title: Enhanced total peripheral vascular responsiveness in hypertension accords with the amplifier hypothesis.
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  To assess whether the vascular amplifier applies to the total peripheral circulation in conscious hypertensive rabbits.
  
  
  METHODS
  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.
  
  
  RESULTS
  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 (r; based on Poiseuille's law) over the full range of vascular tone showed that r was narrower in hypertension, but, in contrast to TPR, the degree of narrowing was almost the same between maximum dilatation and constriction.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Pharmacology, University of Melbourne, Parkville, Victoria, Australia. c.wright@pharmacology.unimelb.edu.au
authors.forename: C E
authors.initials: CE
authors.lastname: Wright
authors.forename: J A
authors.initials: JA
authors.lastname: Angus
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D002476:Cellophane; D004305:Dose-Response Relationship, Drug; D005260:Female; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008729:Methoxamine / Q000494:pharmacology; D008955:Models, Cardiovascular; D011817:Rabbits; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D002476:Cellophane; D008729:Methoxamine; D000241:Adenosine