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Received for publication January 13, 2006.
Revised March 10, 2006.
Accepted for publication March 13, 2006.
The purpose of this study was to test the hypothesis that renal sympathetic nerves modulate angiotensin II-induced renal vasoconstriction in kidneys from genetically hypertensive rats via Y1 receptors activating the Gi pathway. In isolated, perfused kidneys from spontaneously hypertensive rats, the naturally-occuring renal sympathetic co-transmitter neuropeptide Y at 6 nmoles/L enhanced angiotensin II (0.3 nmoles/L)-induced changes in perfusion pressure by 47 ± 7 mm Hg, and this effect was inhibited by BIBP3226 (a selective Y1-receptor antagonist, 1 µmole/L). We next examined whether periarterial nerve stimulation (5 Hz) enhances renal vascular responses to a physiological level of angiotensin II (100 pmoles/L). Kidneys were pretreated with prazosin (a selective 
1-adrenoceptor antagonist) to block nerve stimulation-induced changes in perfusion pressure. In kidneys from spontaneously hypertensive rats, but not normotensive rats, periarterial nerve stimulation significantly augmented angiotensin II-induced changes in perfusion pressure (177 ± 26% of response in absence of stimulation). BIBP3226, but not rauwolscine (a selective 2-adrenoceptor antagonist), abrogated periarterial nerve stimulation-induced enhancement of angiotensin II-mediated renal vasoconstriction. Pretreatment of hypertensive animals with pertussis toxin three days prior to kidney perfusion significantly (P<0.000001) decreased mean blood pressure (203 ± 2 versus 145 ± 6 mm Hg in non-pretreated versus pertussis toxin-pretreated SHR) and abolished periarterial nerve stimulation-induced enhancement of angiotensin II-mediated renal vasoconstriction. We conclude that in spontaneously hypertension rats, but not normotensive rats, sympathetic nerve stimulation enhances renal vascular responses to physiological levels of angiotensin II via a mechanism mainly involving Y1 receptors coupled to Gi proteins.
Key words:
angiotensin II, neuropeptide Y, perfused rat kidney, renal vascular resistance, spontaneously hypertensive rat, sympathetic nervous system
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