A review of changes in vascular smooth muscle functions in hypertension: isolated tissue versus in vivo studies

1985 ◽  
Vol 63 (4) ◽  
pp. 355-365 ◽  
Author(s):  
C. R. Triggle ◽  
I. Laher
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Function ◽  
Spontaneously Hypertensive Rat ◽  
In Vivo Studies ◽  
Neuronal Uptake ◽  
Smooth Muscle Function

The role of altered vascular smooth muscle function in the etiology of essential hypertension has been extensively studied by a number of investigators. The results obtained from in vivo studies do not always correlate with results from in vitro studies and it is not always apparent whether the results reflect differences related to hypertension or to the genetic background of the animal model. In vitro and perfused vascular bed studies in our laboratory have utilized the spontaneously hypertensive rat (SHR), the normotensive Wistar Kyoto rat (WKY), genetically related crossbred rats (F1, F2, and BC1), and also Dahl salt-sensitive (DS) and salt-resistant (DR) rats. The role of altered smooth muscle function in relation to the development of the elevated blood pressure (BP) of the SHR or DS rat was studied and emphasis was placed on determining the role of altered neuronal uptake1 (U1) in hypertensives in masking elevated postsynaptic sensitivity to noradrenaline. In addition, the relationship between postsynaptic sensitivity to cations and BP was assessed. Such studies have indicated that alterations in postsynaptic sensitivity, U1 activity, and sensitivity to cations are not entirely consistent with the etiology of hypertension in the SHR and DS rat but may simply reflect genetic strain differences between the hypertensive and normotensive animals.

scholarly journals Fundamental Roles of Axial Stretch in Isometric and Isobaric Evaluations of Vascular Contractility

2019 ◽  
Vol 141 (3) ◽  
Author(s):  
Alexander W. Caulk ◽  
Jay D. Humphrey ◽  
Sae-Il Murtada
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Function ◽  
Contractile Function ◽  
Contractile Activity ◽  
Comparison Of Methods ◽  
Axial Stretch ◽  
Smooth Muscle Function ◽  
In Vivo Loading

Vascular smooth muscle cells (VSMCs) can regulate arterial mechanics via contractile activity in response to changing mechanical and chemical signals. Contractility is traditionally evaluated via uniaxial isometric testing of isolated rings despite the in vivo environment being very different. Most blood vessels maintain a locally preferred value of in vivo axial stretch while subjected to changes in distending pressure, but both of these phenomena are obscured in uniaxial isometric testing. Few studies have rigorously analyzed the role of in vivo loading conditions in smooth muscle function. Thus, we evaluated effects of uniaxial versus biaxial deformations on smooth muscle contractility by stimulating two regions of the mouse aorta with different vasoconstrictors using one of three testing protocols: (i) uniaxial isometric testing, (ii) biaxial isometric testing, and (iii) axially isometric plus isobaric testing. Comparison of methods (i) and (ii) revealed increased sensitivity and contractile capacity to potassium chloride and phenylephrine (PE) with biaxial isometric testing, and comparison of methods (ii) and (iii) revealed a further increase in contractile capacity with isometric plus isobaric testing. Importantly, regional differences in estimated in vivo axial stretch suggest locally distinct optimal biaxial configurations for achieving maximal smooth muscle contraction, which can only be revealed with biaxial testing. Such differences highlight the importance of considering in vivo loading and geometric configurations when evaluating smooth muscle function. Given the physiologic relevance of axial extension and luminal pressurization, we submit that, when possible, axially isometric plus isobaric testing should be employed to evaluate vascular smooth muscle contractile function.

Mg2+–Ca2+ interaction in contractility of vascular smooth muscle: Mg2+ versus organic calcium channel blockers on myogenic tone and agonist-induced responsiveness of blood vessels

1987 ◽  
Vol 65 (4) ◽  
pp. 729-745 ◽  
Author(s):  
B. M. Altura ◽  
B. T. Altura ◽  
A. Carella ◽  
A. Gebrewold ◽  
T. Murakawa ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Blood Vessels ◽  
Divalent Cations ◽  
Smooth Muscles ◽  
In Vivo Studies ◽  
Channel Blockers ◽  
Arterial Blood

Contractility of all types of invertebrate and vertebrate muscle is dependent upon the actions and interactions of two divalent cations, viz., calcium (Ca2+) and magnesium (Mg2+) ions. The data presented and reviewed herein contrast the actions of several organic Ca2+ channel blockers with the natural, physiologic (inorganic) Ca2+ antagonist, Mg2+, on microvascular and macrovascular smooth muscles. Both direct in vivo studies on microscopic arteriolar and venular smooth muscles and in vitro studies on different types of blood vessels are presented. It is clear from the studies done so far that of all Ca2+ antagonists examined, only Mg2+ has the capability to inhibit myogenic, basal, and hormonal-induced vascular tone in all types of vascular smooth muscle. Data obtained with verapamil, nimopidine, nitrendipine, and nisoldipine on the microvasculature are suggestive of the probability that a heterogeneity of Ca2+ channels, and of Ca2+ binding sites, exists in different microvascular smooth muscles; although some appear to be voltage operated and others, receptor operated, they are probably heterogeneous in composition from one vascular region to another. Mg2+ appears to act on voltage-, receptor-, and leak-operated membrane channels in vascular smooth muscle. The organic Ca2+ channel blockers do not have this uniform capability; they demonstrate a selectivity when compared with Mg2+. Mg2+ appears to be a special kind of Ca2+ channel antagonist in vascular smooth muscle. At vascular membranes it can (i) block Ca2+ entry and exit, (ii) lower peripheral and cerebral vascular resistance, (iii) relieve cerebral, coronary, and peripheral vasospasm, and (iv) lower arterial blood pressure. At micromolar concentrations (i.e., 10–100 μM), Mg2+ can cause significant vasodilatation of intact arterioles and venules in all regional vasculatures so far examined. Although Mg2+ is three to five orders of magnitude less potent than the organic Ca2+ channel blockers, it possesses unique and potentially useful Ca2+ antagonistic properties.

