Structure, function, and endothelium-derived hyperpolarizing factor in the caudal artery of the SHR and WKY rat.
OBJECTIVE
To quantify structural and functional characteristics of the caudal artery from spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats with particular reference to endothelium-derived hyperpolarizing factor (EDHF).


RESULTS
Ultrastructural studies showed that the number of myoendothelial gap junctions, smooth muscle cell (SMC) layers, and medial cross-sectional area were significantly greater in SHR than WKY. Intracellular dye labeling demonstrated hyperplasia of SMCs in SHR. Analysis of nerve-mediated excitatory junction potentials recorded in SMCs at the adventitial and luminal borders demonstrated decreased radial coupling of SMCs in SHR. In both SHR and WKY, in the presence of NG-nitro-L-arginine methyl ester and indomethacin, acetylcholine-elicited EDHF was abolished by charybdotoxin and apamin, while iberiotoxin had no effect, implicating the involvement of small and intermediate, but not large, calcium-activated potassium channels. EDHF was abolished by Gap-mimetic peptides, 18beta-glycyrrhetinic acid, and endothelial removal but not affected by the NO scavengers hydroxocobalamin and carboxy-PTIO.


CONCLUSIONS
Significant differences in SMC morphology and homocellular and heterocellular coupling exist between the caudal artery of SHR and WKY rats. In the caudal artery of SHR, significantly greater heterocellular coupling compensates for other structural changes in the media to maintain a functional role for EDHF.
Sandow
Shaun L
SL
Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT, 0200, Australia. shaun.sandow@anu.edu.au
Bramich
Narelle J
NJ
Bandi
Hari Priya
HP
Rummery
Nicole M
NM
Hill
Caryl E
CE
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001158:Arteries / Q000473:pathology; D001685:Biological Factors / Q000032:analysis / Q000502:physiology*; D018999:Charybdotoxin / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D017629:Gap Junctions / Q000502:physiology / Q000648:ultrastructure; D006965:Hyperplasia; D006973:Hypertension / Q000473:pathology*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology; D024681:Potassium Channels, Calcium-Activated / Q000187:drug effects / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013623:Tail / Q000098:blood supply; D014664:Vasodilation
D001685:Biological Factors; D010455:Peptides; D024681:Potassium Channels, Calcium-Activated; C067410:endothelium-dependent hyperpolarization factor; D018999:Charybdotoxin; D001030:Apamin; C064719:iberiotoxin; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin