Effects of hypoxia, hypercapnia, and pH on the chemoreceptor activity of the carotid body in vitro.

Eyzaguirre, C.; Koyano, H

doi:10.1113/jphysiol.1965.sp007634

Cited by 121 publications

(45 citation statements)

References 31 publications

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“…Anoxia of several minutes duration causes blockade of action potentials in rat optic nerve (Stys, Ransom, Waxman & Davis, 1990). However, it should be noted that action potential height was not diminished in our study, and a previous study reported that the sinus nerve remained functional for nearly 1 h into anoxia (Eyzaguirre & Koyano, 1965). Thus, the mechanism causing the adaptation or depression remains unresolved.…”

Section: Discussionmentioning

confidence: 53%

Maturation of carotid chemoreceptor sensitivity to hypoxia: in vitro studies in the newborn rat.

Kholwadwala

Donnelly

1992

The Journal of Physiology

138

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SUMMARY1. A preparation was developed to record single-fibre chemoreceptor afferent activity from carotid bodies of newborn and adult rats in vitro. The response to severe hypoxia was studied as a function of developmental age in four age groups: 1-2, 4-7, 10-15 days and adult (25-30 days).2. During superfusion with HEPES-saline at room PO and at 26 or 35 0C, afferent chemoreceptor activity could be recorded in all age groups. No significant difference was found among groups in baseline discharge frequency at 26 or 35 'C.3. All chemoreceptors responded to anoxia (PO 20 Torr) with a rapid increase in discharge frequency. At 35 'C, peak discharge frequency of single chemoreceptor afferents was significantly greater in the adult (15 7 + 1P6 Hz, mean + S.E.M., n = 18) and 10-15 days ( 112 + 4 2, n = 8) compared to rats of 1-2 days (4 3 + 0 7, n = 14) and 4-7 days of age (39+10, n= 7).4. At 2 min into the anoxia period, all chemoreceptor activities were reduced from their peak discharge levels. At 35 O, this decrease was significantly greater in the adult compared to the newborn. 5. During the period of decreased activity during anoxia, the chemoreceptor discharge could not be increased by inter-stream injection of acetylcholine (100 /tg) or dopamine (100 jug), although these drugs were effective in increasing discharge rate prior to hypoxia. 6. We conclude that: (1) postnatal maturation of chemoreceptor sensitivity to hypoxia is present in vitro, (2) maturation occurs between the first and second week after birth in the rat, and (3) the decrease in activity during prolonged anoxia is not greater in the newborn compared to the adult. Thus, maturational changes occur in the sensitivity of the glomus cell-nerve ending complex to hypoxia.

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Section: Discussionmentioning

confidence: 53%

Maturation of carotid chemoreceptor sensitivity to hypoxia: in vitro studies in the newborn rat.

Kholwadwala

Donnelly

1992

The Journal of Physiology

138

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“…The latter always are spontaneously active, 19 respond to prolonged ischemia with an irregular and prolonged discharge, 20 and are markedly activated during perfusion of the carotid body with deoxygenated solutions. 21 Moreover, whereas cyanide always excites arterial chemoreceptors, it affects "R" chemoreceptors only when they are already spontaneously active. Although these differences cannot be explained, the answer may be found in differences in the morphology of these two chemoreceptors, for the functional properties of arterial chemoreceptors are highly dependent on the structural relationships occurring between free nerve endings and surrounding glomus cells.…”

Section: Discussionmentioning

confidence: 99%

Renal chemoreceptors in the rat.

Recordati¹,

Moss

Waselkov³

1978

Circulation Research

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There are afferent nerve fibers responsive to alterations of the kidney's chemical environment in the renal nerves of the rat. In anesthetized, artificially ventilated, male Sprague-Dawley rats, single unit recordings were prepared by dissection of the centrally cut nerves of the right kidney. The stimuli used included occlusion of the renal artery, systemic asphyxia, changes in renal arterial and venous pressures, changes in ureteral pressure, and cyanide infusion. We found a population of sensory nerve fibers whose endings are activated only during markedly impaired renal blood flow (produced by clamping the renal artery, severe hypotension below 40 mm Hg, and prolonged occlusion of the renal vein), and during systemic asphyxia. The same units are not responsive to increases and decreases in systemic arterial pressure (range: 40--190 mm Hg), to ureteral pressure (range: 0--50 mm Hg), or to changes in renal venous pressure. None of the 40 single units studied was spontaneously active; their pattern of activation during renal ischemia always was characterized by trains of impulses. These sensory units have functional properties distinctly different from those of known renal mechanoreceptors. They appear to be a homogeneous group of sensory elements, and we have termed them renal ("R") chemoreceptors. Evidence also is presented which is consistent with the concept that a chemical substance released by or accumulated within the kidney might be the agent activating these chemoreceptors during renal ischemia.

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“…Paraffin oil was layered over the superfusate to a depth of less than 3 mm. The whole sinus nerve was placed on two platinum wire electrodes for recording the chemosensory discharge as used by Eyzaguirre and Koyano [20]. In these experiments, the electroneurogram consisted of almost entirely chemoreceptor impulses as characterized by their random pattern of discharge and the responses to nicotine, CO> and oxygen.…”

Section: Carotid Body Perjusion and Superfusionmentioning

confidence: 99%

The primary oxygen sensor of the cat carotid body is cytochrome a₃ of the mitochondrial respiratory chain

et al. 1994

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A~traet Carbon monoxide was shown to be competitive with 02 in oxygen sensing by perfused carotid bodies isolated from cats, afferent electrical activity increasing with either decreasing Oz or increasing CO. The CO-induced increase in afferent activity was fully reversed by bright light. At submaximal light intensities the extent of reversal, after correcting to equal light intensity of light quanta at each wavelength, was maximal for light of 432 + 2 and 590 + 2 nm, with a ratio (432/590) of approximately 6. This spectrum is characteristic of the CO compound of mitochondrial cytochrome a 3. The photo-reversible inhibition of oxygen sensing activity by CO accounts for at least 80% of the oxygen chemosensory activity of the carotid body.

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Effects of hypoxia, hypercapnia, and pH on the chemoreceptor activity of the carotid body in vitro.

Cited by 121 publications

References 31 publications

Maturation of carotid chemoreceptor sensitivity to hypoxia: in vitro studies in the newborn rat.

Maturation of carotid chemoreceptor sensitivity to hypoxia: in vitro studies in the newborn rat.

Renal chemoreceptors in the rat.

The primary oxygen sensor of the cat carotid body is cytochrome a₃ of the mitochondrial respiratory chain

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Effects of hypoxia, hypercapnia, and pH on the chemoreceptor activity of the carotid body in vitro.

Cited by 121 publications

References 31 publications

Maturation of carotid chemoreceptor sensitivity to hypoxia: in vitro studies in the newborn rat.

Maturation of carotid chemoreceptor sensitivity to hypoxia: in vitro studies in the newborn rat.

Renal chemoreceptors in the rat.

The primary oxygen sensor of the cat carotid body is cytochrome a3 of the mitochondrial respiratory chain

Contact Info

Product

Resources

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The primary oxygen sensor of the cat carotid body is cytochrome a₃ of the mitochondrial respiratory chain