The clinical features, pathogenesis, and pharmacologic management of hypertensive crises are reviewed, with emphasis on newer therapies. Hypertensive crises may be divided into hypertensive emergencies and hypertensive urgencies. Hypertensive emergencies, in which acute organ damage exists, require blood pressure reduction within one hour. In hypertensive urgencies no acute end-organ damage has yet occurred; however, blood pressure should be controlled within 24 hours. Factors that may precipitate a hypertensive crisis include renovascular hypertension, acute glomerulonephritis, head injuries, renin- or catecholamine-secreting tumors, antihypertensive-therapy withdrawal syndromes, eclampsia, and ingestion of tyramine by patients receiving monoamine oxidase inhibitors. The traditional drug of choice for therapy of hypertensive emergencies is sodium nitroprusside. Intravenous labetalol produces a prompt, controlled reduction in blood pressure and is a promising alternative. Other agents used are diazoxide, trimethaphan camsylate, hydralazine, nitroglycerin, and phentolamine. However, all these agents have disadvantages, including unpredictable antihypertensive effects, difficult blood pressure titration, and serious potential adverse effects such as profound hypotension, reduced renal blood flow, and increased myocardial workload. Most patients with hypertensive urgencies can be effectively treated with orally or sublingually administered agents. Older regimens of reserpine, methyldopa, or guanethidine, with their slow onsets and long durations of action, have been largely replaced by clonidine and nifedipine. Captopril and minoxidil have also been used with some success. Despite the lack of comparative trials with traditional agents, demonstrated efficacy and desirable pharmacologic characteristics have made several new agents acceptable for therapy of hypertensive crises.