Cardiac chemical reflex control of preload in conscious dogs.

The purpose of our study was to determine the effects of cardiac chemical reflexes on left ventricular (LV) preload in conscious dogs. Adult mongrel dogs were instrumented to measure LV pressure and, with ultrasonic dimension crystals, to measure LV internal diameter. A catheter was inserted in the left circumflex coronary artery for the administration of increasing doses of veratridine, arachidonic acid (AA), and prostacyclin (PGI2). LV end-diastolic diameter (EDD) and end-diastolic pressure (EDP) were used as indexes of preload. Veratridine (0.4 micrograms/kg) reduced EDD 3.0 +/- 0.5% from 36.6 +/- 1.7 mm and EDP 24 +/- 5.0% from 6.1 +/- 0.5 mmHg (P less than 0.05). AA (100 micrograms/kg) reduced EDD by 3.7 +/- 0.5% from 37 +/- 1.1 mm and EDP by 25 +/- 4.4% from 7.0 +/- 0.6 mmHg (P less than 0.05). PGI2 (0.5 micrograms/kg) also reduced EDD by 3.3 +/- 0.5% from 37 +/- 0.5 mm and EDP by 25 +/- 6.0% from 7.8 +/- 0.3 mmHg (P less than 0.05). Although holding heart rate constant by pacing or combined beta-adrenergic and muscarinic receptor blockades did not reduce the preload responses to veratridine, AA, or PGI2, alpha 1-adrenergic blockade or vagotomy abolished them. Systemic arterial barodenervation markedly potentiated the reduction in myocardial size after stimulation of cardiac chemical receptors. Stimulation of inhibitory cardiac receptors, therefore, reduces preload via a vagal reflex by withdrawing peripheral alpha-adrenergic tone to capacitance vessels in the conscious dog.