Abstract

BackgroundChemical lesions of the lateral preoptic area (LPA) enhance water intake induced by subcutaneous injection of hypertonic saline in rats. On the other hand, the LPA section abolishes the increase in intravesical pressure (IP) induced by olfactory tubercle stimulation in dogs. Immunohistochemical labeling has demonstrated the presence of Mas receptors for Angiotensin‐(1–7) in LPA. It is not known whether neurons with Mas receptors in LPA are involved in urinary bladder regulation.AimWe investigated the effects of activation or blockade of Mas receptors for angiotensin‐(1–7) in LPA on intravesical pressure in anesthetized female rats.Materials and methodsFemale Wistar rats (~240 g, N=6) underwent to a stereotaxic surgery for implantation of stainless steel guide cannulas into the LPA under ketamine and xylazin anesthesia. After 7 days, the animals were anesthetized and maintained with 2% isoflurane in 100% O2 and submitted to cannulation of the femoral artery and vein, placement of a miniaturized Doppler flow probe around the left renal artery to measure the renal blood flow and cannulation of the urinary bladder for IP measurements. After baseline IP and cardiovascular parameters recordings for 15 min, angiotensin‐(1–7) (5 nmol/ uL) or saline (1 uL) or A‐779 (Mas receptor antagonist, 50 nmol/uL) was injected into the LPA and the variables were measured for additional 60 min.ResultsUnilateral injection of angiotensin‐(1–7) into LPA evoked a significant increase in IP (187.5±37.2%) compared to saline (−2.1±1.9%). Unilateral injection of A‐779 into LPA decreased the IP (−15.9±2.8%) in comparison to saline (2.0±1.1%). Interestingly, the decrease in IP was enhanced after bilateral injection of A‐779 into LPA (−27.3±3.4%) compared to the unilateral injection of this drug and also in comparison to saline (−2.9±1.6%) bilaterally into LPA. No significant changes in cardiovascular parameters after angiotensin‐(1–7) or saline or A‐779 in APL were observed.ConclusionThe data suggest that LPA is an important part of the circuit that regulates the urinary bladder activity mediated by angiotensin‐(1–7).Support or Funding InformationFinancial support: FAPESP and NEPAS‐FMABCThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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