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   <subfield code="a">10.1007/BF00175465</subfield>
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   <subfield code="a">Activation of β2-adrenoceptors by isoprenaline and adrenaline enhances noradrenaline release in cortical kidney slices of young spontaneously hypertensive rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[L. Rump, M. Schuster, P. Schollmeyer]</subfield>
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   <subfield code="a">Summary: The aim of the present study was to investigate β-adrenoceptor modulation of noradrenaline release from sympathetic nerves in superfused cortical kidney slices of 4-week-old spontaneously hypertensive rats (SHR) and age-matched controls (WKY). After preincubation with 3H-noradrenaline the kidney slices were electrically stimulated in superfusion chambers. The stimulation induced (S-I) outflow of radioactivity was mainly composed of unmetabolized 3H-noradrenaline in both strains and thus taken as an index of noradrenaline release. There was a frequency-dependent (1.25-20 Hz) increase in the S-1 outflow of radioactivity. At all stimulation frequencies tested S-I outflow of radioactivity was similar or even slightly lower in SHR than in WKY kidney slices in either the absence or presence of cocaine (10 μmol/l). The non-selective β-adrenoceptor agonists isoprenaline (0.l gmol/1) and adrenaline (0.01 and 0.1 μmol/l) enhanced S-I outflow of radioactivity. The facilitatory effects of isoprenaline (0.1 μmol/l) and adrenaline (0.1 μmol/l) were blocked by the selective β2-adrenoceptor antagonist ICI 118551 (0.1 μmol/l) but not by the selective β1-adrenoceptor antagonist atenolol (0.3 μmol/l). The cell-permeable CAMP analogue 8-bromo-cAMP (300 μmol/l) enhanced S-1 outflow of radioactivity to a similar extent in both SHR and WKY kidney slices. A combination of 8-bromo-cAMP (300 μmol/l) and adrenaline (0.1 μmol/l) did not enhance S-1 outflow of radioactivity to a greater extent than 8-bromo cAMP (300 μmol/l) alone in both strains. However, the facilitatory effects of isoprenaline (0.1 μmol/l) and adrenaline (0.1 μmol/l) but not that of adrenaline (0.01 μmol/l) were significantly greater in SHR than in WKY. The results suggest that stimulation of prejunctional β2-adrenoceptors by adrenaline even in the absence of a-adrenoceptor blockade enhances noradrenaline release in kidney cortex of young SHR and WKY. This β2-adrenoceptor mediated effect may possibly be dependent on cAMP formation. The greater facilitatory effects of isoprenaline (0.1 μmol/l) and adrenaline (0.1 μmol/l) in SHR as compared to WKY are in accord with receptor binding studies which show a higher density of β2-adrenoceptors in SHR than in WKY kidney cortex.</subfield>
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   <subfield code="a">Springer-Verlag, 1992</subfield>
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   <subfield code="a">3H-noradrenaline release</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">SHR</subfield>
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   <subfield code="a">Kidney</subfield>
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   <subfield code="a">Prejunctional β-adrenoceptors</subfield>
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   <subfield code="a">Adrenaline</subfield>
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   <subfield code="a">Isoprenaline</subfield>
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   <subfield code="a">SHR : Spontaneously hypertensive rats</subfield>
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   <subfield code="a">WKY : WistarKyoto rats</subfield>
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   <subfield code="a">cAMP : 3′-5′-cyclic adenosine monophosphate</subfield>
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   <subfield code="a">S-I : stimulation induced</subfield>
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   <subfield code="a">Rump</subfield>
   <subfield code="D">L.</subfield>
   <subfield code="u">Medizinische Universitatsklinik Freiburg, Innere Medizin IV, Hugstetter Strasse 55, W-7800, Freiburg, Federal Republic of Germany</subfield>
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