Vasopressin (VP)-, neuropeptide FF (NPFF)-, and tyrosine hydroxylase (TH)-expressing neurons were studied by means of single and double immunocytochemistry in the human brainstem of controls who died suddenly due to trauma and of patients who suffered from essential hypertension and died due to acute myocardial infarction, while in one case there was brain hemorrhage. In the control and hypertensive groups VP fibers and NPFF neurons and fibers were the most abundantly present in the dorsal vagal complex, especially in the dorsal motor nucleus of the vagus. Numerous VP and NPFF fibers formed synaptic-like contacts with neuronal profiles in the dorsointermediate, centrointermediate, ventrointermediate, caudointermediate, and caudal parts of the dorsal motor nucleus of vagus as well as adjacent medial and intermediate subnuclei of the solitary nucleus. VP, but not NPFF, positive fibers were found to vastly contact TH-positive neuronal profiles in A2/C2, A2, and ambiguus nucleus (Amb). The density of VP fibers in the dorsal motor nucleus of the vagus and Amb did not differ between hypertensive patients and controls, whereas the density of NPFF fibers in hypertensives was 3.19 times lower in the dorsal motor nucleus of vagus and markedly decreased in the Amb. In both groups, VP and NPFF were scarcely present in the pain pathways, suggesting that these peptides are not crucially involved in nociceptive control in human. The reduction of NPFF release within the dorsal motor nucleus and Amb could serve as a possible cause of the impairment of cardiac vagal control in hypertensive patients.