Effect of plasma from hypertensive patients on contractile response of vascular smooth muscle from normotensive rat

1989 ◽  
Vol 67 (10) ◽  
pp. 1272-1277 ◽  
Author(s):  
G. Pillai ◽  
M. C. Sutter
Keyword(s):  
Smooth Muscle ◽  
Portal Vein ◽  
Vascular Smooth Muscle ◽  
Spontaneous Activity ◽  
Mechanical Response ◽  
Contractile Response ◽  
Contractile Activity ◽  
Plasma Samples ◽  
Hypertensive Patients ◽  
Plasma Factor

This study examines whether incubation with plasma from essential hypertensive patients increases the contractile activity of vascular smooth muscle from rats in response to noradrenaline (NA) and potassium (K+). Plasma samples were obtained from age- and sex-matched essential hypertensive patients and normotensive people. Vascular strips were prepared from aorta and portal veins of normotensive rats and placed in physiological solution in muscle baths for measurement of mechanical response. Aortic strips exposed to hypertensive plasma showed increased responsiveness to NA compared with normotensive plasma, but K+ caused an opposite effect. Portal vein exposed to normotensive or hypertensive plasma did not produce any response to NA, but the responsiveness produced in the presence of normotensive plasma to K+ was higher than that of hypertensive plasma. Portal vein exposed to normotensive plasma or hypertensive plasma showed a dose-dependent increase in the spontaneous activity up to 50% concentration of the plasma samples, but further increase in the concentration of plasma inhibited the spontaneous activity. Spontaneous activity at any given concentration of hypertensive plasma was significantly higher than that of normotensive plasma. The spontaneous activity in the presence of heated or unheated normotensive plasma or unheated normotensive serum was not significantly different from each other. These results indicate that the plasma factor from hypertensive patients, which alters the reactivity of vascular smooth muscle from normotensive rat, is present in the serum fraction and is not heat sensitive.Key words: hypertension, plasma, contractile response, circulating factor, spontaneous activity.

Effect of human plasma proteins on spontaneous contractile activity of rat mesenteric portal vein

1990 ◽  
Vol 68 (6) ◽  
pp. 737-743 ◽  
Author(s):  
G. Pillai ◽  
M. C. Sutter
Keyword(s):  
Portal Vein ◽  
Spontaneous Activity ◽  
Plasma Proteins ◽  
Mechanical Response ◽  
Contractile Activity ◽  
Physiological Salt Solution ◽  
Portal Veins ◽  
6 Hydroxydopamine ◽  
Dose Dependent Increase ◽  
Dose Dependent

This study examines the effect of various plasma proteins from man on the spontaneous contractile activity of the rat portal vein. Albumin, γ-globulin, α-globulin, β-globulin (the major plasma proteins), and immunoglobulin IgG (the major immunoglobulin present in the γ-globulin fraction) were obtained commercially. Mesenteric portal vein strips were prepared from rats and placed in a physiological salt solution in muscle baths for the measurement of longitudinal mechanical response. Portal veins exposed to albumin or γ-globulin showed a dose-dependent increase in the spontaneous activity, whereas those exposed to α-globulin or α - and β-globulin together showed a dose-dependent inhibition of spontaneous activity. Immunoglobulin IgG produced a dose-dependent increase in the spontaneous activity similar to that of γ-globulin. The increased spontaneous activity produced by albumin was not prevented by ouabain but was inhibited by phentolamine. Spontaneous contractile activity was stimulated by albumin in the chemically (6-hydroxydopamine) denervated portal vein. These findings indicate that albumin acts in a manner similar to noradrenaline. The increased spontaneous activity caused by γ-globulin (IgG) was inhibited by ouabain or verapamil. The effect of IgG was not dependent on α-adrenergic, cholinergic, histaminergic, serotoninergic, or renin angiotensin systems nor was it affected by removal of the endothelium. These observations may have implications in the pathophysiology of essential hypertension.Key words: vasomotion, mesenteric portal vein, plasma proteins, albumin, γ-globulin, inhibitory factor, stimulatory factor, IgG.

