Contribution of sarcoplasmic reticulum calcium uptake and L-type calcium channels to altered vascular responsiveness in the aorta of renal hypertensive rats

• Published in: General pharmacology Vol. 33; no. 6; pp. 457 - 466
• Main Authors: Callera, G.E., Bendhack, L.M.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.12.1999; Elsevier
• Subjects: Animals; Aorta - drug effects; Aorta - physiology; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Caffeine - pharmacology; Calcium; Calcium - metabolism; Calcium Channels, L-Type - physiology; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Hypertension, Renal - physiopathology; In Vitro Techniques; Male; Medical sciences; Nifedipine - pharmacology; Phenylephrine - pharmacology; Potassium Chloride - pharmacology; Rat thoracic aorta; Rats; Rats, Wistar; Renal hypertension; Sarcoplasmic reticulum; Sarcoplasmic Reticulum - metabolism; Thapsigargin - pharmacology; Vasoconstriction - drug effects; Calcium; Renal hypertension; Rat thoracic aorta; Sarcoplasmic reticulum; Hypertension; Kidney disease; Urinary system disease; Pathophysiology; Rat; Pathogenesis; Rodentia; Cardiovascular disease; Smooth muscle; Ionic channel; Ionic current; Muscle contraction; Extracellular; In vitro; Artery; Vertebrata; Mammalia; Animal; Blood vessel; Aorta; Intracellular
• ISSN: 0306-3623; 1879-0011
• DOI: 10.1016/S0306-3623(99)00042-7

This study examined whether alterations in intracellular or extracellular Ca 2+ mobilization were related to differences in caffeine and phenylephrine (PHE)-induced contractions between two-kidney, one-clip hypertensive (2K-1C) and normotensive (2K) rat aortas. After depletion and reloading of intracellular Ca 2+ stores, caffeine and PHE-induced contractions in Ca 2+-free solution were increased in 2K-1C. Thapsigargin reduced the contraction to caffeine in 2K-1C and 2K with similar sensitivity. PHE-induced contraction in 1.6-mM Ca 2+ solution was decreased in 2K-1C, and nifedipine was less effective in lowering this response. The responsiveness to extracellular Ca 2+ was decreased in 2K-1C hypertensive rat aortas. Our results indicate an increased intracellular Ca 2+ stores that are not related to alteration in Ca 2+-ATPase function and a lower contribution of L-type channels to the contraction of 2K-1C aortas.