Management of patients with concomitant hypertension and angina pectoris mandates that the physician pay attention to the underlying pathophysiology. The heart, when exposed to years of hypertension, becomes "remodeled." Overall mass is enlarged, the walls are thickened, and initial cavity volume remains normal or relatively small. Left ventricular end-diastolic pressure rises in the setting of a hypertrophic noncompliant ventricle; coronary resistance and coronary perfusion pressure are increased; and coronary vascular reserve, even with widely patent coronary arteries, is decreased. Long-standing hypertension--a risk factor for coronary atherosclerosis--is often accompanied by epicardial coronary stenoses that aggravate these coronary abnormalities. In managing the patient with hypertension and angina pectoris, it is important to determine whether the angina occurs in the setting of hypertensive hypertrophic disease alone or coexists with coronary arterial stenoses. Also important to therapy is whether the ventricle is of normal size with good function or decompensated with dilatation and diminished function. The latter two anatomic considerations, namely, epicardial coronary patency and left ventricular cavity size, will influence the choice of an anti-ischemic regimen. For example, diuretic and nitrate therapy can be hazardous, and digitalis unnecessary, in the setting of a nondilated hypertrophic ventricle with hyperdynamic function. On the other hand, the combined use of beta blocking agents plus calcium antagonists is particularly effective in lowering blood pressure and in improving coronary blood flow. Finally, this combination has been shown to be rapidly effective and to have prolonged benefit in this setting. The choice of these latter agents is also affected by the underlying state of the ventricle. Calcium channel blocking agents without significant negative inotropic effect, such as nifedipine and nitrendipine, would be suitable in patients with decompensated ventricular function and dilated left ventricular cavities. Both of these drugs have been shown to increase cardiac output and contractility via a reflex effect and to have little or no direct negative inotropic effect. In contrast, verapamil has a direct negative inotropic effect. The final choice of agents must be tailored to the needs of the individual patient, and the physician also has to determine the role of specific agents in the natural history of hypertensive heart disease.