Further investigation of myogenic tone and flow mediated responses in mesenteric resistance arteries of pregnant and non-pregnant rats

1996 ◽  
Vol 3 (2) ◽  
pp. 289A
Author(s):  
A COCKELL
Keyword(s):  
Myogenic Tone ◽  
Resistance Arteries ◽  
Pregnant Rats

Enhanced resistance artery sensitivity to agonists under isobaric compared with isometric conditions

1994 ◽  
Vol 266 (1) ◽  
pp. H147-H155 ◽  
Author(s):  
W. R. Dunn ◽  
G. C. Wellman ◽  
J. A. Bevan
Keyword(s):  
Membrane Potential ◽  
Angiotensin Ii ◽  
Myogenic Tone ◽  
Isometric Contractions ◽  
Fundamental Interaction ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Enhanced Resistance ◽  
Increased Sensitivity

We have compared the responsiveness of rabbit mesenteric resistance arteries with agonists under isometric and isobaric conditions. When pressurized (60 mmHg), arteries spontaneously reduced their diameter by 18.1%. An equivalent isometric stress did not generate force in a “wire” myograph. Subsequently, much higher concentrations of norepinephrine (NE) and histamine were required to cause isometric contractions than were needed to reduce vascular diameter of pressurized vessels, whereas angiotensin II produced a maintained response only in pressurized arteries. Reducing transmural pressure to 20 mmHg abolished pressure-induced myogenic tone and decreased arterial sensitivity to NE. Under isometric conditions, partial depolarization with KCl increased sensitivity to NE and histamine to within the concentration range effective in pressurized vessels and also "revealed" responses to angiotensin II. The membrane potential of the vascular smooth muscle cells under partially depolarized conditions was similar to that found in vivo and in vessels studied isobarically. These observations demonstrate a fundamental interaction between pressure-induced myogenic tone and the sensitivity of resistance arteries to vasoactive stimuli. This influence was mimicked in isometrically mounted vessels by partial depolarization, indicating a possible pivotal role for membrane potential in determining the reactivity of the resistance vasculature.

Abstract 485: Novel Mechanisms at Immune-vascular Interfaces Regulates Myogenic Tone of Resistance Arteries and Induce Hypertension in Mice

2018 ◽  
Vol 38 (Suppl_1) ◽  
Author(s):  
Daniela Carnevale ◽  
Iolanda Vinciguerra ◽  
Manuel Casaburo ◽  
Marialuisa Perrotta ◽  
Roberta Iacobucci ◽  
...  
Keyword(s):  
Myogenic Tone ◽  
Resistance Arteries

Mechanisms Leading to Increased Vasodilator Responses to Calcitonin-Gene-Related Peptide in Mesenteric Resistance Arteries of Early Pregnant Rats

2008 ◽  
Vol 45 (4) ◽  
pp. 350-356 ◽  
Author(s):  
H.W.F. van Eijndhoven ◽  
G.M.J. Janssen ◽  
R. Aardenburg ◽  
M.E.A. Spaanderman ◽  
L.L.H. Peeters ◽  
...  
Keyword(s):  
Calcitonin Gene Related Peptide ◽  
Resistance Arteries ◽  
Pregnant Rats ◽  
Related Peptide ◽  
Calcitonin Gene

Role of T-type calcium channels in myogenic tone of skeletal muscle resistance arteries

2002 ◽  
Vol 283 (6) ◽  
pp. H2239-H2243 ◽  
Author(s):  
Ed VanBavel ◽  
Oana Sorop ◽  
Ditte Andreasen ◽  
Martin Pfaffendorf ◽  
Boye L. Jensen
Keyword(s):  
Calcium Channels ◽  
Southern Blotting ◽  
Myogenic Tone ◽  
Cremaster Muscle ◽  
Resistance Arteries ◽  
Rt Pcr ◽  
Response Curves ◽  
Potent Effect ◽  
Channel Expression

