Unusual effects of SCN and lyotropic anions on contractility of vascular smooth muscle from female rats

1991 ◽  
Vol 344 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Aimin Zhang ◽  
Bella T. Altura ◽  
Burton M. Altura

2000 ◽  
Vol 278 (4) ◽  
pp. C834-C844 ◽  
Author(s):  
Jason G. Murphy ◽  
Raouf A. Khalil

The hypothesis that vascular protection in females and its absence in males reflects gender differences in [Ca2+]iand Ca2+mobilization mechanisms of vascular smooth muscle contraction was tested in fura 2-loaded aortic smooth muscle cells isolated from intact and gonadectomized male and female Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. In WKY cells incubated in Hanks' solution (1 mM Ca2+), the resting length and [Ca2+]iwere significantly different in intact males (64.5 ± 1.2 μm and 83 ± 3 nM) than in intact females (76.5 ± 1.5 μm and 64 ± 7 nM). In intact male WKY, phenylephrine (Phe, 10−5M) caused transient increase in [Ca2+]ito 428 ± 13 nM followed by maintained increase to 201 ± 8 nM and 32% cell contraction. In intact female WKY, the Phe-induced [Ca2+]itransient was not significantly different, but the maintained [Ca2+]i(159 ± 7 nM) and cell contraction (26%) were significantly less than in intact male WKY. In Ca2+-free (2 mM EGTA) Hanks', Phe and caffeine (10 mM) caused transient increases in [Ca2+]iand contraction that were not significantly different between males and females. Membrane depolarization by 51 mM KCl caused 31% cell contraction and increased [Ca2+]ito 259 ± 9 nM in intact male WKY, which were significantly greater than a 24% contraction and 214 ± 8 nM [Ca2+]iin intact female WKY. Maintained Phe- and KCl-stimulated cell contraction and [Ca2+]iwere significantly greater in SHR than WKY in all groups of rats. Reduction in cell contraction and [Ca2+]iin intact females compared with intact males was significantly greater in SHR (∼30%) than WKY (∼20%). No significant differences in cell contraction or [Ca2+]iwere observed between castrated males, ovariectomized (OVX) females, and intact males, or between OVX females with 17β-estradiol implants and intact females. Exogenous application of 17β-estradiol (10−8M) to cells from OVX females caused greater reduction in Phe- and KCl-induced contraction and [Ca2+]iin SHR than WKY. Thus the basal, maintained Phe- and depolarization-induced [Ca2+]iand contraction of vascular smooth muscle triggered by Ca2+entry from the extracellular space exhibit differences depending on gender and the presence or absence of female gonads. Cell contraction and [Ca2+]idue to Ca2+release from the intracellular stores are not affected by gender or gonadectomy. Gender-specific reduction in contractility and [Ca2+]iin vascular smooth muscle of female rats is greater in SHR than WKY rats.



Endocrinology ◽  
2008 ◽  
Vol 150 (1) ◽  
pp. 212-219 ◽  
Author(s):  
James P. Stice ◽  
Jason P. Eiserich ◽  
A. A. Knowlton

Although aging is known to lead to increased vascular stiffness, the role of estrogens in the prevention of age-related changes in the vasculature remains to be elucidated. To address this, we measured vascular function in the thoracic aorta in adult and old ovariectomized (ovx) rats with and without immediate 17β-estradiol (E2) replacement. In addition, aortic mRNA and protein were analyzed for proteins known to be involved in vasorelaxation. Aging in combination with the loss of estrogens led to decreased vasorelaxation in response to acetylcholine and sodium nitroprusside, indicating either smooth muscle dysfunction and/or increased fibrosis. Loss of estrogens led to increased vascular tension in response to phenylephrine, which could be partially restored by E2 replacement. Levels of endothelial nitric oxide synthase and inducible nitric oxide synthase did not differ among the groups, nor did total nitrite plus nitrate levels. Old ovx exhibited decreased expression of both the α and β-subunits of soluble guanylyl cyclase (sGC) and had impaired nitric oxide signaling in the vascular smooth muscle. Immediate E2 replacement in the aged ovx prevented both the impairment in vasorelaxation, and the decreased sGC receptor expression and abnormal sGC signaling within the vascular smooth muscle. The combination of loss of estradiol and aging leads to increased constriction (phenylephrine) and decreased relaxation with nitric oxide. Reduced soluble guanylyl cyclase mediates these changes.



Author(s):  
Martin Hagopian ◽  
Michael D. Gershon ◽  
Eladio A. Nunez

The ability of cardiac tissues to take up norepinephrine from an external medium is well known. Two mechanisms, called Uptake and Uptake respectively by Iversen have been differentiated. Uptake is a high affinity system associated with adrenergic neuronal elements. Uptake is a low affinity system, with a higher maximum rate than that of Uptake. Uptake has been associated with extraneuronal tissues such as cardiac muscle, fibroblasts or vascular smooth muscle. At low perfusion concentrations of norepinephrine most of the amine taken up by Uptake is metabolized. In order to study the localization of sites of norepinephrine storage following its uptake in the active bat heart, tritiated norepinephrine (2.5 mCi; 0.064 mg) was given intravenously to 2 bats. Monoamine oxidase had been inhibited with pheniprazine (10 mg/kg) one hour previously to decrease metabolism of norepinephrine.







1991 ◽  
Author(s):  
Cynthia L. Perreault ◽  
◽  
Kathleen G. Morgan ◽  
James P. Morgan


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