Courneya C A
Department of Physiology, University of British Columbia, Vancouver, Canada.
Am J Physiol. 1996 Oct;271(4 Pt 2):H1524-30. doi: 10.1152/ajpheart.1996.271.4.H1524.
It is not known how the intrarenal mechanisms that control renin release, in particular the intrarenal receptor, respond to the structural changes in renal vasculature that are secondary to hypertension. It is also not known whether baroreflex control of renin release is affected by hypertension. We hypothesized impairment at both levels. Thus we compared plasma renin activity (PRA) during hemorrhage between conscious normotensive (NT) and renal-wrap hypertensive (HT) rabbits. Mean arterial pressure (MAP) and PRA were measured before and during hemorrhage at 4 ml/min. To look at intrarenal control of renin we hemorrhaged NT and HT rabbits after pharmacological autonomic nervous system (ANS) blockade, thus eliminating the influence of reflexes. The slope of the log PRA-MAP relationship was significantly (P < 0.002) reduced in ANS-blocked HT compared with NT rabbits, i.e., for a given fall in MAP, HT rabbits had lower plasma levels of PRA. To examine baroreflex control of renin we hemorrhaged rabbits with an intact ANS. The slope of the log PRA-MAP relationship was significantly attenuated (P < 0.0087) in ANS-intact HT compared with NT rabbits. Cardiac receptor denervation had no effect on the slope of this relationship for either NT or HT rabbits, indicating no appreciable role for cardiac receptors in the reflex control of renin under these circumstances. Although sinoaortic denervation significantly attenuated the slope of the log PRA-MAP relationship (suggesting an important role in reflex control of renin) it did so equally in NT (P < 0.0261) and HT (P < 0.0189) rabbits. We concluded that renin release was impaired in ANS-blocked HT rabbits and that the impairment may be due to dysfunction of intrarenal mechanisms (e.g., the intrarenal receptor). These results also support the hypothesis that reflex control of PRA was impaired in HT rabbits; however, no particular role could be ascribed to either cardiac or arterial baroreceptors in contributing to this impairment.
