Estimation of non-autonomic and autonomic components of iliac bed vascular resistance in renal hypertensive rabbits

Abstract

Iliac bed vascular resistance (IVR) was measured before and after pharmacological block of the autonomic effectors in unanaesthetized renal hypertensive and normotensive rabbits with previously implanted Doppler flowmeters. This permitted partitioning the resting IVR into a non-autonomic component (ie, steady-state IVR after block) and an autonomic component (ie, resting IVR minus non-autonomic IVR). When IVR was measured at the same mean arterial pressure (MAP) before and after block in each animal, the increase in estimated non-autonomic IVR accounted entirely for the rise in resting IVR in renal hypertensive rabbits. However, if IVR measurements after block were made at a lower MAP than before block, the estimated non-autonomic and autonomic components were both significantly increased in renal hypertensive rabbits. It is concluded that in the latter experiment non-autonomic IVR in renal hypertension was underestimated, whilst the autonomic component was overestimated. The rise in non-autonomic IVR in renal hypertension was partly due to structural changes in the iliac bed, since IVR remained higher in hypertensive than in normotensive rabbits after abolishing smooth muscle tone with vasodilator drugs.

Guanethidine‐induced Vasodilatation in the Rabbit, Mediated by Endogenous Histamine

“…In the course of other studies in the rabbit we observed that the intravenous injection of guanethidine elicited a prolonged vasodilatation (White, 1967;West, Angus & Korner, 1975). Such a response has been reported previously in the rabbit (Kadzielawa, 1962).…”

“…Administration of guanethidine resulted in pronounced reduction in blood pressure and HVR ( Figure 1, left panels). When the guanethidine injection was repeated 1 h later in these autonomically blocked animals, the haemodynamic effects were similar to those observed after the first injection ( Figure 1, middle) despite good evidence of effective neural block at this time (West et al, 1975). When the sympathetic vasoconstriction was initially blocked with phenoxybenzamine (6 mg/kg) instead of guanethidine (12.5 mg/kg), injection of guanethidine again resulted in a marked fall in HVR (Figure 1, right).…”

“…Lumbar sympathetic nerve stimulation experiments in anaesthetized rabbits show that the above dose of guanethidine blocks transmission in sympathetic nerves to strong electrical stimuli (6.5 V, 1 ms, 8 Hz) for a period of 4 to 6 h (West et al, 1975). Guanethidine does not interfere with secretion of adrenal catecholamines but the doses of propranolol and phentolamine were adequate to block heart rate and peripheral fi-and a-adrenoceptor mediated effects produced by 4 pg of isoprenaline sulphate and by 2 pg/kg noradrenaline injected intravenously.…”

“…Arterial pressure, heart rate, lower aortic blood flow (taken to be hindlimb blood flow, HBF) and hindlimb vascular resistance (HVR, computed by an analogue divider as arterial pressure/ HBF) were determined as described previously (White, McRitchie & Porges, 1974;West et al, 1975). As used, the flow transducer becomes firmly adherent to the artery and the calibration lines are independent of perfusion pressure between the limits tested in these experiments of 60 to 160 mmHg.…”

“…The drug regime to block the autonomic effectors was as described by Korner & Uther (1969), with the modifications described by West et al (1975). A large dose of guanethidine sulphate (12.5 mg/kg i.v.)…”