While diving, harbour seals (Phoca vitulina) manage their oxygen stores through cardiovascular adjustments, including bradycardia, a concurrent reduction in cardiac output, and peripheral vasoconstriction. At the surface, post-dive tachycardia facilitates rapid reloading of oxygen stores. Although harbour seals can tolerate >20 min of submergence, the majority of their natural dives are only 2-6 min and are usually followed by surface intervals that are <1 min, so they spend approximately 80% of their time submerged. Given that harbour seals meet their ecological needs through repetitive short aerobic dives, we were interested in the functional role, if any, of the dive response during these short dives. During voluntary diving in an 11 m deep tank, the cardiovascular responses to submergence of five harbour seals were manipulated using specific pharmacological antagonists, and the effects on diving behaviour were observed. Effects of pharmacological blockade on heart rate were also examined to assess the autonomic control of heart rate during voluntary diving. Heart rate was recorded using subcutaneous electrodes and data loggers, while diving behaviour was monitored using a video camera. The muscarinic blocker methoctramine blocked diving bradycardia, the alpha-adrenergic blocker prazosin blocked diving vasoconstriction, and the beta-adrenergic blocker metoprolol blocked post-dive tachycardia. Heart-rate analysis indicated that diving bradycardia is primarily modulated by the vagus, while post-dive tachycardia results from parasympathetic withdrawal as well as increased sympathetic stimulation of the heart. None of the pharmacological blockers had any effect on average dive or surface interval duration. Seals maintained a high percentage of time spent diving in all treatments. Thus, harbour seals do not appear to need the dive response during short dives in order to maintain an efficient dive strategy.