Role of GADD153 (growth arrest- and DNA damage-inducible gene 153) in vascular smooth muscle cell apoptosis

2001 ◽  
Vol 100 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Michiya IGASE ◽  
Takafumi OKURA ◽  
Michitsugu NAKAMURA ◽  
Yasunori TAKATA ◽  
Yutaka KITAMI ◽  
...  
Keyword(s):  
Dna Damage ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Molecular Mechanisms ◽  
Growth Arrest ◽  
Cell Contact ◽  
Inducible Gene

GADD153 (growth arrest- and DNA damage-inducible gene 153) is expressed at very low levels in growing cells, but is markedly induced in response to a variety of cellular stresses, including glucose deprivation, exposure to genotoxic agents and other growth-arresting situations. Forced expression of GADD153 induces cell cycle arrest in many types of cells. It is also reported that GADD153 is directly associated with apoptosis. Recently we have reported that platelet-derived growth factor (PDGF)-BB induces apoptosis in cultured vascular smooth muscle cells (VSMC), but only when 100% confluency is reached. These results suggested that cell–cell contact inhibition (cell growth arrest) may be a critical factor for induction of VSMC apoptosis by PDGF-BB. In the present study, we explored the role of GADD153, one of a number of growth-arrest-related gene products, in the molecular mechanisms of VSMC apoptosis in vitro and in vivo. GADD153 was markedly induced at both the mRNA and protein levels, in parallel with the induction of VSMC apoptosis, after treatment with PDGF-BB. Moreover, overexpression of GADD153 in VSMC significantly reduced cell viability and induced apoptosis. In the carotid artery balloon injury model in rats, GADD153 protein was expressed in apoptotic VSMC which were positively stained by in situ DNA labelling. These results demonstrate an important role for GADD153 in the molecular mechanisms of VSMC apoptosis.

Gallbladder motor function in gallstone patients: sonographic and in vitro studies on the role of gallstones, smooth muscle function and gallbladder wall inflammation

1994 ◽  
Vol 21 (3) ◽  
pp. 430-440 ◽  
Author(s):  
Piero Portincasa ◽  
Agostino Di Ciaula ◽  
Giuseppe Baldassarre ◽  
Vincenzo Palmieri ◽  
Antonia Gentile ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Motor Function ◽  
Muscle Function ◽  
Gallbladder Wall ◽  
In Vitro Studies ◽  
Smooth Muscle Function

The Role of Endogenous NADPH Oxidases in Airway and Pulmonary Vascular Smooth Muscle Function

2003 ◽  
Vol 5 (6) ◽  
pp. 751-758 ◽  
Author(s):  
John R. Hoidal ◽  
S.S. Brar ◽  
Anne B. Sturrock ◽  
Karl A. Sanders ◽  
Bruce Dinger ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Function ◽  
Nadph Oxidases ◽  
Smooth Muscle Function

Ambient particulate matter induces relaxation of rat aortic rings in vitro

2001 ◽  
Vol 20 (5) ◽  
pp. 259-265 ◽  
Author(s):  
A M Knaapen ◽  
G J den Hartog ◽  
A Bast ◽  
P JA Borm
Keyword(s):  
Smooth Muscle ◽  
Particulate Matter ◽  
Muscle Function ◽  
Ultrafine Particles ◽  
Epidemiological Studies ◽  
Suspended Particulate ◽  
Smooth Muscle Function ◽  
Underlying Mechanisms

Epidemiological studies have shown an association between ambient levels of particulate matter (PM) and increased mortality from cardiovascular diseases. However, the underlying mechanisms are still not clear. We hypothesised that PM, when translocated after inhalation, could affect vascular smooth muscle function. Therefore, total suspended particulate matter (TSP) was sampled and investigated for its ability to affect aortic muscle contraction. Both TSP and TSP supernatant (TSP-sup) induced a concentration-dependent relaxation of phenylephrine (PE)-precontracted aortic rings. Relaxation induced by 100 jg/ml TSP was 51.5 t 3.1% of total contraction. At 60 and 100 Hg/ ml, relaxation induced by TSP was significantly higher compared to TSP-sup. Ultrafine TiO2, used as a model to investigate the role of ultrafine particles, did not show an effect. Soluble iron, present in TSP suspensions, seems not to be involved, as chelating with deferoxamine did not affect TSP-induced relaxation. However, TSP effects were inhibited by Trolox, suggesting a role of oxidants. Nudation of aortic rings showed that effects of TSP were only partly endothelium-dependent, while preincubation with LNAME increased TSP-induced relaxation. From these data, we conclude that both the particle core and soluble components of TSP can affect the smooth muscle function, leading to changes in the vascular contractile response.

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