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(Hypertension. 1995;25:1224-1231.)
© 1995 American Heart Association, Inc.
Articles |
-Adrenoceptor Modulation of Norepinephrine and ATP Release in Isolated Kidneys of Spontaneously Hypertensive Rats
From Medizinische Universitätsklinik Freiburg, Innere Medizin IV, and Pharmakologisches Institut (I.v.K.), Freiburg im Breisgau, Germany.
Abstract The present study investigates sympathetic
cotransmission and its 
-adrenoceptor–mediated modulation in kidneys
of spontaneously hypertensive rats (SHR, 12 to 14 weeks) and
age-matched normotensive Wistar-Kyoto rats (WKY). In the presence of
cocaine and corticosterone, renal nerve stimulation at 1 Hz (30
seconds) induced a greater outflow of norepinephrine in SHR (4.2±0.2
pmol/g kidney) than in WKY (3.0±0.2 pmol/g kidney). The
2-adrenoceptor antagonist rauwolscine (0.01 to 1
µmol/L) increased the stimulation-induced norepinephrine outflow to a
greater extent in SHR than in WKY. In contrast, the
1-adrenoceptor antagonist prazosin (0.03 to 3 µmol/L)
increased the stimulation-induced norepinephrine outflow to a greater
extent in WKY than in SHR. This difference was not observed in the
presence of the P1-purinoceptor antagonist
8-(p-sulfophenyl)theophylline (100 µmol/L).
Stimulation at 4 Hz (30 seconds) induced an outflow of ATP (SHR,
12.7±3.3 pmol/g kidney; WKY, 16.7±2.1 pmol/g kidney; perfusion
solution without cocaine and corticosterone). Prazosin (0.03 µmol/L)
markedly reduced pressor responses to stimulation and inhibited the
induced ATP outflow by 60% to 70%. When prazosin (0.03 µmol/L) was
present, rauwolscine (0.1 µmol/L) increased the induced
outflow of norepinephrine and ATP and markedly enhanced
prazosin-resistant pressor responses. These pressor responses were
abolished by the P2-purinoceptor antagonist suramin (300
µmol/L). The results demonstrate an increased
2-adrenoceptor–mediated automodulation of
norepinephrine release in SHR kidneys caused by increased intrasynaptic
norepinephrine levels. 1-Adrenoceptor–mediated
transjunctional modulation of norepinephrine release by
endogenous adenosine is defective in SHR kidneys and may be
responsible for the greater norepinephrine release in this strain.
Norepinephrine and ATP are coreleased in SHR and WKY kidneys and both
mediate pressor responses to stimulation. The release of ATP is
identical in SHR and WKY and is, like that of norepinephrine, modulated
by 2-adrenoceptor–mediated autoinhibition.
Key Words: hypertension, experimental • kidney • norepinephrine • purines • sympathetic nervous system • rats, inbred SHR • receptors, adrenergic, alpha • receptors, purinergic
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