Cardiovascular and renal effects of hypoxia in conscious carotid body-denervated rats

1993 ◽  
Vol 74 (6) ◽  
pp. 2795-2800 ◽  
Author(s):  
R. Behm ◽  
H. Mewes ◽  
W. H. DeMuinck Keizer ◽  
T. Unger ◽  
R. Rettig

The contribution of peripheral arterial chemoreceptors to cardiovascular and renal responses to acute hypocapnic hypoxia is currently not well understood. We compared the effects of normobaric hypoxia on mean arterial blood pressure (MABP), heart rate, glomerular filtration rate (GFR), renal blood flow (RBF), and renal volume and electrolyte excretion in conscious unilaterally nephrectomized carotid body-denervated (n = 10) and sham-operated (n = 10) control rats. Thirty minutes of normobaric hypoxia (12.5% O2) resulted in significant reductions in arterial PO2 and PCO2 as well as decreases in MABP, GFR, RBF, and renal sodium, potassium, and water excretion. These effects occurred more rapidly and/or were significantly more pronounced in carotid body-denervated than in sham-operated rats. These data indicate that moderate acute hypocapnic hypoxia has profound effects on systemic and renal hemodynamics as well as on renal excretory function in conscious rats. We conclude that stimulation of the peripheral arterial chemoreceptors can partially offset the hypoxia-induced decreases in MABP, RBF, GFR, urine flow, and urinary sodium and potassium excretion, thereby helping to maintain cardiovascular as well as fluid and electrolyte homeostasis.

1993 ◽  
Vol 75 (3) ◽  
pp. 1035-1043 ◽  
Author(s):  
S. Lahiri ◽  
W. L. Rumsey ◽  
D. F. Wilson ◽  
R. Iturriaga

To understand the interplay between microcirculatory control and carotid body (CB) function, we simultaneously measured carotid body microvascular PO2 (CBM PO2) and chemosensory activity in the cat in vivo under several experimental conditions. Cats were anesthetized with pentobarbital sodium, paralyzed, and artificially ventilated. CBs were exposed, and steady-state CBM PO2 was measured by the O2-dependent quenching of the phosphorescence of Pd-meso-tetra-(4-carboxyphenyl)porphine, which was administered intravenously. A few fibers of the carotid sinus nerve were used to record chemosensory discharges. At arterial PO2 (PaO2) of 103.4 +/- 4.1 Torr, CBM PO2 was 52.5 +/- 3.6 Torr (n = 9). Graded lowering of PaO2 from 160 to 50 Torr resulted in nearly proportional decreases in CBM PO2, but at lower PaO2 the decrease in CBM PO2 became more substantial. As PaO2 decreased, chemosensory discharge increased in parallel with CBM PO2. Hypercapnia and hypocapnia did not significantly change the relationship between PaO2 and CBM PO2, although the chemosensory discharge responded significantly. CBM PO2 and chemosensory discharge were not affected by hemorrhagic hypotension until arterial blood pressure fell below approximately 50 Torr and then CBM PO2 decreased and chemosensory discharge increased. The lack of a significant effect of hemorrhagic hypotension indicated that O2 delivery to CB was almost independent of the systemic blood pressure. Taken together, the observations suggest that CB microcirculation and PO2 are subject to control by intrinsic mechanisms and that CBM PO2 is compatible with oxidative metabolism playing a role in O2 chemoreception during hypoxia.


2011 ◽  
Vol 10 (5) ◽  
pp. 101-105 ◽  
Author(s):  
O. S. Talalayeva ◽  
A. Yu. Zharikov ◽  
S. A. Fedoreyev ◽  
Ya. F. Zverev ◽  
V. M. Bryukhanov ◽  
...  

The aim of present investigation was to establish possible histochrome's effect on the renal excretory function. During 10 days was being administrated histochrome by subcutaneous injections in dose 10 mg/kg. Every 2 days was being detected daily renal excretions of water, creatinin, sodium and potassium. Long-term histochrome's administration was followed by a fivefold increasing of water excretion and comparable amplification of creatinin. Sodium's and potassium's excretions were increasing to a lesser degree. The revealed histochrome's diuretic effect qualitatively reminds action of diuretic plants, but quantitatively it was compared with thiazid's one.


1985 ◽  
Vol 58 (6) ◽  
pp. 1901-1908 ◽  
Author(s):  
S. Lahiri ◽  
C. Hsiao ◽  
R. Zhang ◽  
A. Mokashi ◽  
T. Nishino

