We investigated the direct effects verapamil, which was infused into the A-V node artery at two doses of 0.01 and 0.1 microgram/kg/min on the A-V conduction and the A-V junctional automaticity in the dog with experimentally induced A-V junctional rhythm. Verapamil significantly prolonged the A-H interval, but not the H-V interval, in the His bundle electrogram during atrial pacing at a rate of 100 beats/min. Effective and functional refractory periods of the A-V node also were prolonged significantly by verapamil. On the other hand, verapamil showed less propensity to decrease the spontaneous A-V junctional rate and to prolong the A-V junctional recovery time after atrial overdrive at a rate of 100 beats/min for 60 s. These results indicate that suppressive effects of verapamil on the A-V junctional automaticity are much weaker when compared with that on the A-V conduction.

Animals↗

PubMedDate not supplied

Dynamic responses of active and inactive renin in patients with essential and renovascular hypertension.

We studied the dynamic responses of inactive renin and the form of renin released by the kidney in the hypertensive patients. Significant increase of active renin concentration (p less than 0.01) and decrease of the percentage of inactive renin concentration (p less than 0.01) after sodium depletion was observed in 15 essential hypertensive subjects with normal plasma renin activity. In eight of 15 patients, significant increase of inactive renin concentration (p less than 0.01) was observed after sodium depletion. In the remaining seven patients, no significant change of inactive renin concentration was demonstrated. A small increase of active and inactive renin concentration was observed following sodium depletion in six essential hypertensive subjects with low plasma renin activity (PRA). In the unilateral renal hypertension after upright tilting, active renin concentration in the renal vein of the affected kidney was significantly (p less than 0.02) higher than that in the renal vein of the non-affected kidney and the inferior vena cava. Inactive renin concentration in the renal vein of the affected kidney was significantly (p less than 0.02) lower than that in the renal vein of the nonaffected kidney and the inferior vena cava. In four of five cases, the inactive renin concentration in the femoral artery was less than that in the inferior vena cava. Therefore, we might conclude that only active renin was released from the affected kidney, and active renin became inactive by unknown mechanisms; the ischemic kidney might also activate inactive renin.

Adolescent↗