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Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7545
Experiments were conducted to gain insight into mechanisms
responsible for exaggerated renal vascular reactivity to ANG II and
vasopressin (AVP) in spontaneously hypertensive rats (SHR) during the
development of hypertension. Cytosolic calcium concentration ([Ca2+]i)
was measured by ratiometric fura 2 fluorescence and a microscope-based photometer. Vascular smooth muscle cells (SMC) from preglomerular arterioles were isolated and dispersed using an iron oxide-sieving method plus collagenase treatment. ANG II and AVP produced rapid and
sustained increases in
[Ca2+]i.
ANG II elicited similar dose-dependent increases in
[Ca2+]i
in SMC from SHR and Wistar-Kyoto rats (WKY). In contrast, AVP caused
almost twofold larger responses in afferent arteriolar SMC from SHR.
ANG II effects were inhibited by the
AT1 receptor antagonist losartan.
AVP action was blocked by the V1
receptor antagonist
[d(CH2)5,Tyr(NH2)9]AVP.
In SMC pretreated with nifedipine, neither ANG II nor AVP elicited
[Ca2+]i
responses. Poststimulation nifedipine reversed elevated
[Ca2+]i
to basal levels. Short-term reductions in external
[Ca2+]i
(EGTA) mimicked the nifedipine effects. Our study shows that AT1 and
V1 receptors stimulate
[Ca2+]i
by a common mechanism characterized by preferential action on
voltage-gated L-type channels sensitive to dihydropyridines. Calcium
signaling elicited by AT1
receptors does not differ between SHR and WKY; thus the in vivo
exaggerated reactivity may be dependent on interactions with other cell
types, e.g., endothelium. In contrast, AVP produced larger changes in
[Ca2+]i
in arteriolar SMC from SHR, and such direct effects can account for the
exaggerated renal blood flow responses.
smooth muscle cells; calcium channel; voltage-gated channel; dihydropyridine; nifedipine; spontaneously hypertensive rat; inbred rats; renal circulation; glomerular filtration rate; segmental vascular resistance; angiotensin AT1 receptor; vasopressin V1 receptor
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