T-type calcium channels may be involved in the maintenance of myogenic tone. We tested their role in isolated rat cremaster arterioles obtained after CO2anesthesia and decapitation. Total RNA was analyzed by RT-PCR and Southern blotting for calcium channel expression. We observed expression of voltage-operated calcium (CaV) channels CaV3.1 (T-type), CaV3.2 (T-type), and CaV1.2 (L-type) in cremaster arterioles ( n= 3 rats). Amplification products were observed only in the presence of reverse transcriptase and cDNA. Concentration-response curves of the relatively specific L-type blocker verapamil and the relatively specific T-type blockers mibefradil and nickel were made on cannulated vessels with either myogenic tone (75 mmHg) or a similar level of constriction induced by 30 mM K+ at 35 mmHg. Mibefradil and nickel were, respectively, 162-fold and 300-fold more potent in inhibiting myogenic tone compared with K+-induced constriction [log(IC50, M): mibefradil, basal −7.3 ± 0.2 ( n = 9) and K+ −5.1 ± 0.1 ( n = 5); nickel, basal −4.1 ± 0.2 ( n = 5) and K+ −1.6 ± 0.5 ( n = 5); means ± SE]. Verapamil had a 17-fold more potent effect [log(IC50, M): basal −6.6 ± 0.1 ( n = 5); K+ −5.4 ± 0.3 ( n = 4); all log(IC50) P < 0.05, basal vs. K+]. These data suggest that T-type calcium channels are expressed and involved in maintenance of myogenic tone in rat cremaster muscle arterioles.

Myogenic tone, reactivity, and forced dilatation: a three-phase model of in vitro arterial myogenic behavior

2002 ◽  
Vol 283 (6) ◽  
pp. H2260-H2267 ◽  
Author(s):  
George Osol ◽  
Johan Fredrik Brekke ◽  
Keara McElroy-Yaggy ◽  
Natalia I. Gokina
Keyword(s):  
Cerebral Arteries ◽  
Peripheral Resistance ◽  
Force Production ◽  
Cytosolic Calcium ◽  
Myogenic Tone ◽  
Wall Tension ◽  
Resistance Arteries ◽  
Cellular Mechanisms ◽  
Initial Development

Myogenic behavior, prevalent in resistance arteries and arterioles, involves arterial constriction in response to intravascular pressure. This process is often studied in vitro by using cannulated, pressurized arterial segments from different regional circulations. We propose a comprehensive model for myogenicity that consists of three interrelated but dissociable phases: 1) the initial development of myogenic tone (MT), 2) myogenic reactivity to subsequent changes in pressure (MR), and 3) forced dilatation at high transmural pressures (FD). The three phases span the physiological range of transmural pressures (e.g., MT, 40–60 mmHg; MR, 60–140 mmHg; FD, >140 mmHg in cerebral arteries) and are characterized by distinct changes in cytosolic calcium ([Ca2+]i), which do not parallel arterial diameter or wall tension, and therefore suggest the existence of additional regulatory mechanisms. Specifically, the development of MT is accompanied by a substantial (200%) elevation in [Ca2+]i and a reduction in lumen diameter and wall tension, whereas MR is associated with relatively small [Ca2+]i increments (<20% over the entire pressure range) despite considerable increases in wall tension and force production but little or no change in diameter. FD is characterized by a significant additional elevation in [Ca2+]i (>50%), complete loss of force production, and a rapid increase in wall tension. The utility of this model is that it provides a framework for comparing myogenic behavior of vessels of different size and anatomic origin and for investigating the underlying cellular mechanisms that govern vascular smooth muscle mechanotransduction and contribute to the regulation of peripheral resistance.

Cardiac transplantation and resistance artery myogenic tone

2004 ◽  
Vol 82 (10) ◽  
pp. 840-848 ◽  
Author(s):  
Farzad Moien-Afshari ◽  
Peter L Skarsgard ◽  
Bruce M McManus ◽  
Ismail Laher
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Contractile Function ◽  
Myogenic Tone ◽  
Resistance Arteries ◽  
Interstitial Edema ◽  
Functional Changes ◽  
Ventricular Compliance ◽  
Myogenic Regulation ◽  
Oxide Synthase

Transplantation is an effective treatment for end-stage heart disease; however, most grafts eventually fail by progressive cardiac failure. Primarily, failure is ischemic due to the occlusive nature of transplant vascular disease (TVD). Early after transplantation and preceding TVD, alterations in coronary physiology such as reduced vascular myogenic tone occur. Resistance arteries possess an inherent ability to constrict in response to transmural pressure; this constrictive response (myogenic tone) is important in fluid homeostasis. Recent evidence suggests that a decline in myogenic tone leads to deficits in cardiac contractility. Factors that reduce myogenic tone in transplantation include constitutive nitric oxide synthase and inducible nitric oxide synthase catalyzed, NO-mediated vasodilation as well as deficits in arterial contractile function. Reduced myogenic tone in allograft resistance arteries increases coronary blood flow such that hydrostatic pressure surpasses oncotic pressure, causing cardiac interstitial edema. This generalized edema decreases ventricular compliance leading to heart failure during the course of acute immune rejection of the graft. Cyclosporine A treatment reduces immune mediated dysregulation of myogenic tone, resulting in reduced interstitial edema and improved cardiac function. In this review, we discuss aspects of TVD and myogenic tone signaling mechanisms and how aberrations in myogenic regulation of arterial tone contribute to functional changes observed in cardiac transplant.Key words: myogenic tone, smooth muscle, nitric oxide, transplantation, edema.

