PMID- 8430823
OWN - NLM
STAT- MEDLINE
DCOM- 19930305
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 264
IP  - 1 Pt 2
DP  - 1993 Jan
TI  - KCl and angiotensin responses in isolated rat renal arterioles: effects of 
      diltiazem and low-calcium medium.
PG  - F134-40
AB  - Studies in intact renovascular models have shown that calcium entry blockers 
      inhibit angiotensin (ANG II)-induced vasoconstriction in afferent (AA) but not 
      efferent arterioles (EA), suggesting that increases in smooth muscle cell 
      cytosolic calcium, the initiating intracellular message, result from entry 
      through potential-operated channels in AA, but from organelle storage 
      mobilization or entry through nonpotential-operated channels in EA. The present 
      study examined the effects of diltiazem (10(-5) M) on the constrictor responses 
      to KCl (50 mM) and half-maximal constricting concentrations (EC50) of ANG II and 
      the effects of low-calcium bathing medium on EC50 ANG II responses in isolated 
      rat AA and EA. KCl caused slightly greater decreases in lumen diameter in AA than 
      in EA (P < 0.05) that were completely inhibited by diltiazem in both. 
      Vasoconstriction to ANG II was significantly inhibited by diltiazem (29 +/- 12 
      vs. 67 +/- 31%; P < 0.02) in AA. However, constrictor response to ANG II in EA 
      was unchanged by diltiazem (42 +/- 32 vs. 41 +/- 31%). Constriction to ANG II of 
      AA in low-calcium medium was significantly attenuated (8 +/- 13 vs. 54 +/- 12%; P 
      < 0.01); however, EA constrictor response was not affected (43 +/- 22 vs. 51 +/- 
      19%). These data indicate that EC50 ANG II-induced AA constriction requires 
      calcium entry primarily through potential-operated channels. While 
      potential-operated calcium entry channels can be functionally expressed in EA, 
      intracellular calcium mobilization is the primary mechanism for ANG II-induced 
      constriction.
FAU - Conger, J D
AU  - Conger JD
AD  - Department of Medicine, University of Colorado Health Sciences Center, Denver 
      80220.
FAU - Falk, S A
AU  - Falk SA
LA  - eng
GR  - R01-DK-41294/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Culture Media)
RN  - 11128-99-7 (Angiotensin II)
RN  - 660YQ98I10 (Potassium Chloride)
RN  - EE92BBP03H (Diltiazem)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Angiotensin II/*pharmacology
MH  - Animals
MH  - Arterioles/drug effects
MH  - Calcium/pharmacology
MH  - Culture Media
MH  - Diltiazem/pharmacology
MH  - In Vitro Techniques
MH  - Potassium Chloride/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Renal Circulation/*drug effects
MH  - Vasoconstriction/drug effects
EDAT- 1993/01/01 00:00
MHDA- 1993/01/01 00:01
CRDT- 1993/01/01 00:00
PHST- 1993/01/01 00:00 [pubmed]
PHST- 1993/01/01 00:01 [medline]
PHST- 1993/01/01 00:00 [entrez]
AID - 10.1152/ajprenal.1993.264.1.F134 [doi]
PST - ppublish
SO  - Am J Physiol. 1993 Jan;264(1 Pt 2):F134-40. doi: 
      10.1152/ajprenal.1993.264.1.F134.