Aortic and inferior vena caval balloons were used to alter mean arterial blood pressure, pulse pressure ( PP ), and right atrial pressure ( RAP ) in unanesthetized rabbits and to reflexly evoke changes in heart period (pulse interval). Curves relating mean arterial blood pressure to heart period were compared in different groups of rabbits at similar Δ PP and Δ RAP . Median blood pressure ( BP 50 ), average gain (G), and heart period range (maximum to minimum heart period) were calculated from the S-shaped curves. The reflex was evoked from arterial baroreceptors and probably from cardiac and pulmonary baroreceptors. Curves relating mean arterial blood pressure and heart period differed with regard to BP 50 and G in sham-operated, thalamic, and pontine rabbits, indicating that suprabulbar centers normally play a role in the reflex. Curves from sham-operated and pontine rabbits treated with atropine also differed, suggesting suprabulbar control of sympathetic effectors. In intact rabbits, forebrain and diencephalic centers caused vagal and sympathetic effectors to respond over the same arterial blood pressure range, but, in pontine rabbits, the effectors responded over dissimilar ranges. In intact rabbits, changes in mean arterial blood pressure evoked reciprocal and nearly equal changes in vagal and sympathetic effectors, but, in pontine rabbits, a given pressure change altered heart period predominantly through one effector. In sham-operated rabbits, vagal effects on heart period were lower by a constant amount at every level of mean arterial blood pressure than they were in pontine rabbits, suggesting that suprabulbar centers exerted a tonic inhibitory effect on vagal motoneurons not involved in the reflex.

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.

The circulatory effects of blocking cardiac and peripheral autonomic effectors were studied in 32 subjects with established essential hypertension, and in 15 normotensives. The mean resting arterial pressure, heart rate and total peripheral resistance index (TPRI) were significantly higher in the hypertensives, but cardiac index was the same in both groups. In subjects with blocked cardiac effectors (atropine + beta-blocking drugs, i.v.) the sympathetic constrictor effects on TPRI were estimated from the changes after giving i.v. guanethidine + phentolamine. The autonomic component of TPRI was higher in hypertensives than in normotensives. The residual resistance after `total' autonomic block (non-autonomic TPRI) was higher in hypertensives, accounting for 60 to 80% of the initial difference in resting TPRI between the two groups. With an increase in non-autonomic TPRI, the increased autonomic TPRI effect in hypertension is not necessarily due to increased sympathetic nerve activity. Vagal and cardiac sympathetic effects on heart rate were compared in the two groups. Each estimate was based on the average of the responses to the appropriate blocking drug (1) in subjects not previously given a blocking drug, and (2) in subjects with the other cardiac effector pathway already blocked. The higher heart rate in established hypertension was predominantly due to change in vagal rather than cardiac sympathetic effects.