Mechanisms of myogenic enhancement by norepinephrine

Mechanisms contributing to the ability of norepinephrine (NE) to enhance arteriolar myogenic responsiveness were studied in the rat cremaster muscle. Anesthetized rats were enclosed in an airtight box that could be pressurized to increase intravascular pressure in the cremaster, which was exteriorized into a tissue bath. Vessel diameter, intravascular pressure, and red cell velocity were measured in the first-order (1A) arteriole during box pressure increases of 10, 20, and 30 mmHg. Control arterioles [diameter = 113 +/- 3 (SE) microns] did not exhibit myogenic constriction in response to step increases in intravascular pressure (e.g., + 30 mmHg, diameter = 122 +/- 5 microns), whereas after 25% constriction with NE (diameter = 85 +/- 2 microns) arterioles exhibited significant myogenic constriction (e.g., +30 mmHg, diameter = 70 +/- 4 microns). The NE effect on myogenic reactivity was augmented by Ca2+ channel agonists and inhibited by antagonists, suggesting a role for voltage-operated Ca2+ channels. In contrast to NE, exposure to KCl (30 mM) did not enhance myogenic responsiveness, suggesting that factors in addition to voltage-operated channels were involved in the NE effect. The protein kinase C (PKC) activator indolactam (1 microM) was found to increase vascular tone in the 1A arterioles (diameter = 109 +/- 6 to 89 +/- 7 microns) and to induce significant myogenic responsiveness similar to that produced by NE (e.g., +30 mmHg, diameter = 65 +/- 9 microns). Staurosporine (0.1 microM) and calphostin C (1 microM), inhibitors of PKC, significantly attenuated the NE-induced myogenic response.(ABSTRACT TRUNCATED AT 250 WORDS)

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Attenuation of blood flow-induced dilation in arterioles after muscle contraction

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.5.h2114 ◽

1994 ◽

Vol 266 (5) ◽

pp. H2114-H2121 ◽

Cited By ~ 6

Author(s):

M. Cabel ◽

V. Smiesko ◽

P. C. Johnson

Keyword(s):

Shear Rate ◽

Muscle Contraction ◽

Vessel Diameter ◽

Similar Degree ◽

Red Cell ◽

Cremaster Muscle ◽

Third Order ◽

Cell Velocity ◽

Luminal Flow ◽

Red Cell Velocity

The response of third-order arterioles (n = 15) in rat cremaster muscle to increased luminal flow was studied after brief (20-30 s) occlusion of a neighboring arteriole in pentobarbital-anesthetized rats. Red cell velocity increased almost fivefold (485 +/- 54% of control) during occlusion, and vessel diameter increased 63 +/- 11%. Initially, the calculated wall shear rate increased to 430 +/- 40% of control during occlusion but then decreased to 308 +/- 35% of control as a consequence of arteriolar dilation. The muscle was subsequently stimulated to contract for 1 min, and the occlusion procedure was repeated after arteriolar diameter and red cell velocity had returned to control levels. In this instance the vessel dilation was 34 +/- 10% or about one-half of that seen during the previous occlusion, although velocity and shear rate rose to a similar degree (474 +/- 54 and 397 +/- 35%, respectively). Dilation during a third occlusion 2-7 min after the vessel recovered from the second occlusion was as great as during the first occlusion (77 +/- 20%). The results indicate that flow-induced dilation in arterioles of rat cremaster muscle is transiently attenuated after muscle contraction.

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Erythrocyte flow and dynamic hematocrit in the renal papilla of the rat

AJP Renal Physiology ◽

10.1152/ajprenal.1985.249.6.f898 ◽

1985 ◽

Vol 249 (6) ◽

pp. F898-F902 ◽

Cited By ~ 5

Author(s):

B. Zimmerhackl ◽

R. Dussel ◽

M. Steinhausen

Keyword(s):

