Autoregulation of hind‐limb blood flow in conscious dogs.

Britton, Steven L.; Metting, Patricia J.; Ronau, T. F.; Strader, J. R.; Weldy, David L.

doi:10.1113/jphysiol.1985.sp015865

Cited by 14 publications

(13 citation statements)

References 23 publications

(28 reference statements)

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“…Therefore, the results of our investigation suggest that the effect of an increase in vasomotor tone (tending to decrease blood flow) from chemoreceptor stimulation can be reversed passively by a rise in blood pressure in the muscle bed but not in the renal bed. This difference in the effects in two vascular beds may be related to the difference in autoregulatory phenomenon, which is absent in resting muscle (Britton et al 1985), and very prominent in the kidney (Johnson, 1986). An increase in muscle blood flow, therefore, does not necessarily mean inhibition or withdrawal of the sympathetic vasoconstrictor tone as claimed by Hilton & Marshall (1982).…”

Section: Discussionmentioning

confidence: 99%

“…Since the response of the cutaneous veins to chemoreceptor stimulation is a vasodilatation (Calvelo, Abboud, Ballard & Abdel-Sayed, 1970;Koike, Mark, Heistad & Schmid, 1975), it is not certain whether the vasodilatation of the whole limb was the result of the effect of chemoreceptors on the venous system, or due to the increase in systemic arterial pressure which was not controlled in the experiments of Marshall (1981Marshall ( , 1987 and Hilton & Marshall (1982). An increase in systemic arterial pressure can mechanically raise the flow, particularly when autoregulation in the muscle vascular bed is absent in the resting condition (Britton, Metting, Ronau, Strader & Weldy, 1985).…”

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confidence: 99%

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Primary effects of carotid chemoreceptor stimulation on gracilis muscle and renal blood flow and renal function in dogs.

Al-Obaidi

Karim

1992

The Journal of Physiology

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SUMMARY1. In chloralose-anaesthetized and artificially ventilated dogs, the carotid sinus regions were vascularly isolated and perfused either with arterial or mixed (arterial and venous) blood (partial pressure of 02 (PO2) 43 8 + 2-4 mmHg, mean + S.E.M. n = 14) to stimulate the carotid chemoreceptors. The carotid sinus pressure was held constant at 142-0 + 2-8 mmHg. Measurements were made of renal and gracilis muscle blood flow by wrap-round electromagnetic flow probes placed around the renal and gracilis arteries, glomerular filtration rate by creatine clearance, urinary sodium excretion by flame photometry and solute excretion by osmometry.2. In ten dogs, with intact cervical vagosympathetic trunks, carotid chemoreceptor stimulation produced significant increases in aortic pressure (AoP) of 12-7+ 1-1 % (n = 10, P < 0-001), in glomerular filtration rate (GFR) of 14-7+441 % (P < 0-001), urine flow rate (V) of 16-5+3-5% (P < 0002), in urinary sodium excretion (UNaV) of 17-5+2-5% (P < 0005) and in urinary osmolar excretion (UOSm V) of 13-2 + 22 % (P < 0-00 1), but a significant decrease in renal blood flow (RBF) of 5-8 + 1P8 % (P < 0 02). In six of these dogs in which gracilis muscle blood flow (MBF) was also recorded, carotid chemoreceptor stimulation caused significant increases in AoP of 12-8+P14% (n = 6, P < 0-001) and in MBF of 10-0+1-6% (P < 0 002), and a small but significant decrease in RBF of 3-6 + 1P5 % (P < 0-02).3. In fourteen dogs, with sectioned cervical vagosympathetic trunks, carotid chemoreceptor stimulation produced increases in AoP of 220 + 26 % (n = 14, P < 0-001), in GFR of 36-9 + 4-2 % (P < 0-001), in V of 301 + 4-4 % (P < 0-001 ), in UNaV of 31-4+5-3% (P < 0-001), and in UosmV of 25-7+5-8% (P < 0-001). However, it produced a greater decrease in RBF of 10-5 + 1P9 % (P < 0-001). In ten of these dogs, where MBF was recorded, carotid chemoreceptor stimulation caused greater increase in AoP of 22-4+3-0% (n = 10, P < 0-001) and in MBF of 32-8+3-7% (P < 0-001), and a greater decrease in RBF of 9-8+ 1-9% (P < 0-001).4. In fourteen dogs, with sectioned vagosympathetic trunks and controlled AoP, carotid chemoreceptor stimulation caused significant decreases in RBF of 19-1+1-6% (n = 14, P < 0001), in GFR of 17-7+2-2% (P < 0-001), in V of 23-4+2-5% (P < 0-001), in UNaV of 22-0+2-4% (P < 0-001) and in Uosm V of * To whom reprint request should be addressed. MS 9678AI. AL-OBAIDI AND F. KARIM 16 7 + 241 % (P < 0-001). In ten of these dogs, in which MBF was measured, carotid chemoreceptor stimulation produced a large decrease (a reverse effect) in MBF of 18 8+21 % (n = 10, P < 0)001) and in a further decrease in RBF of 19-7+2-0%

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Primary effects of carotid chemoreceptor stimulation on gracilis muscle and renal blood flow and renal function in dogs.

