MEAN BLOOD-PRESSURE - EFFECTS OF CLONIDIN E

Objective: To study the relationship of blood presure (BP), its variab ility (BPV) and reactivity (BPR), we gave to a group oi 12 essential h ypertensives clonide to decrease adrenergic activity from the CNS. Met hods: 24-h BP and BPV were meassured with 24 h non invasive blood pres ure recording. BPR was studies with isometric exercise (IE). We determ ined plasma catecholamines (PCA), plasma renin activity (PRA) and plas ma aldosterone. (PAL). All the protocol was carried out before and aft er clonidine treatment. Results: PCA decreased with clonidine: NE, fro m 251 +/- 106 to 145 +/- 40. E, from 49 +/- 35 to 25 +/- 17 and DA, fr om 73 +/- 41 to 59 +/- 38, pg/ml. 24 h BP (mmHg) and HR decrease also: from 159.13 +/- 13/98.36 +/- 6 to 145.34 +/- 14/90.09 +/- 6, p < 0.00 09/p < 0.0003; HR (bpm) from 65 +/- 8 to 56 +/- 8, p < 0.0009. No chan ge was observed in 24 h BPV (mmHg): SBPV/DBPV 12.33 +/- 2/9.14 +/- 4 v s 12.72 +/- 3/8.19 +/- 1, NS. HR 6 +/- 2 vs 6 +/- 2, NS. Clonidine cou ld not avoid the BP and PCA increase after IE. SPB +43, DBP +28 mmHg; HR +26 bpm. Following clodine they were: SBP +49 mmHg; DBP +28 mmHg; H R +23 bpm, NS. Something similar happened with PCAS, increasing afther IE: NE, 49 %; E, 122 %, only DA decreased, -4 %. Those increments als o persisted with clonidine: NE, 67 %, E, 160 % and DA, 24 %. When comp ared with values before treatment only changes in DA became significan t, p < 0.000001. The RAAS activity was lowered by clonidine: PRA decre ased from 1.2 +/- 1.2 to 0,2 +/- 0.1, ng/ml/h., p < 0.01. PAL from 0.3 +/- 0.1 to 0.2 +/- 0.1, nmol/L, p < 0.03, such a lowering in activity help in keeping BP down but could nort change BPV and could not avoid the increase in BPR values nor increment in PCA after IE. Comments: B P, BPV and BPR seem to be different compnents of 24 h BP, decreasing C NS adrenergic activity with clonidine controls BP but not BPV nor BPR. It may seem that the center control for those components is different , and that BPR to the IE overcomes the buffering mechnism from the bar orreceptors. There is no antihypertensive drug that would substantiall y lowers the increments in BP to IE nor BPV. One final consideration w ould De that even if BPV and BPR are not regulated they do so from a l ower level of BP which may have ist clinical importance.