Renal Sympathetic Nerve Activity – Controlled by Renal Afferent Sympathoexcitatory or ‐Inhibitory Nerves ?

Abstract

Renal sympathetic nerve activity (RSNA) is important in hypertension, volume disorders or renal disease. It is unclear if increases of RSNA in disease are due to sympathoexcitatory or impaired sympathoinhibitory renal afferent nerves. We present data from nephritic rats suggesting the latter.Nephritis due to OX7‐antibodies. Methohexital anesthetized nephritic rats & controls instrumented to stimulate renal afferent nerve activity (ARNA) in order to influence RSNA: ipsilateral renal arterial catheter for intrarenal administration (IRA) of the TRPV1 agonist capsaicin to stimulate ARNA (CAP 6.6*10‐7M) and induce release of the tachykinin receptor agonist SP from renal afferents; contralateral stainless steel electrode for RSNA recording; before and after IRA CAP the tachykinin‐receptor blocker RP67580 was given. Baseline RSNA & ARNA were assessed. Some nephritic rats pretreated with tachykinin receptor antagonists to prove increased SP effects.IRA CAP decreased RSNA from 67.5±12.0 µV*sec to 14.8±4.2 µV*sec (p<0.05) over 60 minutes while in nephritis RSNA suppression was abolished. Suppressed RSNA in controls was transiently reversed by the tachykinin inhibitor. Under resting conditions RSNA was higher, ARNA lower in nephritis as compared to controls. Tachykinreceptor antagonism ameliorated damage in renal nephritis suggesting increased SP release from renal afferent nerves despite lack of the tachykinin dependant sympathoinhibition seen in controls.Our data suggest that a tachykinin dependant reno‐sympathetic reflex mechanism exerts sympathoinhibitory effects being impaired under pathophysiological circumstances.