EFFECT OF VASOPRESSIN ON LEFT-VENTRICULAR PERFORMANCE

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 mum. kg-1.min-1 for 2 min) the plasma AVP was elevated from 3.9 +/-0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1.min, P < 0.01) and arterial elastance (E(a)) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dt(max))-end-diastolic volume (V(ED)) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg-s-1.ml-1, P < 0.05), and the stroke work-V(ED) relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in E(a) produced by methoxamine did not depress LV performance. The cardiodepressant effect of AVP was also present after autonomic blockade. When changes in heart rate were prevented by pacing, this effect was reversed by AVP V1-receptor blockade. We conclude that, in conscious animals, physiologically relevant concentrations of AVP directly depress LV contractile performance, and this effect is prevented by an AVP V1-receptor antagonist.