Patients suffering from pHPT show beside elevated PTH blood levels also hypertension. The aetology for this paradoxical hypertension is till unknown. The aim of is study was to investigate whether a desensitisation of the PTH1-r is contributed on this effect. Isolated rat hearts (Langendorff) were perfused under flow-constant conditions. Heartrate (HR), perfusion pressure (AP) and the left ventricular developed pressure (LVDP) were determinated. In all experiments hearts were pre-constricted by addition of L-nitro arginine (L-NA). A single application of PTH increased HR (8%), reduced LVDP (9%) and abolished the increased AP, mediated by L-NA, within minutes completely. A second application of PTH (also in presence of L-NA) showed no effect on LVDP, but increased HR (10%) and reduced the L-NA effect (40%). For investigation of the receptor kinetic we used the related peptide PTHrP (PTH-1r agonist). Using in the first treating period PTHrP instead of PTH, an application of PTH in the second treating period had no effect on HR, AP and LVDP furthermore. But if we repeated the experiment, using PTH in the first treating period and PTHrP in the second one, an application of PTHrP increased HR (12%), reduced LVDP (10%) and abolished the L-NA effect completely. In conclusion it seems unlikely, that a desensitisation of the PTH-1r is responsible for the paradoxical hypertension in pHPT.