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This Article Full Text Full Text (PDF) All Versions of this Article: 288/6/F1249    most recent 00363.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Vagnes, O. B. Articles by Arendshorst, W. J. Search for Related Content PubMed PubMed Citation Articles by Vagnes, O. B. Articles by Arendshorst, W. J.

Enhanced Ca²⁺ response to AVP in preglomerular vessels from rats with genetic hypertension during different hydration states

¹Renal Research Group, Institute of Medicine, University of Bergen and Department of Medicine, Haukeland University Hospital, Bergen, Norway; and ²Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

Submitted 27 September 2004 ; accepted in final form 12 January 2005

Exaggerated arginine vasopressin (AVP)-induced calcium signaling and renal vasoconstriction, characteristic in young spontaneously hypertensive rats (SHR) during euvolemia, are related to greater amounts of V_1a receptor mRNA and V_1a protein in preglomerular resistance arterioles. The present study determined whether V_1a receptor density and calcium signal transduction in the renal vasculature of young SHR is regulated appropriately during physiological changes in hydration state. [³H]AVP ligand binding documented two- to threefold greater density of V_1a receptors in euvolemic SHR vs. Wistar-Kyoto (WKY) rats. Parallel changes in V_1a receptor density were observed in both strains during chronic water loading (plus 50 fmol/mg) and during dehydration (minus 50 fmol/mg). Affinity was unchanged. Real-time RT-PCR demonstrated that V_1a mRNA in preglomerular arterioles was three times greater in euvolemic SHR. Dehydration decreased expression 50% in renal vessels independent of rat strain; water loading increased V_1a mRNA. Thus V_1a receptor regulation correlated with changes in mRNA in a normal manner in response to chronic changes in AVP concentration, albeit set at a higher level in SHR. In dehydrated animals, AVP increased the cytosolic Ca²⁺ concentration ([Ca²⁺]_i) by 60 ± 5 and 112 ± 13 nM cytosolic Ca²⁺ in WKY and SHR, respectively (P < 0.01), whereas in hydrated animals the [Ca²⁺]_i increase was 168 ± 10 and 220 ± 18 nM, respectively (P < 0.05). In all hydration states, calcium signaling was greater in SHR compared with WKY (P < 0.05). Calcium signaling paralleled changes in the receptor density and mRNA. Mechanisms other than hydration state per se are likely to be responsible for the two- to threefold difference in the V_1a receptor density between WKY and SHR in the renal vasculature at the critical age of 6 wk.

renal circulation; afferent arteriole; receptor regulation; spontaneously hypertensive rat; calcium ion; arginine vasopressin; spontaneoulsy hypertensive rat

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