Adenine-induced chronic renal failure in rats decreases aortic relaxation rate and alters expression of proteins involved in vascular smooth muscle calcium handling

2016 ◽  
Vol 218 (4) ◽  
pp. 250-264 ◽  
Author(s):  
L. Nguy ◽  
E. Shubbar ◽  
M. Jernås ◽  
I. Nookaew ◽  
J. Lundgren ◽  
...  
Keyword(s):  
Renal Failure ◽  
Smooth Muscle ◽  
Chronic Renal Failure ◽  
Vascular Smooth Muscle ◽  
Relaxation Rate ◽  
Calcium Handling ◽  
Muscle Calcium

Evidence against the role of α1-adrenoceptor reserve in buffering the inhibitory effect of nifedipine on the contractility of canine vascular smooth muscle

1990 ◽  
Vol 68 (10) ◽  
pp. 1346-1350 ◽  
Author(s):  
Yong-Yuan Guan ◽  
Chiu-Yin Kwan ◽  
Edwin E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Saphenous Vein ◽  
Mesenteric Artery ◽  
Inhibitory Effect ◽  
Contractile Responses ◽  
Intracellular Ca ◽  
Adrenoceptor Agonists ◽  
The Difference ◽  
Muscle Calcium

The relationship between the postsynaptic α1-adrenoceptor reserve and the sensitivity of vasoconstriction induced by α-adrenoceptor agonists to the dihydropyridine Ca2+ entry blocker nifedipine was investigated in isolated muscle strips of dog mesenteric artery (DMA) and saphenous vein (DSV). The amplitudes of the contractile responses of DMA induced by phenylephrine were the same as those in DSV in the presence and in the absence of extracellular Ca2+. The use of 3 × 10−9 M phenoxybenzamine to irreversibly block the α1-adrenoceptors revealed a marked difference in the size of the α1-adrenoceptor reserve between DMA (40%) and DSV (7%). In spite of a larger receptor reserve, the contractile responses induced by phenylephrine in DMA were more sensitive to nifedipine compared with those in DSV. These results suggest that the postsynaptic α1-adrenoceptor reserve in vascular smooth muscle, at least in DMA and DSV, does not play an important role in buffering the inhibitory effect of nifedipine on the contractile response to a full agonist of α1-adrenoceptors. Other factors, such as the difference in the membrane depolarizing effect, the ability to utilize intracellular Ca2+ for contraction, and the possible existence of α1-adrenoceptor subtypes, may contribute to the different inhibitory effects of nifedipine on these blood vessels.Key words: adrenoceptors, nifedipine, smooth muscle, calcium, saphenous vein, mesenteric artery.

scholarly journals Altered Calcium Handling Between Healthy And Atherosclerotic Vascular Smooth Muscle

2009 ◽  
Vol 96 (3) ◽  
pp. 117a ◽  
Author(s):  
Marie-Ann Ewart ◽  
Susan Currie ◽  
John G. McCarron ◽  
Simon Kennedy
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Calcium Handling

Dysfunction of calcium handling by smooth muscle in hypertension

1985 ◽  
Vol 63 (4) ◽  
pp. 366-374 ◽  
Author(s):  
C. Y. Kwan
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cardiovascular System ◽  
Control Systems ◽  
Active Transport ◽  
Smooth Muscles ◽  
Peripheral Resistance ◽  
Calcium Handling ◽  
Experimental Hypertension

Dysfunction of ion handling, including binding and fluxes (passive and active transport) of physiologically important ions such as potassium, sodium, calcium, and magnesium, by vascular smooth muscle cell membranes has repeatedly been reported to be associated with the pathophysiology of hypertension. The specific purpose of this review is to summarize and evaluate the evidence for alterations of calcium ion (Ca2+) handling by vascular smooth muscle in various forms of hypertension in the animal model on the basis that regulation of cytoplasmic Ca2+ concentration is a complex and yet vitally important process for a normal function of vascular smooth muscle and that derangement of such a regulation may result in excessive retention of cytoplasmic Ca2+, contribute toward increase of total peripheral resistance, and ultimately lead to elevation of blood pressure. Emphasis is placed upon the consideration of the usefulness of the subcellular membrane fractionation technique in studies of binding and transport of Ca2+ by vascular and nonvascular smooth muscle membranes from genetic as well as experimental hypertensive rats. The limitations of the interpretation of data using such an approach are also considered. Decreased active transport of Ca2+ across isolated plasma membrane vesicles from large and small arteries occurs in several but not all forms of hypertension. This membrane abnormality also occurs in nonvascular smooth muscles and other tissues or cells not confined to the cardiovascular system in genetic hypertension, but not in experimental hypertension. A hypothesis of general membrane defects in spontaneous hypertension is proposed. Since the long-term regulation of blood pressure at the sites of resistant blood vessels is under finely integrated and interacting control systems, namely, the myogenic, neurogenic, and humoral controls, involving many tissues or cells not necessarily confined to cardiovascular system, membrane abnormalities in Ca2+ handling by tissues in each or a combination of these control systems can conceivably lead to hypertension.

Effects of Dietary Calcium on Blood Pressure, Vascular Reactivity and Vascular Smooth Muscle Calcium Efflux Rate in Zucker Rats

1991 ◽  
Vol 4 (7_Pt_1) ◽  
pp. 592-596 ◽  
Author(s):  
Susan L. Ambrozy ◽  
Stacey E. Shehin ◽  
Cho-Yen Chiou ◽  
James R. Sowers ◽  
Michael B. Zemel
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Reactivity ◽  
Dietary Calcium ◽  
Zucker Rats ◽  
Calcium Efflux ◽  
Efflux Rate ◽  
Muscle Calcium
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