PMID- 1334994
OWN - NLM
STAT- MEDLINE
DCOM- 19930126
LR  - 20190819
IS  - 0263-6352 (Print)
IS  - 0263-6352 (Linking)
VI  - 10
IP  - 10
DP  - 1992 Oct
TI  - Extracellular calcium, contractile activity and membrane potential in tail 
      arteries from genetically hypertensive rats.
PG  - 1137-43
AB  - OBJECTIVE AND DESIGN: This study compares the effect of extracellular calcium on 
      contractile responsiveness and membrane potential (E(m)) in arteries from 
      stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto 
      normotensive (WKY) rats. METHODS: Isometric force and E(m) were measured in 
      isolated tail artery strips using standard muscle bath and microelectrode 
      techniques, respectively. RESULTS: The resting contractile force in SHRSP and WKY 
      arteries was not influenced by the extracellular calcium concentration. However, 
      the rate of force development in response to norepinephrine (3 x 10(-8) mol/l) 
      was slowed when calcium was elevated and increased when calcium was reduced. 
      Compared with WKY rats, this stabilizing action of calcium on contractions to 
      norepinephrine was reduced in SHRSP. In 1.6 mmol/l calcium, resting E(m) in SHRSP 
      did not differ from that in WKY rats. Calcium-free buffer caused depolarization 
      in SHRSP and WKY rats. Reductions in calcium below physiological levels resulted 
      in depolarization, whereas elevations in calcium caused hyperpolarization. 
      Regardless of the calcium concentration, E(m) values in SHRSP did not differ from 
      those in WKY rats. Norepinephrine (3 x 10(-8) mol/l) caused a depolarization in 
      WKY rat and SHRSP arteries, and the magnitude of this depolarization was not 
      influenced by calcium. Endothelium removal did not alter the stabilizing effects 
      of calcium on the membrane potential or contractile activity in WKY rats or 
      SHRSP. CONCLUSIONS: The reduced stabilizing effect of calcium on the contractile 
      activity in SHRSP arteries is not due to an alteration in the general effect of 
      the cation on the membrane potential.
FAU - Chai, S
AU  - Chai S
AD  - Department of Physiology, University of Michigan Medical School, Ann Arbor.
FAU - Webb, R C
AU  - Webb RC
LA  - eng
GR  - HL18575/HL/NHLBI NIH HHS/United States
GR  - HL27020/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - J Hypertens
JT  - Journal of hypertension
JID - 8306882
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Arteries/physiology/physiopathology
MH  - Biomechanical Phenomena
MH  - Calcium/*physiology
MH  - Cerebrovascular Disorders
MH  - Extracellular Space
MH  - Male
MH  - Membrane Potentials/*physiology
MH  - Muscle Contraction/*physiology
MH  - Muscle, Smooth, Vascular/physiology/*physiopathology
MH  - Rats
MH  - Rats, Inbred SHR/*physiology
MH  - Rats, Inbred WKY
MH  - Tail/blood supply
EDAT- 1992/10/01 00:00
MHDA- 1992/10/01 00:01
CRDT- 1992/10/01 00:00
PHST- 1992/10/01 00:00 [pubmed]
PHST- 1992/10/01 00:01 [medline]
PHST- 1992/10/01 00:00 [entrez]
AID - 10.1097/00004872-199210000-00005 [doi]
PST - ppublish
SO  - J Hypertens. 1992 Oct;10(10):1137-43. doi: 10.1097/00004872-199210000-00005.