High Sensitivity ◽

Vessel Diameter ◽

Systemic Circulation ◽

Red Cells ◽

Red Cell ◽

Renal Papilla ◽

Television System ◽

Vasa Recta ◽

Cell Velocity ◽

Red Cell Velocity

The microcirculation of the renal papilla was investigated in 32 vasa recta of Wistar rats. Using fluorescence microscopy in combination with a high-sensitivity television system we measured the velocity and flux of fluorescent-tagged erythrocytes in descending (DVR) and ascending vasa recta (AVR). After staining the plasma with fluorescent high molecular weight dextran we determined the diameters of DVR and AVR. Red cell flux (Qrbc) was determined from the ratio of the frequency of fluorescent-tagged red cells detected per unit time (fFITC) to the number of fluorescent-tagged red cells per nanoliter packed red cells (NFITC). From red cell velocity (Vrbc) and vessel diameter (D) we calculated the volume flow (Vapp). The dynamic hematocrit was directly derived as the ratio of Qrbc to Vapp. During antidiuresis Vrbc was 1.35 +/- 0.15 mm X s-1 (mean +/- SE) in DVR and 0.47 +/- 0.07 mm X s-1 in AVR. Qrbc in the same vessels averaged 3.26 +/- 0.9 and 1.72 +/- 0.35 nl X min-1, respectively. The diameter in DVR was 14.3 +/- 0.9 and in AVR 17.9 +/- 0.9 micron. From these values we calculated a dynamic hematocrit of 26 +/- 4 in DVR and 25 +/- 4% in AVR. The systemic hematocrit was 44 +/- 1%. The dynamic hematocrit in vasa recta represented 59 +/- 9 and 57 +/- 8% of the value in the systemic circulation, respectively.

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Role of EDRFs in the control of arteriolar diameter during increased metabolism of striated muscle

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.1.h195 ◽

1994 ◽

Vol 267 (1) ◽

pp. H195-H200 ◽

Cited By ~ 4

Author(s):

Y. Saito ◽

A. Eraslan ◽

R. L. Hester

Keyword(s):

Sodium Nitroprusside ◽

Striated Muscle ◽

Distal Portion ◽

Distal Region ◽

Red Cell ◽

First Order ◽

Cell Velocity ◽

Red Cell Velocity ◽

Arteriolar Vasodilation ◽

Arteriolar Diameter

This experiment was designed to determine the role that the release of endothelium-derived relaxing factors (EDRFs), endothelium-derived nitric oxide (EDNO), or prostaglandins have in the control of arteriolar vasodilation during an increased metabolic rate in striated muscle. A silicone stopcock grease dam was placed across the distal portion of the cremaster muscle of pentobarbital-anesthetized hamsters to localize the application of the metabolic stimulator 2,4-dinitrophenol (DNP). Application of DNP (10 mM) to the distal region resulted in significant increases in red cell velocity (from 6 +/- 1 to 10 +/- 2 mm/s) and arteriolar diameter (from 75 +/- 3 to 91 +/- 5 microns) (P < 0.05; n = 6) in the first-order arterioles located approximately 11 mm upstream from the silicone dam. Administration of N omega-nitro-L-arginine methyl ester (L-NAME; 2 mg iv) resulted in significant vasoconstriction of the first-order arterioles and a significant decrease in the vasodilator response to acetylcholine (1 microM). Addition of sodium nitroprusside (380 microM) to the superfusion solution during L-NAME treatment resulted in a return of arteriolar diameter to control levels. DNP treatment during L-NAME and sodium nitroprusside treatment did not inhibit the arteriolar vasodilation [75 +/- 3 to 87 +/- 4 microns (P > 0.05)] after a significant increase in red cell velocity from 7 +/- 1 to 11 +/- 1 mm/s. Before indomethacin treatment, DNP treatment resulted in an increase in arteriolar diameter from 72 +/- 3 to 90 +/- 3 microns, preceded by an increase in red cell velocity from 6 +/- 1 to 10 +/- 1 mm/s. (ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of NO-Donors on Thrombus Formation and Microcirculation in Cerebral Vessels of the Rat

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650532 ◽

1996 ◽

Vol 76 (01) ◽

pp. 111-117 ◽

Cited By ~ 10

Author(s):

Yasuto Sasaki ◽

Junji Seki ◽

John C Giddings ◽

Junichiro Yamamoto

Keyword(s):

Blood Flow ◽

Thrombus Formation ◽

Dependent Manner ◽

Red Cell ◽

Cell Velocity ◽

Red Cell Velocity ◽

The Mean ◽

Wall Shear ◽

Dose Dependent

SummarySodium nitroprusside (SNP) and 3-morpholinosydnonimine (SIN-1), are known to liberate nitric oxide (NO). In this study the effects of SNP and SIN-1 on thrombus formation in rat cerebral arterioles and venules in vivo were assessed using a helium-neon (He-Ne) laser. SNP infused at doses from 10 Μg/kg/h significantly inhibited thrombus formation in a dose dependent manner. This inhibition of thrombus formation was suppressed by methylene blue. SIN-1 at a dose of 100 Μg/kg/h also demonstrated a significant antithrombotic effect. Moreover, treatment with SNP increased vessel diameter in a dose dependent manner and enhanced the mean red cell velocity measured with a fiber-optic laser-Doppler anemometer microscope (FLDAM). Blood flow, calculated from the mean red cell velocity and vessel diameters was increased significantly during infusion. In contrast, mean wall shear rates in the arterioles and venules were not changed by SNP infusion. The results indicated that SNP and SIN-1 possessed potent antithrombotic activities, whilst SNP increased cerebral blood flow without changing wall shear rate. The findings suggest that the NO released by SNP and SIN-1 may be beneficial for the treatment and protection of cerebral infarction

