changes in borderline than in sustained hypertensive patients, with a significant increase in arterial blood pressure and total peripheral resistance and a significant decrease in stroke volume and cardiac index. 4. Indomethacin significantly decreased arterial PGE2 in borderline hypertensive patients. The decrease was less important in sustained hypertensive patients. 5. In the overall population, a significant positive correlation between arterial PGE2 concentration and cardiac index was observed before and after indomethacin treatment. 6. The study suggests an important role of PGE2 in the regulation of cardiac output (positive inotropic effect) and blood pressure of essential hypertensive patients.