Mechanisms of Hydrogen Sulfide Effects on Contractile Activity of Vascular Smooth Muscle in Rats

2012 ◽  
Vol 3 (2) ◽  
pp. 149-160
Author(s):  
Olena M. Semenykhina ◽  
Olga V. Bazilyuk ◽  
Yulia P. Korkach ◽  
Vadim F. Sagach
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Contractile Activity

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.

scholarly journals Adrenergic airway vascular smooth muscle responsiveness in healthy and asthmatic subjects

2001 ◽  
Vol 90 (2) ◽  
pp. 665-669 ◽  
Author(s):  
Jorge Brieva ◽  
Adam Wanner
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Dead Space ◽  
Healthy Subjects ◽  
Contractile Response ◽  
Mucosal Blood Flow ◽  
Forced Expiratory Volume ◽  
Baseline Values ◽  
The Mean

The purpose of the present study was to determine the responsiveness of airway vascular smooth muscle (AVSM) as assessed by airway mucosal blood flow (Q˙aw) to inhaled methoxamine (α1-agonist; 0.6–2.3 mg) and albuterol (β2-agonist; 0.2–1.2 mg) in healthy [ n = 11; forced expiratory volume in 1 s, 92 ± 4 (SE) % of predicted] and asthmatic ( n = 11, mean forced expiratory volume in 1 s, 81 ± 5%) adults. Mean baseline values for Q˙aw were 43.8 ± 0.7 and 54.3 ± 0.8 μl · min−1· ml−1of anatomic dead space in healthy and asthmatic subjects, respectively ( P < 0.05). After methoxamine inhalation, the maximal mean change in Q˙aw was −13.5 ± 1.0 μl · min−1· ml−1in asthmatic and −7.1 ± 2.1 μl · min−1· ml−1in healthy subjects ( P < 0.05). After albuterol, the mean maximal change in Q˙aw was 3.0 ± 0.8 μl · min−1· ml−1in asthmatic and 14.0 ± 1.1 μl · min−1· ml−1in healthy subjects ( P < 0.05). These results demonstrate that the contractile response of AVSM to α1-adrenoceptor activation is enhanced and the dilator response of AVSM to β2-adrenoceptor activation is blunted in asthmatic subjects.

Effect of acute experimental colitis on rabbit colonic smooth muscle

1986 ◽  
Vol 251 (4) ◽  
pp. G538-G545 ◽  
Author(s):  
J. D. Cohen ◽  
H. W. Kao ◽  
S. T. Tan ◽  
J. Lechago ◽  
W. J. Snape
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Current Pulse ◽  
Mechanical Response ◽  
Contractile Activity ◽  
Experimental Colitis ◽  
Isometric Tension ◽  
Mucosal Inflammation ◽  
Resting Membrane Potential ◽  
Circular Smooth Muscle

The membrane potential and contractile activity of colonic circular smooth muscle from New Zealand White rabbits were studied after the production of acute experimental colitis. Colitis was induced in the distal colon by rectal infusion of formaldehyde solution, followed by an intravenous bolus of soluble immune complexes. Despite active mucosal inflammation, there are only occasional inflammatory cells in the muscularis. Electrophysiological studies on tissue from control rabbits and rabbits with colitis were performed using double sucrose gap and intracellular microelectrode techniques. The resting membrane potential was lower (-44 +/- 3 mV) in muscle from rabbits with colitis compared with control animals (-54 +/- 2 mV) (P less than 0.02). Amplitude of the electrotonic potential after a hyperpolarizing current pulse was decreased (P less than 0.05) and the time constant was shortened (P less than 0.01) in muscle from animals with colitis compared with normal animals. Amplitude (13.1 +/- 2.3 mV) and maximum rate of rise (0.24 +/- 0.06 V/s) of the spike potential, initiated by a depolarizing current pulse, were decreased in muscle from animals with colitis compared with muscle from healthy animals (P less than 0.001). Isometric tension generation after electrical and chemical depolarization of the membrane or bethanechol administration was decreased (P less than 0.001) in muscle from colitic animals. These studies suggest 1) membrane resistance and membrane potential are decreased in muscle strips from animals with colitis; and 2) there is a disturbance in the electrical and mechanical response of these tissues after stimulation.