Al-Obaidi

Karim

1992

The Journal of Physiology

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“…Autoregulation of blood flow is absent or weak in resting skeletal muscle (23), and the cutaneous circulation is generally described as a passive vascular bed (24). Because systemic vascular autoregulation results from the net autoregulatory contribution of all of the regional vascular beds, redistribution of blood flow from A number of studies have shown that the effectiveness of autoregulation is enhanced when tissues operate near their nutritive limit (12,14,23,25); only vasopressin caused a significant decrease in baseline cardiac output (Table I), which would bring tissues closer to this limit. This may be another reason for finding a greater contribution of autoregulation in the hemodynamic response to vasopressin compared to angiotensin II or norepinephrine.…”

Section: Discussionmentioning

confidence: 99%

Quantitative contribution of systemic vascular autoregulation in acute hypertension in conscious dogs.

Metting¹,

Kostrzewski²,

Stein³

et al. 1989

J. Clin. Invest.

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Experiments were performed in nine conscious dogs to quantitate the contribution of systemic vascular autoregulation to the increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) produced by angiotensin II (ANG II), arginine vasopressin (AVP), and norepinephrine (NE). We hypothesized that if autoregulatory vasoconstriction is significant, then the increase in TPR produced by vasoconstrictor infusion will be greater when MAP is controlled at hypertensive values than when the increase in pressure is prevented by controlling MAP at the animal's normotensive value. Each drug was infused at a dose sufficient to increase MAP by 50%. Then, a constant rate of vasoconstrictor infusion was maintained while MAP was controlled at hypertensive or normotensive levels for 15-min periods using a gravity reservoir connected to the left common carotid artery. During AVP infusion, TPR was significantly greater when MAP was controlled at hypertensive than at normotensive values. This autoregulatory-mediated vasoconstriction accounted for approximately three-fourths of the increase in MAP produced by AVP. No significant autoregulatory component was identified for the increases in TPR and MAP produced by ANG II or NE. We conclude that systemic vascular autoregulation is a powerful physiological property that contributes to the hemodynamic response to pressor doses of AVP.

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“…Outputs from Doppler flow channels were recorded in kilohertz of Doppler frequency shift. Calibration of the flow probes was performed in situ at the completion of all experiments while the animals were anaesthetized (Britton, Metting, Ronau, Strader & Weldy, 1985). Alternatively, the flow in ml min-' was calculated using the Doppler equation (Ishida, Lewis, Hartley, Entman & Field, 1983).…”

Section: Mea8urementsmentioning

confidence: 99%

Adenosine is not essential for exercise hyperaemia in the hindlimb in conscious dogs.

Koch

Britton

Metting

1990

The Journal of Physiology

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SUMMARY1. The contribution of endogenous adenosine to the increase in hindlimb blood flow that occurs during treadmill exercise was evaluated in conscious dogs. We postulated that if adenosine is essential for the hindlimb hyperaemic response, then pharmacological treatment of the animals with adenosine receptor antagonists should decrease hindlimb blood flow during treadmill exercise.2. A total of twenty-three dogs were chronically instrumented for measurement of aortic blood pressure and hindlimb blood flow using electromagnetic or Doppler flow probes on the left external iliac artery. Measurements of arterial blood pressure, hindlimb blood flow and heart rate were made during steady-state treadmill exercise in both the presence and the absence of adenosine receptor antagonists. Four different protocols were performed using different routes of administration of two adenosine receptor antagonists. Aminophylline was used in most of the experiments, and the effects of the more potent antagonist, 8-phenyltheophylline, were also evaluated. In addition, the dogs exercised at varying intensities ranging from a low level of 5 5 km h-1 at 0 % gradient to a high intensity of 5-5 km h-' at 21 % gradient.3. Aminophylline given as a single intravenous dose, or as a constant infusion either intravenously or directly into the hindlimb artery, did not decrease hindlimb blood flow at low, moderate or high intensities of exercise. Likewise, the blockade of adenosine receptors with 8-phenyltheophylline, given systemically or as a bolus injection administered directly into the hindlimb circulation during moderate exercise, did not attenuate the hindlimb blood flow response.4. Our data demonstrate that exercise hyperaemia of the hindlimb is not reduced by antagonism of adenosine receptors. These findings are consistent with the hypothesis that adenosine is not an essential mediator of hindlimb vasodilatation during exercise.

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Autoregulation of hind‐limb blood flow in conscious dogs.

Cited by 14 publications

References 23 publications

Primary effects of carotid chemoreceptor stimulation on gracilis muscle and renal blood flow and renal function in dogs.

Primary effects of carotid chemoreceptor stimulation on gracilis muscle and renal blood flow and renal function in dogs.

Quantitative contribution of systemic vascular autoregulation in acute hypertension in conscious dogs.

Adenosine is not essential for exercise hyperaemia in the hindlimb in conscious dogs.

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