Relaxin increases sympathetic nerve activity and activates spinally-projecting neurons in the paraventricular nucleus of nonpregnant, but not pregnant, rats

      Pregnancy is characterized by increased blood volume and baseline sympathetic nerve activity (SNA), vasodilation, and tachycardia. Relaxin (RLX), an ovarian hormone elevated in pregnancy, activates forebrain sites involved in control of blood volume and SNA, and contributes to adaptations during pregnancy. In anesthetized arterial baroreceptor denervated nonpregnant (NP) rats, RLX microinjected into the subfornical organ (SFO, 0.77 pmol in 50 nl) produced sustained increases in lumbar SNA (8 ± 3%) and mean arterial pressure (MAP, 26 ± 4 mmHg). Intra-carotid artery (ica) infusion of human RLX-2 (155 pmol/ml/hr; 1.5 hr) increased heart rate (+50 ± 5) and transiently increased MAP (+13 ± 1 mmHg) in conscious NP, but not near-term pregnant (P), rats. In NP rats, ica RLX activated neurons (increased Fos-IR) in the SFO and in spinally-projecting (19 ± 2%) and AVP-IR (21 ± 5%) cells in the PVN. Fos-IR due to RLX was significantly less in P rats, and not different from Fos-IR in saline treated (SAL, 1 ml/hr) NP or P rats. Although the SFO of P rats was not activated by exogenous RLX, mRNA and protein for RLX receptors in the SFO were preserved in pregnancy. These data provide an anatomical substrate for a role of RLX in resetting of AVP secretion and increased baseline SNA in pregnancy. Since expression of RLX receptors was preserved in the SFO of P rats, the lack of response to exogenous RLX may be due to maximal activation by elevated endogenous levels of RLX in near-term pregnancy.
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