Myogenic vascular regulation in skeletal muscle <i>in vivo</i> is not dependent of endothelium‐derived nitric oxide

Ekelund, Ulf; Björnberg, J.; Grände, Per‐Olof; Albert, U; Mellander, Stefan

doi:10.1111/j.1748-1716.1992.tb09286.x

Cited by 51 publications

(37 citation statements)

References 19 publications

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“…The NO responsible is largely produced by nNOS in macula densa cells (154,192,210). Although NO has also been reported to attenuate MR in vessels from skin (63), myocardium (151,158,198), mesentery (150), spleen (25), and skeletal muscle (46,93,141), other studies failed to confirm such an effect at least in the skeletal muscle circulation (50,51,97,184). The picture is even less consistent in the kidney.…”

Section: Modulation Of the Contribution Of The Autoregulatory Mechanismsmentioning

confidence: 99%

Mechanisms of renal blood flow autoregulation: dynamics and contributions

Just

2007

American Journal of Physiology-Regulatory, Integrative and Comp

163

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Autoregulation of renal blood flow (RBF) is caused by the myogenic response (MR), tubuloglomerular feedback (TGF), and a third regulatory mechanism that is independent of TGF but slower than MR. The underlying cause of the third regulatory mechanism remains unclear; possibilities include ATP, ANG II, or a slow component of MR. Other mechanisms, which, however, exert their action through modulation of MR and TGF are pressure-dependent change of proximal tubular reabsorption, resetting of RBF and TGF, as well as modulating influences of ANG II and nitric oxide (NO). MR requires < 10 s for completion in the kidney and normally follows first-order kinetics without rate-sensitive components. TGF takes 30–60 s and shows spontaneous oscillations at 0.025–0.033 Hz. The third regulatory component requires 30–60 s; changes in proximal tubular reabsorption develop over 5 min and more slowly for up to 30 min, while RBF and TGF resetting stretch out over 20–60 min. Due to these kinetic differences, the relative contribution of the autoregulatory mechanisms determines the amount and spectrum of pressure fluctuations reaching glomerular and postglomerular capillaries and thereby potentially impinge on filtration, reabsorption, medullary perfusion, and hypertensive renal damage. Under resting conditions, MR contributes ∼50% to overall RBF autoregulation, TGF 35–50%, and the third mechanism < 15%. NO attenuates the strength, speed, and contribution of MR, whereas ANG II does not modify the balance of the autoregulatory mechanisms.

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Section: Modulation Of the Contribution Of The Autoregulatory Mechanismsmentioning

confidence: 99%

Mechanisms of renal blood flow autoregulation: dynamics and contributions

Just

2007

American Journal of Physiology-Regulatory, Integrative and Comp

163

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“…This profile contrasts with that found in the current study. Ekelund et al (1992) used the a-adrenoceptor agonist phenylephrine to control for the hypertensive effect of NO synthase inhibition upon responses. The pharmacodynamic profile of phenylephrine may be different from that of NO synthase inhibitors and is therefore not the best means of controlling for the loss of endogenous levels of NO.…”

Section: Discussionmentioning

confidence: 99%

The effect of NG‐nitro‐L‐arginine methyl ester upon hindlimb blood flow responses to muscle contraction in the anaesthetized cat

Poucher

1995

Experimental Physiology

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SUMMARYThe aim of the present experiment was to investigate the relative contribution of nitric oxide produced in endothelial cells to functional and reactive hyperaemia in the hindlimb of anaesthetized cats. Cats (2-5-3.4 kg) were anaesthetized with alphadalone-alphalaxone, and breathed spontaneously following tracheotomy. Left hindlimb blood flow was measured with a flow probe and hyperaemia responses were monitored following 10 s occlusion of the left external iliac artery and during 20 min stimulation of the sciatic and femoral nerves at 3 Hz. This was repeated following nitric oxide synthase inhibition with NG-nitro-L-arginine methyl ester (L-NAME, 100 mg kg-', i.v.). Following L-NAME administration, baseline hindlimb blood flow and arterial blood pressure were restored by infusion of sodium nitroprusside (range, 0-3-2-25 ,ug kg-l min-', i.v.). Following arterial occlusion, L-NAME reduced the peak reactive hyperaemia (6-5 ± 0-8 vs. 4.5 + 1.0 ml min-' kg-', P <0.05) and blood flow repayment (9-9 + 2-3 vs.6-1 + 2-6 ml, P < 0-05) responses. In contrast, the total functional hyperaemia response during hindlimb contraction was not altered (264-7 + 68-2 vs. 264-4 + 62-8 ml kg-', n.s.). The results of the study suggest that the production of nitric oxide from endothelial cells does not contribute to functional hyperaemia in contracting skeletal muscle, but plays a large role in reactive hyperaemia. The results imply that flow-dependent dilatation of feed arteries is mediated by NO in reactive hyperaemia.