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A method to obtain volumetric blood flow and red cell velocity in the microvascular network

Microvascular Research ◽

10.1016/0026-2862(84)90067-0 ◽

1984 ◽

Vol 27 (3) ◽

pp. 379-384 ◽

Cited By ~ 1

Author(s):

Isaac I.H. Chen ◽

John N. Diana

Keyword(s):

Blood Flow ◽

Red Cell ◽

Microvascular Network ◽

Cell Velocity ◽

Red Cell Velocity

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ET-1 induced alterations of hepatic microcirculation: sinusoidal and extrasinusoidal sites of action

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1994.267.1.g143 ◽

1994 ◽

Vol 267 (1) ◽

pp. G143-G149 ◽

Cited By ~ 16

Author(s):

M. Bauer ◽

J. X. Zhang ◽

I. Bauer ◽

M. G. Clemens

Keyword(s):

Recovery Period ◽

Epifluorescence Microscopy ◽

Microvascular Blood Flow ◽

Red Cell ◽

Hepatic Microcirculation ◽

Cell Velocity ◽

Red Cell Velocity ◽

Sites Of Action ◽

Systemic Application

Using epifluorescence microscopy, we investigated the dynamic changes in hepatic sinusoidal hemodynamics in vivo during continuous infusion of endothelin-1 (ET-1) in pentobarbital-anesthetized rats. ET-1 was infused for 20 min at rates of 2 or 10 pmol/min either systemically or into the portal vein, followed by a 90-min recovery period. In contrast to systemic application of ET-1 that did not cause a consistent hepatic microvascular effect, we observed two different patterns of microcirculatory alterations during portal application. Infusion of 2 pmol/min elicited a rapid, reversible decrease in sinusoidal diameter that was paralleled by a slight increase in red cell velocity, resulting in conservation of volumetric flow and sinusoid density. Infusion of 10 pmol/min resulted in a biphasic narrowing followed by transient increase in sinusoidal diameter and a profound and lasting decrease in red cell velocity, leading to an almost complete cessation of hepatic microvascular blood flow. These results indicate that ET-1 is a potent constrictor in the liver microcirculation in vivo and acts at both extrasinusoidal and sinusoidal sites, although the sinusoidal sites appear to be more sensitive to lower concentrations.

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Red cell perfusion in skeletal muscle at rest and after mild and severe contractions

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.252.3.h485 ◽

1987 ◽

Vol 252 (3) ◽

pp. H485-H493 ◽

Cited By ~ 2

Author(s):

K. Tyml

Keyword(s):

Sartorius Muscle ◽

Red Cell ◽

Capillary Length ◽

Mean Values ◽

Pooled Data ◽

Cell Velocity ◽

Red Cell Velocity ◽

The Mean ◽

O2 Supply ◽

First Time

The aim of this study was to evaluate the distribution of red cell perfusion in sartorius muscle of anesthetized frogs by analyzing simultaneously red cell velocity (VRBC), number of cells per unit capillary length (NRBC), and density of perfused capillaries (CD) in a 2.07 X 2.71-mm region of the muscle visualized microscopically at very low magnification. In the 16 muscles studied, a severe 1-min electrical stimulation induced statistically significant increases in the mean values, VRBC, NRBC, and CD, as well as significant decreases in heterogeneities (SD/mean) of these three parameters when going from rest to postcontraction hyperemia. A mild 3-s stimulation caused significant increases only in VRBC and NRBC. Red cell perfusion, computed as a product of the three parameters divided by the mean capillary length, increased significantly from 87.4 +/- 81.9 to 417.9 +/- 118.2 (SD) and from 96.9 +/- 75.7 to 192.5 +/- 190.2 (SD) cells X s-1 X mm-3, respectively. In both stimulations, the postcontraction increase of red cell supply to the muscle, expressed in cells per second per cubic millimeter, was larger than any individual increase in the three parameters. Based on pooled data from all muscles, both NRBC and CD were determined to be dependent on VRBC. The present study supports the view that VRBC, NRBC, CD, and heterogeneity of red cell distribution depend on vascular tone and demonstrates for the first time that these four dependencies can operate both concurrently and synergistically to increase O2 supply to muscle after contraction.

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