title: Norepinephrine-induced calcium signaling pathways in afferent arterioles of genetically hypertensive rats.
abstract: This study provides new information about the relative importance of calcium mobilization and entry in the renal vascular response to adrenoceptor activation in afferent arterioles isolated from 7- to 8-wk-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Intracellular free calcium concentration ([Ca(2+)](i)) was measured in microdissected arterioles utilizing ratiometric photometry of fura 2 fluorescence. There was no significant strain difference in baseline [Ca(2+)](i). Norepinephrine (NE; 10(-6) and 10(-7) M) elicited immediate, sustained increases in [Ca(2+)](i). The general temporal pattern of response to 10(-6) M NE consisted of an initial peak and a maintained plateau phase. The response to NE was partially blocked by nifedipine (10(-6) M) or 8-(N,N-diethylamino) octyl-3,4,5-trimetoxybenzoate (TMB-8; 10(-5) M). A calcium-free external solution abolished the sustained [Ca(2+)](i) plateau response to NE, with less influence on the peak response. In the absence of calcium entry, TMB-8 (10(-5) M) completely blocked the calcium response to NE in WKY but not SHR, suggesting strain differences in mobilization. A higher concentration of TMB-8 (10(-4) M), however, blocked all discernible mobilization in both strains. We conclude that there are differences in Ca(2+) handling in renal resistance vessels between young WKY and SHR with respect to mobilization stimulated by alpha-adrenoceptors. Afferent arterioles of young SHR appear to have a larger inositol-1,4,5-trisphosphate-sensitive pool or release from a site less accessible to TMB-8.
authors.affiliation: Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7545, USA.
authors.forename: M
authors.initials: M
authors.lastname: Salomonsson
authors.forename: W J
authors.initials: WJ
authors.lastname: Arendshorst
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D020013:Calcium Signaling; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D005707:Gallic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D006973:Hypertension / Q000378:metabolism*; D066298:In Vitro Techniques; D007668:Kidney / Q000033:anatomy & histology / Q000098:blood supply*; D009543:Nifedipine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002614:Chelating Agents; D014662:Vasoconstrictor Agents; D004533:Egtazic Acid; C006014:8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; D005707:Gallic Acid; D009543:Nifedipine; D002118:Calcium; D009638:Norepinephrine