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OBJECTIVE To test the hypotheses that vascular supersensitivity correlates with the appearance of contractile oscillations; vascular oscillations are mediated by gap junctions; and gap junctional communication is altered in the vasculature in stroke-prone spontaneously hypertensive (SHRSP) compared with Wistar-Kyoto (WKY) rats. METHODS Helical strips of mesenteric and tail arteries from SHRSP and WKY rats were mounted in tissue baths for measurement of isometric force. Cultures of mesenteric arterial cells were used for measurement of Lucifer yellow dye transfer and abundance of connexin43 mRNA, a monomer of gap junctions. RESULTS Mesenteric arteries from SHRSP that displayed spontaneous oscillations were more sensitive to the contractile agonist 5-hydroxytryptamine than those from SHRSP and WKY rats that displayed no oscillations. In addition, SHRSP tail arteries displayed norepinephrine-induced oscillations. The putative gap junction up-regulator tetraethylammonium (10(-3)-10(-1) mol/l) induced oscillations (1-5 cycle/min) in arteries from both rat strains. These oscillations were not altered by endothelium removal or phentolamine and were blocked by heptanol (10(-3) mol/l). Although tetraethylammonium and heptanol caused similar effects in both arteries, heptanol-sensitive agonist-induced oscillations persisted only in the tail artery of SHRSP. Tetraethylammonium increased dye transfer between contiguous cells approximately 35% above basal levels both for SHRSP and WKY cells. In both cell lines, heptanol reduced basal- and tetraethylammonium-stimulated dye transfer. Total RNA from WKY rat and SHRSP cultured cells hybridized strongly and to a similar magnitude with a complementary DNA probe for messenger RNA for connexin43. CONCLUSIONS Gap junctional communication is important in vascular reactivity and might play a part in the development of oscillations. Altered gap junctional communication could not be demonstrated in cell cultures nor in some contractile experiments. It is possible that the culture conditions failed to mimic conditions in vivo that differentially regulate gap junctions in the hypertensive state, but it is also possible that gap junctional activity is not abnormal in hypertension.
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
November 1994,
Clinical and experimental hypertension (New York, N.Y. : 1993),
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
December 1999,
Journal of hypertension,
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
June 1995,
Journal of pharmacological and toxicological methods,
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
April 1998,
The Journal of physiology,
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
November 1996,
Hypertension (Dallas, Tex. : 1979),
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
July 1995,
Hypertension (Dallas, Tex. : 1979),
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
January 1994,
Annals of clinical and laboratory science,
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
January 1998,
International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition,
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
January 1981,
Annual review of physiology,
M L Tsai, and
S W Watts, and
R Loch-Caruso, and
R C Webb
January 1983,
Hypertension (Dallas, Tex. : 1979),
