Vasopressin (AVP) is an effective pressor agent in circulatory shock. We compared effects of the 5-HT1A-receptor agonist, 8 OH-DPAT, with AVP on mean circulatory filling pressure (MCFP) and renal sympathetic nerve activity (RSNA) in rats in hypovolemic shock. Male Sprague-Dawley rats were fit with renal sympathetic nerve electrodes, vascular catheters and right atrial balloons (for measurement of MCFP) under sodium pentobarbital anesthesia. Rats were hemorrhaged to 50 mmHg for 25 min, after which 8 OH-DPAT (30 nmol/kg, iv bolus, n=7), AVP (2 ng/kg/min, iv, n=9) or saline (33 μl/kg/min, iv, n=9) was given. Hemorrhage decreased MCFP from 6.1 ± 0.2 to 0.9 ± 0.4 mmHg (P<0.01). 8 OH-DPAT produced a sustained rise in MAP (+36 ± 3 vs. +13 ± 6 mmHg, 35 min post-injection, P<0.01 vs. Saline), a transient rise in RSNA (+112 ± 34 vs. +17 ± 12 % of baseline, 5 min post-injection, P<0.01 vs. Saline) and a sustained rise in MCFP (2.2 ± 0.6∗, 2.7 ± 0.3∗∗, 2.9 ± 0.2∗∗, and 2.7 ± 0.2∗ mmHg at 5, 15, 25 and 35 min post-injection; ∗,∗∗P<0.05, 0.01 vs. Saline). An equipressor dose of AVP did not raise MCFP (1.5 ± 0.3, 1.6 ± 0.3, 1.0 ± 0.4∗∗, and 1.7 ± 0.3 mmHg; ∗∗P<0.01 vs. 8 OH-DPAT), but suppressed RSNA (103 ± 34∗ vs. 186 ± 70 and 102 ± 37∗ vs. 182 ± 67% of baseline, 10 and 15 min post-injection; ∗P<0.05 vs. Saline). 8 OH-DPAT increases MCFP more than AVP during hypovolemic shock, possibly through sympathetic mobilization of blood stores. Supported by HL 076162 and 072354