Recent insights into the interactions between the baroreflex and the kidneys in hypertension.
Recent findings in chronically instrumented animals challenge the classic concept that baroreflexes do not play a role in the chronic regulation of arterial pressure. As alterations in renal excretory function are of paramount importance in the chronic regulation of arterial pressure, several of these recent studies have focused on the long-term interactions between the baroreflex and the kidneys during chronic perturbations in arterial pressure and body fluid volumes. An emerging body of evidence indicates that the baroreflex is chronically activated in several experimental models of hypertension, but in most cases, the duration of these studies has not exceeded 2 wk. Although these studies suggest that the baroreflex may play a compensatory role in attenuating the severity of the hypertension, possibly even in primary hypertension with uncertain causes of sympathetic activation, there has been only limited assessment of the quantitative importance of this interaction in the regulation of arterial pressure. In experimental models of secondary hypertension, baroreflex suppression of renal sympathetic nerve activity is sustained and chronically promotes sodium excretion. This raises the possibility that the renal nerves may be the critical efferent link for baroreceptor-induced suppression of central sympathetic output through which long-term compensatory reductions in arterial pressure are produced. This contention is supported by strong theoretical evidence but must be corroborated by experimental studies. Finally, although it is now clear that pressure-induced increases in baroreflex activity persist for longer periods of time than previously suggested, studies using new tools and novel approaches and extending beyond 2 wk of hypertension are needed to elucidate the true role of the baroreflex in the pathogenesis of clinical hypertension.
Lohmeier
Thomas E
TE
Dept. of Physiology and Biophysics, Univ. of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505, USA. tlohmeier@physiology.umsmed.edu.
Hildebrandt
Drew A
DA
Warren
Susan
S
May
Paul J
PJ
Cunningham
J Thomas
JT
D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D003714:Denervation; D006801:Humans; D006977:Hypertension, Renal / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology; D012849:Sinoatrial Node / Q000502:physiology; D012964:Sodium / Q000652:urine*
D000804:Angiotensin II; D012964:Sodium