HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 290/2/R331    most recent 00317.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Eppel, G. A. Articles by Evans, R. G. Search for Related Content PubMed PubMed Citation Articles by Eppel, G. A. Articles by Evans, R. G.

RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

Type 1 neuropeptide Y receptors and ₁-adrenoceptors in the neural control of regional renal perfusion

¹Department of Physiology and ²Monash Micro Imaging, Monash University, Melbourne, Australia

Submitted 4 May 2005 ; accepted in final form 22 September 2005

The aim of this study was to determine the contribution of neuropeptide Y (NPY) Y₁ receptors in neurally mediated reductions in renal medullary perfusion. In pentobarbital sodium-anesthetized rabbits, electrical stimulation of the renal nerves (RNS, 0.5–16 Hz) decreased renal perfusion in a frequency-dependent manner. Under control conditions, 4 Hz reduced cortical and medullary perfusion by –85 ± 3% and –43 ± 7%, whereas 8 Hz reduced them by –93 ± 2% and –73 ± 4%, respectively. After Y₁ receptor antagonism with BIBO3304TF (0.1 mg/kg plus 0.2 mg·kg·^–1·h^–1), RNS reduced perfusion less (by –65 ± 9% and –12 ± 8% at 4 Hz). ₁-Adrenoceptor antagonism with prazosin (0.2 mg/kg plus 0.2 mg kg^–1h^–1) also inhibited RNS-induced reductions in renal perfusion (–80 ± 4% and –37 ± 10% reductions in the cortex and medulla, respectively, at 8 Hz). When given after BIBO3304TF treatment, prazosin inhibited RNS-induced reductions in cortical and medullary perfusion more profoundly (–57 ± 12% and –25 ± 9% reductions, respectively, at 8 Hz). Y₁ receptor- and ₁-adrenoceptor-blockade were confirmed by testing vascular responses to renal arterial NPY and phenylephrine boluses. NPY-positive immunolabeling was observed around interlobular arteries, afferent and efferent arterioles, and in the outer medulla. In conclusion, Y₁ receptors and ₁-adrenoceptors contribute to RNS-induced vasoconstriction in the vessels that control both cortical and medullary perfusion. Consistent with this, NPY immunostaining was associated with blood vessels that control perfusion in both regions. There also seems to be an interaction between Y₁ receptors and ₁-adrenoceptor-mediated neurotransmission in the control of renal perfusion.

renal medullary blood flow; sympathetic nervous system; BIBO3304TF

This article has been cited by other articles:

				N. W. Rajapakse, G. A. Eppel, R. E. Widdop, and R. G. Evans ANG II type 2 receptors and neural control of intrarenal blood flow Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2006; 291(6): R1669 - R1676. [Abstract] [Full Text] [PDF]