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1 Internal Medicine, University of California, Davis, Davis, California, United States
2 Div. of Cardiovascular Medicine, University of California, Davis, Davis, California, United States
* To whom correspondence should be addressed. E-mail: mpkaufman{at}ucdavis.edu.
The renal vasoconstriction induced by the sympathetic outflow during exercise serves to direct blood flow from the kidney towards the exercising muscles. The renal circulation seems to be particularly important in this regard because it receives a substantial part of the cardiac output, which in resting humans has been estimated to be 20 %. The role played by group III mechanoreceptors in causing the reflex renal sympathetic response to static contraction remains an open question. To shed some light on this question, we recorded the renal sympathetic nerve responses to static contraction before and after injecting gadolinium into the arterial supply of the statically contracting triceps surae muscles of both decerebrated unanesthetized and chloralose anesthetized cats. Gadolinium has been shown to be a selective blocker of mechanogated channels in thin fiber muscle afferents, which comprise the afferent arm of the exercise pressor reflex arc. In both decerebrated (n=15) and chloralose anesthetized (n=12) cats, we found that gadolinium (10mM; 1 ml) significantly attenuated the renal sympathetic nerve and pressor responses to static contraction (60 seconds) after a latent period of 60 minutes; both responses recovered after a latent period of 120 minutes. We conclude that thin fiber mechanoreceptors supplying contracting muscle are capable of playing a role in causing some the renal vasoconstriction evoked by the exercise pressor reflex.
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