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“…A component of the autoregulatory adjustment is termed the myogenic response, which was first identified by Bayliss in 1902 (15,38). This response can occur independent of sympathetic and endothelium influences (13,50).…”

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confidence: 94%

Sex differences in limb vasoconstriction responses to increases in transmural pressures

Lott

Hogeman

Herr

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Women compared with men are more likely to have orthostatic intolerance. The purpose of this study was to examine whether sex affects limb vasoconstrictor response to increases in transmural pressure. Brachial and femoral mean blood velocity (MBV) and diameter (Doppler Ultrasound) were measured in 10 women and 10 men as transmural pressure was altered by applying local suction (Ϫ25, Ϫ50, Ϫ75, and Ϫ100 mmHg) via pressurized-limb tanks for 1 min to a single arm and leg. With the abrupt application of forearm suction (Ϫ75 and Ϫ100 mmHg), women compared with men had a greater initial rise in MBV (peak), followed by a quicker dynamic rate of velocity reduction. In the leg, women had a tendency for higher peak MBV but had similar dynamic velocity reductions compared with men. After 60 s of suction, women compared with men had attenuated reductions in brachial flow and conductance (Ϫ8.05 Ϯ 1.71 vs. Ϫ16.25 Ϯ 1.71 ml/min; Ϫ0.12 Ϯ 0.03 vs. Ϫ0.20 Ϯ 0.03 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; main effect, P Ͻ 0.05), as well as attenuated femoral flow and conductance to sustained leg negative pressure at Ϫ100 mmHg (P Ͻ 0.05). When the data were expressed as percent change, women compared with men continued to have attenuated brachial flow responses (Ϫ24 Ϯ 2 vs. Ϫ36 Ϯ 2%, main effect, P Ͻ 0.05), with a trend toward attenuation at the highest leg pressure (Ϫ25 Ϯ 11 vs. Ϫ46 Ϯ 4%; P ϭ 0.08). These sex differences remained after normalizing the flow responses by limb volume (percent change). Our findings suggest that young women compared with men have attenuated brachial and femoral vasoconstrictor responses to increases in transmural pressure, which may have implications for the greater incidence of orthostatic intolerance in women.gender; myogenic response; autoregulation; sympathetic nervous system SYNCOPE, ESPECIALLY DURING postural stress, is more common in women then men (6, 22, 52). Most studies (4,7,16,19,21,28,46,55,61,63), but not all (26), have demonstrated that orthostatic tolerance is impaired in women compared with men. The suggested causes of the reduced orthostatic tolerance in women compared with men include altered central volume adjustments (20,21) and vasoconstriction responses (56). As human subjects rise from lying or sitting to the standing position, transmural pressure in the levels of the lower limbs rise. Postural stress evokes sympathetic engagement and autoregulatory constrictor responses to the rise in transmural pressure. In contrast to the effect of sex on neurally mediated cardiovascular responses to orthostatic stress, very few studies have examined the impact of sex on autoregulatory constrictor responses. A component of the autoregulatory adjustment is termed the myogenic response, which was first identified by Bayliss in 1902 (15, 38). This response can occur independent of sympathetic and endothelium influences (13, 50).In vitro animal studies have yielded mixed findings regarding the effects of sex on the myogenic response.Step increases in transmural pressure (i.e., 20 up to 140 mmHg) evoked attenuated myo...

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Myogenic vascular regulation in skeletal muscle in vivo is not dependent of endothelium‐derived nitric oxide

Cited by 51 publications

References 19 publications

Mechanisms of renal blood flow autoregulation: dynamics and contributions

Mechanisms of renal blood flow autoregulation: dynamics and contributions

The effect of NG‐nitro‐L‐arginine methyl ester upon hindlimb blood flow responses to muscle contraction in the anaesthetized cat

Sex differences in limb vasoconstriction responses to increases in transmural pressures

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