Microsurgical renal denervation of the rat has been reported to increase blood loss and bleeding time after a standardized kidney resection. To investigate the vascular effects of denervation, isolated intrarenal arteries were studied using sensitive ‘isometric’ recording equipment. Four pieces of evidence were obtained to indicate an effective functional denervation 1 week after renal nerve transection: (i) Phentolamine reduced the K+‐induced contraction in controls but not in denervated arteries, (ii) The K+‐induced contraction was significantly smaller in denervated than in control arteries, (iii) Noradrenaline (NA) was a significantly more potent vasoconstrictor (4 x) in denervated than in control arteries, (iv) Cocaine increased the NA sensitivity in control arteries (3 x), whereas it failed to do so in denervated vessels. Vasopressin, 5‐hydroxytryptamine (5‐HT), NA (in the presence of cocaine), prostaglandin F2α(PGF2:α) and dopamine (DA) produced concentration‐dependent contractions in the mentioned order of potency. Denervated arteries were found to be about two to three times more sensitive to the vasoconstrictors than control arteries. Angiotensin I and II had no contractile effect in any of the vessel segments examined. Indomethacin‐pretreated arteries also failed to respond to angiotensin II. Neuropeptide Y produced only weak contractions and failed to influence the NA concentration‐response relationship in either control or denervated arteries. In conclusion, renal denervation caused a general supersensitivity of the vascular smooth muscle cells to both circulating and non‐circulating vasoconstrictors. Our results cannot explain the increased blood loss and bleeding time seen after denervation, but rather support the view that the enhanced bleeding was caused by an interrupted vasoconstrictor influence of t