title: Acute hypercalcemia-induced hypertension: the roles of calcium channel and alpha-1 adrenergic receptor.
abstract: OBJECTIVE
  To study the mechanism(s) of acute hypercalcemia-induced hypertension in dogs.
  
  
  METHODS
  Adult male mongrel dogs were intravenously infused with: 1) normal saline solution, 2) CaCl2 solution, 3) CaCl2 + calcium channel blocker (verapamil), 4) CaCl2 + selective alpha-1 adrenergic receptor blocker (prazosin), or 5) CaCl2 + verapamil + prazosin. Either verapamil or prazosin treatment was started at forty minutes before CaCl2 infusion and then was co-administered throughout the three-hour experimental period. Systemic and renal hemodynamics parameters were determined.
  
  
  RESULTS
  Infusion of CaCl2 caused increases in mean arterial blood pressure (p < 0.01), total peripheral resistance (p < 0.001), and renal vascular resistance (p < 0.001). Prior treatment with either verapamil or prazosin lowered baseline blood pressure (p < 0.01) and could prevent hypercalcemia-induced hypertension. This occurred accompanying regaining to near normal values of abnormal systemic hemodynamics parameters. Combination of both drugs showed more profound effects, particularly on lowering renal vascular resistance.
  
  
  CONCLUSIONS
  Acute hypercalemic hypertension is caused by an increase in vascular resistance mediated via the direct effect of calcium on vascular smooth muscle as well as the indirect effect of calcium induced hypercatecholaminemia. The stimulatory effect of hypercalcemia on renal vascular resistance is more prominent than that on peripheral vascular resistance.
authors.affiliation: Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. EiamOng@netscape.net
authors.forename: Somchit
authors.initials: S
authors.lastname: Eiam-Ong
authors.forename: Somchai
authors.initials: S
authors.lastname: Eiam-Ong
authors.forename: Pongsak
authors.initials: P
authors.lastname: Punsin
authors.forename: Visith
authors.initials: V
authors.lastname: Sitprija
authors.forename: Narongsak
authors.initials: N
authors.lastname: Chaiyabutr
mesh_terms: D000208:Acute Disease; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D002395:Catecholamines / Q000097:blood*; D004285:Dogs; D006934:Hypercalcemia / Q000097:blood* / Q000150:complications / Q000503:physiopathology*; D006973:Hypertension / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*
chemical_list: D000317:Adrenergic alpha-Antagonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002395:Catecholamines