Contractile Responses to Bay K 8644 in Rats with Coarctation-Induced Hypertension

Deborah S. Storm, R Clinton Webb

Research output: Contribution to journalArticle

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Abstract

This study examines potential-operated calcium channel function in rats made hypertensive by aortic coarctation. The hypothesis that channel function is influenced by elevated arterial pressure was tested by comparing contractile responses to elevated K+and to the potential-operated calcium channel agonist, Bay K 8644, in aortic segments above (thoracic) and below (abdominal) the coarctation that are exposed to hypertensive and normotensive pressures, respectively. To control for vessel differences, the effects of Bay K 8644 were also examined in abdominal aortae from two-kidney, one-clip hypertensive rats. Sensitivity to K+(EC15) was significantly greater in both thoracic and abdominal aortae from coarctation-hypertensive rats than in those from normotensive sham rats. In the thoracic aorta, maximal contractile response to Bay K 8644 (normalized to contraction produced by 100 mM K+) was significantly greater in coarctation-hypertensive rats (124 ± 9%) than in sham rats (12 ± 6%). However, Bay K 8644 did not elicit contraction in abdominal aortae from either group. When [K+]°was increased (19.2 mM), thoracic aortae from coarctation-hypertensive rats were more sensitive to Bay K 8644, but there were no differences in maximal responses among thoracic and abdominal aortae. Bay K 8644 evoked dose-dependent contraction in all abdominal aortic strips from two-kidney, one-clip hypertensive rats (maximum = 68 ± 11%). In summary, vascular responsiveness to Bay K 8644 is increased in the thoracic but not abdominal aorta from coarctation-hypertensive rats, whereas sensitivity to elevated K+is increased in both vessels. Enhanced K+sensitivity in the abdominal aorta may be related to general effects of the cation on membrane potential. However, augmented responsiveness to Bay K 8644 suggests a specific alteration in the function of potential-operated calcium channels that is dependent upon elevated blood pressure and is not due to differences in responsiveness between the thoracic and abdominal aortae.

Original languageEnglish (US)
Pages (from-to)92-99
Number of pages8
JournalProceedings of the Society for Experimental Biology and Medicine
Volume203
Issue number1
DOIs
StatePublished - Jan 1 1993

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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
Abdominal Aorta
Rats
Hypertension
Thoracic Aorta
Calcium Channels
Surgical Instruments
Thorax
Calcium Channel Agonists
Kidney
Aortic Coarctation
Blood pressure
Membrane Potentials
Blood Vessels
Cations
Arterial Pressure
Blood Pressure
Membranes
Pressure

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Contractile Responses to Bay K 8644 in Rats with Coarctation-Induced Hypertension. / Storm, Deborah S.; Webb, R Clinton.

In: Proceedings of the Society for Experimental Biology and Medicine, Vol. 203, No. 1, 01.01.1993, p. 92-99.

Research output: Contribution to journalArticle

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abstract = "This study examines potential-operated calcium channel function in rats made hypertensive by aortic coarctation. The hypothesis that channel function is influenced by elevated arterial pressure was tested by comparing contractile responses to elevated K+and to the potential-operated calcium channel agonist, Bay K 8644, in aortic segments above (thoracic) and below (abdominal) the coarctation that are exposed to hypertensive and normotensive pressures, respectively. To control for vessel differences, the effects of Bay K 8644 were also examined in abdominal aortae from two-kidney, one-clip hypertensive rats. Sensitivity to K+(EC15) was significantly greater in both thoracic and abdominal aortae from coarctation-hypertensive rats than in those from normotensive sham rats. In the thoracic aorta, maximal contractile response to Bay K 8644 (normalized to contraction produced by 100 mM K+) was significantly greater in coarctation-hypertensive rats (124 ± 9{\%}) than in sham rats (12 ± 6{\%}). However, Bay K 8644 did not elicit contraction in abdominal aortae from either group. When [K+]°was increased (19.2 mM), thoracic aortae from coarctation-hypertensive rats were more sensitive to Bay K 8644, but there were no differences in maximal responses among thoracic and abdominal aortae. Bay K 8644 evoked dose-dependent contraction in all abdominal aortic strips from two-kidney, one-clip hypertensive rats (maximum = 68 ± 11{\%}). In summary, vascular responsiveness to Bay K 8644 is increased in the thoracic but not abdominal aorta from coarctation-hypertensive rats, whereas sensitivity to elevated K+is increased in both vessels. Enhanced K+sensitivity in the abdominal aorta may be related to general effects of the cation on membrane potential. However, augmented responsiveness to Bay K 8644 suggests a specific alteration in the function of potential-operated calcium channels that is dependent upon elevated blood pressure and is not due to differences in responsiveness between the thoracic and abdominal aortae.",
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