1 In the present study, the role of metabotropic glutamate receptors (mGluRs) in central cardiovascular regulation in conscious rats was examined. To this end, agonists and antagonists for type I and II mGluRs were administered intrathecally, and the temporal changes in blood pressure and heart rate were recorded. 2 L-glutamate (1 mmol) and the prototypical mGluR agonist (1S,3R)-ACPD (0.1 and 0.3 mmol) both increased mean arterial pressure (MAP) and heart rate (HR), implicating functional mGluRs in the spinal cord. The type I mGluR agonist DHPG (0.01 ± 0.1 mmol) evoked increases in MAP (max=25+5 mmHg) and HR (max=88+23 beats min 71 ). The duration of action, but not the maximum e ects, were dose-related and ranged from approximately 10 min to 590 min and 1 min to 490 min for MAP and HR, respectively. 3 The type I/II mGluR agonist CCG-1 (0.1 and 0.3 mmol) caused smaller, variable increases in MAP and HR of intermediate duration (5 ± 20 min), whereas the type II MGluR agonist APDC (0.1 and 1.0 mmol) caused marked, but transient (3 ± 5 min), pressor and tachycardic responses. The highest doses of DHPG and CCG-1, but not APDC, also evoked behavioural responses similar to a spontaneous nociceptive behavioural e ect reported previously. 4 The type I and II mGluR antagonists (AIDA and LY307452, respectively) were also given approximately 5 min before the administration of the respective type I and II mGluR agonists (DHPG and APDC). Both compounds caused pressor and tachycardic responses, with the e ect of AIDA, but not LY307452, returning to control levels before mGluR agonist administration. AIDA signi®cantly attenuated the overall cardiovascular e ects of DHPG, while LY307452 signi®cantly attenuated the overall cardiovascular e ects of APDC. 5 These results indicate that functional type I and II mGluRs exist in the spinal cord, and that their activation evokes prolonged cardiovascular e ects.