Continued inputs of fertilizer and manure in excess of crop requirements have led to a build‐up of soil phosphorus (P) levels and increased P runoff from agricultural soils. The objectives of this study were to determine the effects of two tillage practices (no‐till and chisel plow) and a range of soil P levels on the concentration and loads of dissolved reactive phosphorus (DRP), algal‐available phosphorus (AAP), and total phosphorus (TP) losses in runoff, and to evaluate the P loss immediately following tillage in the fall, and after six months, in the spring. Rain simulations were conducted on a Typic Argiudoll under a corn (Zea mays L.)–soybean [Glycine max (L.) Merr.] rotation. Elapsed time after tillage (fall vs. spring) was not related to any form of P in runoff. No‐till runoff averaged 0.40 mg L−1 and 0.05 kg ha−1 DRP and chisel‐plow plots averaged 0.24 mg L−1 and 0.02 kg ha−1 DRP concentration and loads, respectively. The relationship between DRP and Bray P1 extraction values was approximated by a logistic function (S‐shaped curve) for no‐till plots and by a linear function for tilled plots. No significant differences were observed between tillage systems for TP and AAP in runoff. Bray P1 soil extraction values and sediment concentration in runoff were significantly related to the concentrations and amounts of AAP and TP in runoff. These results suggest that soil Bray P1 extraction values and runoff sediment concentration are two easily measured variables for adequate prediction of P runoff from agricultural fields.

The action of different antihypertensive drugs on Ca 2+ concentration in human platelets was studied under in vitro conditions and during the treatment of hypertensive persons. Several calcium antagonists (verapamil, nifedipine, and nicardipine) acted to block an increase of Ca 2+ concentration in platelets which was induced by platelet activating factor (PAF), adenosine diphosphate, and U46619, the stable analog of thromboxane A 2 . All calcium antagonists suppressed dose-dependent calcium responses induced by each agonist. In a group of stable hypertensive patients, the basal Ca + level in platelets was significantly higher than the level in mildly hypertensive or normotensive individuals. The induced increase in Ca 2+ in the platelets of stable hypertensive patients was also higher, but this difference was not significant. Treatment of hypertensive patients with nifedipine for 3 weeks led to a decrease in calcium responses induced by all activators, but this decrease was significant only when PAF was used for platelet stimulation. Nifedipine added to platelets induced a nearly identical decrease in PAF-dependent calcium responses before and after therapy. Treatment with nifedipine in combination with furosemide and propranolol led to a more significant decrease in calcium responses than that expressed with monotherapy. In vitro experiments showed that furosemide has a calcium-blocking action on platelets, but that it is less expressed than the action of calcium antagonists. Low doses of propranolol did not influence calcium platelet responses, but high doses potentiated them slightly. A significant correlation was found