Length-dependent sensitivity in vascular smooth muscle

Price, J. M.; Davis, Darrell L.; Knauss, Elizabeth B.

doi:10.1152/ajpheart.1981.241.4.h557

Cited by 53 publications

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“…The alteration of wall tension may activate or inactivate the contraction of vascular smooth muscle and the signal pathways of endothelial cells mediated by mechanotransductions such as integrins and G protein-coupled receptors (9, 17, 25, 26). It has been suggested that the change in distension or stretch affects vascular reactivity (3,6,22,27). In the present study, we extended the pressure and stretch to a pathological range (e.g., hypertensive pressures or stretches) and verified that the effect on the vasorelaxation of blood vessel is substantial (Fig.…”

Section: Discussionsupporting

confidence: 80%

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Kassab

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Lu X, Kassab GS. Assessment of endothelial function of large, medium, and small vessels: a unified myograph. Am J Physiol Heart Circ Physiol 300: H94 -H100, 2011. First published November 12, 2010; doi:10.1152/ajpheart.00708.2010.-Endothelial dysfunction precedes the development of morphological atherosclerotic changes and can also contribute to lesion development in cardiovascular diseases. Currently, there is a lack of a single method to determine endothelial function of the entire range of vessel dimensions from aorta to arterioles. Here we assessed endothelial function of a large range of size arteries using a unified isovolumic myograph method. The method maintains a constant volume of fluid in the lumen of the vessel during contraction and relaxation, which are characterized by an increase and a decrease of pressure, respectively. Segments of six aortas, six common femoral arteries, and six mesenteric arteries from rats; six carotid arteries from mice; and six coronary and carotid arteries from pigs were used. The endothelium-dependent dose-response vasorelaxation was determined with endothelium-dependent vasodilators while arterial preconstriction was induced with vasoconstrictors at a submaximal dose. The circumferential midtension during vascular reactivity varied from 43.1 Ϯ 7.9 to 2.59 Ϯ 0.46 mN/mm (from large to small arteries), whereas the circumferential midstress showed a much smaller variation from 217 Ϯ 23.5 to 123 Ϯ 15.3 kPa (in the same range of vessels). We also found that overinflation and axial overelongation compromised endothelium-dependent vasorelaxation to underscore the significance of vessel preload. In conclusion, an isovolumic myograph was used to unify arterial vasoreactivity from large to small arteries and shows the uniformity of wall stress and %tension throughout the range of vessel sizes. isovolumic myograph; wire myograph; pressure myograph VASCULAR ENDOTHELIAL DYSFUNCTION is widely considered to be a consequence, a biomarker, and a mediator of the adverse effects of cardiovascular risk factors (2,4,5,11,15,18,21). Endothelial dysfunction precedes the development of morphological atherosclerotic changes and can also contribute to lesion development and later clinical complications (15,23,24). Endothelial dysfunction has also been shown to be a predictor of adverse outcomes in patients with coronary artery disease (10,11,20). Although endothelial dysfunction may be indicated by several biomarkers such as the expression of endothelial nitric oxide (NO) synthase, the expression of cyclooxygenase, and the production of nitric oxide or prostacyclin, the vasodilation of blood vessel in response to endothelium-dependent agonists is the gold standard.The wire and pressure myographs have been used extensively to study the vasoreactivity and pharmacology of large and small vessels, respectively (7-9, 12-16, 19, 26). The applicability of wire myograph is in vessels with a diameter range from large vessels (aorta) down to about 500 m. The attachment of vessel rings to hooks, however, ca...

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Section: Discussionsupporting

confidence: 80%

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Kassab

2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, force development induced by U-46619 in Ca2+- sensitivity for vasocontraction of a longer muscle, as observed by Price et al (1981), is not necessarily associated with increases in [Ca2+]i, but can be explained by a further potentiation of Ca2+ sensitivity of contractile apparatus during agonist stimulation by stretch, as evidenced by the present study (Fig. 6D) (Chatterjee & Murphy, 1983;Moreland & Murphy, 1986) and co-operative cycling of cross-bridges ).…”

Section: Methodssupporting

confidence: 62%

Resting load regulates cytosolic calcium‐force relationship of the contraction of bovine cerebrovascular smooth muscle.

Miyagi¹,

Kobayashi²,

Nishimura³

et al. 1995

The Journal of Physiology

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1. We determined the effects of a change in preload, or resting load, on the development of force and on cytosolic calcium concentration ([Ca2+] Contraction of vascular smooth muscle is regulated and [Ca2+]i has made it clear that these two factors do not mainly by changes in cytosolic calcium concentration always move in parallel and dissociations between ([Ca2+]i), and thus development of force has been regarded changes in these two factors are currently major problems as a good indicator of an increase in [Ca2+]i (Brading, for workers studying the contractile regulation in smooth 1979). However, the simultaneous measurement of force muscle (Somlyo & Himpens, 1989).

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“…Thus, the optimal tension determined in vitro is in the range of physiological wall tension. Affinity of adrenergic receptors in arterial smooth muscle is influenced by alterations in wall tension (Raffa and Tallarida, 1981;Price et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

Prejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in canine coronary arteries.

Cohen¹,

Shepherd²,

Vanhoutte³

1983

Circulation Research

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SUMMARY. The effects of endogenous and of exogenous norepinephrine were studied in isolated rings of canine left circumflex coronary artery and its first ventricular branch. Norepinephrine was released from adrenergic nerve endings by transmural electrical stimulation and by tyramine. In rings contracted with prostaglandin ¥20, transmural electrical stimulation resulted in frequencydependent relaxations which were blocked by propranolol or tetrodotoxin; tyramine and exogenous norepinephrine caused concentration-dependent relaxations which were blocked by propranolol. The tyramine-induced relaxations also were inhibited by cocaine. The left circumflex artery was less sensitive than its branch to /S-adrenergic activation; this difference was significant even between rings of the two vessels immediately adjacent to the branching point and was abolished by phentolamine. In the presence of propranolol, transmural electrical stimulation, tyramine and phenylephrine, produced contractions of the left circumflex artery, but not the branch; these contractions were prevented by phentolamine. Phentolamine, but not prazosin, augmented the /?-adrenergic response of left circumflex artery to low frequency stimulation; in arteries preincubated with 3 H-norepinephrine, this was accompanied by an increased overflow of tritiated neurotransmitter. The prejunctional effect of phentolamine was also evident in branch coronary arteries which exhibit no postjunctional a-adrenergic responses. With high frequency stimulation, both a-adrenergic antagonists equally augmented the relaxation of left circumflex artery; the efflux of tritiated norepinephrine was not different from untreated arteries. These experiments demonstrate, in isolated coronary arteries, that the primary adrenergic response to released endogenous norepinephrine is /S-adrenergic relaxation. The prejunctional effects of nonspecific a-adrenergic antagonists preclude their use in determining the importance of postjunctional coronary a-adrenergic receptor activation caused by sympathetic nerve stimulation. (Circ Res 52: 16-25, 1983)

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Length-dependent sensitivity in vascular smooth muscle

Cited by 53 publications

References 0 publications

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Resting load regulates cytosolic calcium‐force relationship of the contraction of bovine cerebrovascular smooth muscle.

Prejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in canine coronary arteries.

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