The effects of physiological left ventricular hypertrophy on coronary reactivity and reserve were examined by comparing greyhounds with their remarkable myocardial hypertrophy with mongrel dogs (left ventricular body weight ratios 7.7(0.1) and 4.4(0.1) g X kg-1 respectively). Peak reactive hyperaemia and flow debt repayment after 15 s coronary occlusions were virtually identical in both groups at baseline heart rates and paced atrial rates up to 270 beats X min-1. Furthermore, the changes in myocardial blood flow and its transmural distribution after release of a 45 s coronary occlusion both at baseline heart rate and during atrial pacing at 210 beats X min-1 were similar in both greyhounds and mongrel dogs. Collateral flow during a 1 min coronary occlusion in conscious animals and myocardial flows and distribution during treadmill exercise were also similar. To determine minimal coronary vascular resistance intracoronary adenosine (400-600 micrograms X min-1) was infused to dilate maximally the coronary vasculature without having appreciable systemic effects. In both groups of dogs adenosine increased coronary flow six to seven fold. Coronary vascular resistance per gram of left ventricle decreased equally, and the minimal resistance was 2200(147) kPa X litre-1 X min X g (RU X g-1) in greyhounds and 2360(453) RU X g-1 in mongrels, thus indicating similar maximal vascularity in each gram of the hypertrophied and mongrel left ventricles. Because of the larger greyhound heart, the minimal coronary vascular resistance for the entire left ventricle (11.7(0.7)RU) was 50% of that in mongrel dogs (24.1(0.7)RU). Thus all forms of left ventricular hypertrophy cannot be assumed to have similar effects on the coronary vasculature. Whereas the pathological hypertrophy associated with renovascular hypertension and aortic banding is accompanied by decreased coronary vascularity, the myocardial hypertrophy of the greyhound is accompanied by increased total vascularity and preserved coronary reserve.