β-Adrenoceptor activation and PKA regulate delayed rectifier K+ channels of vascular smooth muscle cells

1998 ◽  
Vol 275 (2) ◽  
pp. H448-H459 ◽  
Author(s):  
E. Alejandro Aiello ◽  
A. Todd Malcolm ◽  
Michael P. Walsh ◽  
William C. Cole
Keyword(s):  
Signal Transduction ◽  
Smooth Muscle ◽  
Portal Vein ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Catalytic Subunit ◽  
Delayed Rectifier ◽  
Rabbit Portal Vein

Macroscopic 4-aminopyridine (4-AP)-sensitive, delayed rectifier K+ current of vascular smooth muscle cells is increased during β-adrenoceptor activation with isoproterenol via a signal transduction pathway involving adenylyl cyclase and cAMP-dependent protein kinase (PKA) (Aiello, E. A., M. P. Walsh, and W. C. Cole. Am. J. Physiol. 268 ( Heart Circ. Physiol. 37): H926–H934, 1995.). In this study, we identified the single delayed rectifier K+(KDR) channel(s) of rabbit portal vein myocytes affected by treatment with isoproterenol or the catalytic subunit of PKA. 4-AP-sensitive KDR channels of 15.3 ± 0.6 pS ( n = 5) and 14.8 ± 0.6 pS ( n = 5) conductance, respectively, were observed in inside-out (I-O) and cell-attached (C-A) membrane patches in symmetrical KCl recording conditions. The kinetics of activation (time constant of 10.7 ± 3.02 ms) and inactivation (fast and slow time constants of 0.3 and 2.5 s, respectively) of ensemble currents produced by these channels mimicked those reported for inactivating, 4-AP-sensitive whole cell KDR current of vascular myocytes. Under control conditions, the open probability ( NP o) of KDR channels of C-A membrane patches at −40 mV was 0.014 ± 0.005 ( n = 8). Treatment with 1 μM isoproterenol caused a significant, approximately threefold increase in NP o to 0.041 ± 0.02 ( P < 0.05). KDR channels of I-O patches exhibited rundown after ∼5 min, which was not affected by ATP (5 mM) in the bath solution. Treatment with the purified catalytic subunit of PKA (50 nM; 5 mM ATP) restored KDRchannel activity and caused NP o to increase from 0.011 ± 0.003 to 0.138 ± 0.03 ( P < 0.05; n = 11). These data indicate that small-conductance, 15-pS KDRchannels are responsible for inactivating the macroscopic delayed rectifier K+ current of rabbit portal vein myocytes and that the activity of these channels is enhanced by a signal transduction mechanism involving β-adrenoceptors and phosphorylation by PKA at a membrane potential consistent with that observed in the myocytes in situ.

Regulation of vascular smooth muscle tone

1994 ◽  
Vol 72 (8) ◽  
pp. 919-936 ◽  
Author(s):  
Michael P. Walsh
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Light Chain ◽  
Myosin Light Chain Kinase ◽  
Myosin Light Chain ◽  
Contractile Response ◽  
Muscle Tone ◽  
Myosin Phosphorylation ◽  
Smooth Muscle Tone ◽  
Vascular Smooth Muscle Tone

Vascular smooth muscle tone is regulated primarily by the sarcoplasmic free Ca2+ concentration, which determines the level of myosin phosphorylation. Stimulation of the muscle results in an increase in free [Ca2+], whereupon Ca2+ binds to calmodulin, inducing a conformational change enabling calmodulin to interact with and activate myosin light chain kinase. The active Ca2+∙calmodulin∙myosin light chain kinase complex catalyses the phosphorylation of serine-19 of the two 20-kDa light chains of myosin; this triggers cross-bridge cycling and the development of force. Relaxation follows restoration of free [Ca2+] to the resting level, whereupon calmodulin dissociates from myosin light chain kinase, which is thereby inactivated, and myosin is dephosphorylated by myosin light chain phosphatase and remains detached from actin. Overwhelming evidence now exists in favour of the central role of myosin phosphorylation–dephosphorylation in smooth muscle contraction–relaxation. However, considerable evidence supports the existence of additional, secondary mechanisms that can modulate the contractile state of smooth muscle either by altering the Ca2+ sensitivity of the contractile response or otherwise modulating one of the molecular events occurring downstream of the Ca2+ signal, e.g., the interaction of phosphorylated myosin heads with actin. The interplay of several regulatory elements confers on the contractile response of vascular smooth muscle the high degree of flexibility and adaptability required for the effective regulation of blood pressure.Key words: calcium, myosin, protein kinases, protein phosphatases, signal transduction, regulation of contraction, caldesmon, calponin.

A novel human plasma factor(S) capable of mobilizing intracellular Ca2+ in cultured rat vascular smooth muscle cells

1988 ◽  
Vol 153 (3) ◽  
pp. 1068-1075 ◽  
Author(s):  
Hiroki Yoshimi ◽  
Yukio Hirata ◽  
Shoichiro Takata ◽  
Yasuyuki Takagi ◽  
Yuka Fukuda ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Human Plasma ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Plasma Factor
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