NEUROHUMORAL MECHANISMS AND THE ROLE OF ARTERIAL BARORECEPTORS IN THE RENOVASCULAR RESPONSE TO HEMORRHAGE IN RABBITS

1. Conscious rabbits, with implanted renal artery Doppler flow probes were bled at a constant rate (4 ml min-1). We assessed the contribution of autonomic, hormonal and local factors to the renal vasoconstrictor response to 20% loss of blood volume (BV) and the role of the sinoaortic baroreceptors in the neurohumoral response. 2. With intact autonomic effectors, 20% BV loss was associated with a small fall in vascular conductance, which was completely unaffected by inhibition or blockade of the combined effects of the two major pressor hormones angiotensin II (AII) and arginine vasopressin (AVP). Combined blockade of the autonomic effects plus those of the two pressor hormones resulted in marked elevation of vascular conductance, considered to be due to the local effects of haemorrhage. This response provided the baseline for assessing the constrictor response in the intact animal which, during 20% BV loss, was entirely due to reflex activity through the sympatho-adrenal system. 3. In contrast to the early phase of haemorrhage (< 20% BV removal) both hormones played a role in the maintenance of mean arterial pressure immediately after haemorrhage and in the maintenance of renal vascular tone. This suggested that the contribution by hormones occurs only after more pronounced blood loss and hypotension. 4. In the presence of autonomic blockade with mecamylamine plus methscopolamine (plus a constant infusion of noradrenaline to maintain resting blood pressure) the renal vasoconstrictor response was similar to that of the intact animal. We have previously found that this regime is associated with greatly enhanced release of AVP and plasma renin activity. Sinoaortic denervation had no effect on this hormonally mediated vasoconstriction. 5. When the autonomic nervous system was intact but the effects of AII and AVP were blocked to prevent the accentuated hormonally mediated vasoconstriction, sinoaortic denervation completely abolished the normal autonomic renal constrictor response, which is thus largely under control of the arterial baroreceptors.