scholarly journals PC-PLC/sphingomyelin synthase activity plays a central role in the development of myogenic tone in murine resistance arteries

2015 ◽  
Vol 308 (12) ◽  
pp. H1517-H1524 ◽  
Author(s):  
Joseph R. H. Mauban ◽  
Joseph Zacharia ◽  
Seth Fairfax ◽  
Withrow Gil Wier
Keyword(s):  
Specific Inhibitor ◽  
Intrinsic Property ◽  
Tissue Perfusion ◽  
Pressure Control ◽  
Mesenteric Arteries ◽  
Myogenic Tone ◽  
Resistance Arteries ◽  
Virtual Absence ◽  
Sphingomyelin Synthase

Myogenic tone is an intrinsic property of the vasculature that contributes to blood pressure control and tissue perfusion. Earlier investigations assigned a key role in myogenic tone to phospholipase C (PLC) and its products, inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). Here, we used the PLC inhibitor, U-73122, and two other, specific inhibitors of PLC subtypes (PI-PLC and PC-PLC) to delineate the role of PLC in myogenic tone of pressurized murine mesenteric arteries. U-73122 inhibited depolarization-induced contractions (high external K+ concentration), thus confirming reports of nonspecific actions of U-73122 and its limited utility for studies of myogenic tone. Edelfosine, a specific inhibitor of PI-PLC, did not affect depolarization-induced contractions but modulated myogenic tone. Because PI-PLC produces IP3, we investigated the effect of blocking IP3 receptor-mediated Ca2+ release on myogenic tone. Incubation of arteries with xestospongin C did not affect tone, consistent with the virtual absence of Ca2+ waves in arteries with myogenic tone. D-609, an inhibitor of PC-PLC and sphingomyelin synthase, strongly inhibited myogenic tone and had no effect on depolarization-induced contraction. D-609 appeared to act by lowering cytoplasmic Ca2+ concentration to levels below those that activate contraction. Importantly, incubation of pressurized arteries with a membrane-permeable analog of DAG induced vasoconstriction. The results therefore mandate a reexamination of the signaling pathways activated by the Bayliss mechanism. Our results suggest that PI-PLC and IP3 are not required in maintaining myogenic tone, but DAG, produced by PC-PLC and/or SM synthase, is likely through multiple mechanisms to increase Ca2+ entry and promote vasoconstriction.

scholarly journals Serum Response Factor involvement in myogenic tone regulation in resistance arteries

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Kevin Retailleau ◽  
Bertrand Toutain ◽  
Mathias Mericskay ◽  
Zhenlin Li ◽  
Daniel Henrion ◽  
...  
Keyword(s):  
Serum Response Factor ◽  
Myogenic Tone ◽  
Response Factor ◽  
Resistance Arteries ◽  
Serum Response

scholarly journals Myogenic Tone in Peripheral Resistance Arteries and Arterioles: The Pressure Is On!

2021 ◽  
Vol 12 ◽  
Author(s):  
William F. Jackson
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Steady State ◽  
Vascular Smooth Muscle ◽  
Signaling Pathways ◽  
Vascular Resistance ◽  
Myogenic Tone ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Fluid Exchange

Resistance arteries and downstream arterioles in the peripheral microcirculation contribute substantially to peripheral vascular resistance, control of blood pressure, the distribution of blood flow to and within tissues, capillary pressure, and microvascular fluid exchange. A hall-mark feature of these vessels is myogenic tone. This pressure-induced, steady-state level of vascular smooth muscle activity maintains arteriolar and resistance artery internal diameter at 50–80% of their maximum passive diameter providing these vessels with the ability to dilate, reducing vascular resistance, and increasing blood flow, or constrict to produce the opposite effect. Despite the central importance of resistance artery and arteriolar myogenic tone in cardiovascular physiology and pathophysiology, our understanding of signaling pathways underlying this key microvascular property remains incomplete. This brief review will present our current understanding of the multiple mechanisms that appear to underlie myogenic tone, including the roles played by G-protein-coupled receptors, a variety of ion channels, and several kinases that have been linked to pressure-induced, steady-state activity of vascular smooth muscle cells (VSMCs) in the wall of resistance arteries and arterioles. Emphasis will be placed on the portions of the signaling pathways underlying myogenic tone for which there is lack of consensus in the literature and areas where our understanding is clearly incomplete.

Sign in / Sign up

Export Citation Format

Share Document