Increases in vascular resistance (or the reciprocal, vascular conductance) in response to constrictor drugs are amplified (or attenuated) in the hindquarter vascular bed of hypertensive rats and rabbits. However, such changes have not been observed for the total peripheral circulation.
To assess whether the vascular amplifier applies to the total peripheral circulation in conscious hypertensive rabbits.
Rabbits were implanted with a flow probe for measuring cardiac output, a left atrial catheter for infusing dilator (adenosine) and constrictor (methoxamine) drugs, and ear artery and vein catheters for measuring mean arterial pressure (MAP) and for giving ganglion blockade. Data from full dose-total peripheral resistance (TPR) or total peripheral conductance (TPC) response curves to adenosine and methoxamine were combined into a logistic function extending from near full dilatation to near maximum constriction.
Changes in MAP induced by methoxamine and adenosine were markedly greater in the ‘wrap’ rabbits (those with renal cellophane wrapping) compared with the sham animals. In the ‘wrap’ rabbits, the slopes and ranges of the adenosine-TPR response curve and the methoxamine-TPC response curve were 200% and 60%, respectively, of sham values. These data show that TPR changes are amplified, and TPC changes attenuated, to dilator and constrictor stimuli. The relationship between dose-average vascular radius (𝙧̅; based on Poiseuille's law) over the full range of vascular tone showed that 𝙧̅ was narrower in hypertension, but, in contrast to TPR, the degree of narrowing was almost the same between maximum dilatation and constriction.
The total peripheral circulation in experimental hypertension is a TPR amplifier, or TPC attenuator, in the rabbit, consistent with well-established data in the major vascular beds.
1Department of Pharmacology, University of Melbourne, Australia.
2Correspondence and requests for reprints to Dr Christine E. Wright, Department of Pharmacology, University of Melbourne, Grattan Street, Parkville, Victoria 3052, Australia.
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Sponsorship: This work was supported in part by a Grant-in-Aid from the National Heart Foundation of Australia.
Received 18 March 1999 Revised 24 May 1999 Accepted 3 August 1999