Studies of the interaction between the renin-angiotensin system and sympathetic nervous system in man
There is considerble evidence for an interaction between the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) from animal studies but the evidence in man is conflicting. The present investigations sought evidence for such an interaction in healthy man. The studies were in two...
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University of Edinburgh
1992
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| Online Access: | http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.661726 |
| Summary: | There is considerble evidence for an interaction between the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) from animal studies but the evidence in man is conflicting. The present investigations sought evidence for such an interaction in healthy man. The studies were in two main groups, those that sought a postsynaptic interaction whereby angiotensin II (AII) augments the effect of released noradrenaline (NA), and those that sought a presynaptic interaction whereby AII augments the release of NA. The first study sought a postsynaptic interaction by infusion of AII and NA alone and in combination. There was a significant synergistic effect of AII/NA with respect to systolic blood pressure (BP). There was no interaction with regard to diastolic BP. The fact that this interaction was limited to systolic BP suggests that this interaction occurs in the myocardium rather than the peripheral vasculature or may be an effect on intravascular volume. A renal AII/NA interaction causing retention of sodium/fluid might account for this. A series of experiments were performed to investigate a possible renal tubular antinatiuretic interaction. These showed that both AII and NA had direct antinatriuretic effects. There was however no synergistic antinatriuretic effect. It seems unlikely that the postynaptic AII/NA interaction is due to sodium/fluid retention. The next study therefore investigated the possibility that AII augments the inotropic response to beta receptor stimulation. The combination of AII/isoprenaline caused a marked increase in stroke volume above that seen with isoprenaline alone. There are several possible mechanisms but a regional redistribution of venous blood from the splanchnic bed increasing cardiac filling seems most likely. |
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