Inhibition of human neutrophil function by tolfenamic acid involves inhibition of Ca2+ influx.

The present work was designed to study the pharmacological control of the receptor-mediated activation of human neutrophils by tolfenamic acid (2(-)[(3-chloro-2-methylphenyl)-amino]benzoic acid). Tolfenamic acid inhibited in a concentration-dependent manner the degranulation response and Ca2+ influx in neutrophils activated either by the chemotactic peptide fMLP (N-formyl-methionyl-leucylphenylalanine) or Ca2+ ionophore A23187 (calcimycin). When fMLP was used to activate neutrophils, tolfenamic acid (30 microM) reduced Ca2+ influx by 50% and degranulation by 20%.

The effect of high calcium intake on Ca2+ ATPase and the tissue Na:K ratio in spontaneously hypertensive rats.

The effects of oral calcium loading on the development of hypertension were studied in spontaneously hypertensive rats (SHR). Forty-eight male SHR were divided into four groups according to treatment: control, calcium, deoxycorticosterone (DOC) and DOC + calcium. Both calcium groups received ad libitum 1.

Deoxycorticosterone prevents the blood pressure-lowering effect of calcium in spontaneously hypertensive rats.

To study the effects of prolonged oral calcium loading on the development of hypertension in spontaneously hypertensive rats (SHR), 48 male animals (age 9 weeks) were divided into four groups according to the treatment: control, calcium, deoxycorticosterone (DOC) and calcium/DOC. Both calcium groups received 1.5% calcium chloride solution ad libitum as their drinking fluid.