The hypothesis that instability of cardiorespiratory control may depend on the response and sensitivity of carotid body chemoreceptors to arterial blood gases was studied in anesthetized cats under three different experimental conditions. 1) Following administration of the peripheral dopamine receptor blocker [domperidone (0.6–0.8 mg X kg-1, iv)], carotid chemoreceptor activity and its sensitivity to CO2 during hypoxia increased, leading to cardiorespiratory oscillations at low arterial PO2 in four of eight cats. Inhalation of 100% O2 promptly decreased chemoreceptor activity and eliminated the oscillations. Inhalation of CO2 stimulated the chemoreceptor activity and ventilation but did not eliminate the oscillations. Bilateral section of carotid sinus nerves abolished the cardiorespiratory oscillations. The implication is that the dopaminergic system in the carotid body keeps chemoreceptor responses to blood gas stimuli suppressed and hence cardiorespiratory oscillations damped. 2) Hypotension and circulatory delay induced by the partial occlusion of venous return led to cardiorespiratory oscillations at low but not at high arterial PO2. 3) A few cats developed cardiorespiratory oscillations without any particular experimental intervention. These oscillations were independent of arterial PO2 and chemoreceptor activity. Thus it is reasonable to conclude that the peripheral chemoreflex can play a critical role in developing cardiorespiratory oscillations in certain instances.


1980 ◽  
Vol 48 (2) ◽  
pp. 243-248 ◽  
Author(s):  
T. V. Peterson ◽  
J. P. Gilmore ◽  
I. H. Zucker

Experiments were performed in anesthetized Macaca fascicularis monkeys to determine if the initial renal responses of these animals to head-out vertical water immersion and isoncotic, isotonic volume expansion are similar, especially with regard to the onset of any changes in solute or water excretion. Significant increases in urine flow, sodium excretion, and osmolar clearance occurred after 10 min of immersion but not until 30 min after volume expansion. Potassium excretion increased during immersion but decreased after volume expansion. Mean arterial blood pressure increased after 30 min of immersion but was unchanged after volume expansion. Indices of vascular filling, central venous pressure in the immersed animals and left ventricular end-diastolic pressure in the volume-expanded animals, increased immediately after the intervention. Effective renal plasma flow increased in both groups but glomerular filtration rate was not consistently elevated. These results suggest that, in the nonhuman primate, immersion and volume expansion exert their renal effects through different afferent and/or efferent mechanisms and should not be considered as similar volume stimuli.


1962 ◽  
Vol 202 (5) ◽  
pp. 901-904 ◽  
Author(s):  
R. Rosas ◽  
L. Barnafi ◽  
T. Pereda ◽  
H. Croxatto

The common action of oxytocin on the smooth musculature of the uterus and on the renal excretion of sodium, potassium, and water suggests a relationship between the two effects. In order to investigate this possibility, the action of oxytocin treated with chymotrypsin and with sodium thioglycollate on sodium, potassium, and water excretion was studied. These agents greatly reduce the uterotonic activity of the hormone as well as its effect on electrolyte and water excretion in rats. Equivalent uterotonic doses of oxytocin, Val3-oxytocin, and Phe2-Tyr3-oxytocin were assayed on the excretion of electrolytes and water. Excretion of sodium and potassium produced by Val3-oxytocin was less than that produced by oxytocin. Phe2-Tyr3-oxytocin was approximately one-ninth as active as oxytocin in this respect. In studies with low doses of oxytocin it was established that 0.25 mU was necessary to increase sodium excretion while 0.5 mU had to be administered in order to increase potassium as well.


1981 ◽  
Vol 59 (6) ◽  
pp. 562-566 ◽  
Author(s):  
Don W. Watkins ◽  
Lucy D. Antoniou ◽  
Robert J. Shalhoub

Urinary excretion of zinc, sodium, potassium, and calcium was studied in anesthetized dogs under conditions of volume expansion by saline infusion and volume expansion plus chlorothiazide administration. Zinc excretion was positively correlated to the fractional water excretion, as well as to the excretion of the other cations, during volume expansion. Chlorothiazide administration during volume expansion increased the zinc, sodium, and potassium excretion without changing that of calcium. The enhanced zinc excretion during chlorothiazide diuresis was equal to that expected on the basis of the increase in fractional water excretion alone. The urinary concentration of zinc appeared inversely related to the urine flow rate, reaching a minimum below that of the plasma ultrafilterable zinc concentration. The ratio of the clearance of zinc to that of sodium was 0.28, indicating a greater degree of net reabsorption for zinc than for calcium. These findings suggest that zinc and sodium reabsorption may be inhibited to a similar degree at chlorothiazide-sensitive sites in the tubule. Furthermore, the zinc reabsorptive mechanism seems capable of lowering urinary zinc concentration below that of ultrafiltrate and appears related in some way to sodium reabsorption.


2003 ◽  
Vol 284 (1) ◽  
pp. R13-R27 ◽  
Author(s):  
David L. Mattson

The control of renal medullary perfusion and the impact of alterations in medullary blood flow on renal function have been topics of research interest for almost four decades. Many studies have examined the vascular architecture of the renal medulla, the factors that regulate renal medullary blood flow, and the influence of medullary perfusion on sodium and water excretion and arterial pressure. Despite these studies, there are still a number of important unanswered questions in regard to the control of medullary perfusion and the influence of medullary blood flow on renal excretory function and blood pressure. This review will first address the vascular architecture of the renal medulla and the potential mechanisms whereby medullary perfusion may be regulated. The known extrarenal and local systems that influence the medullary vasculature will then be summarized. Finally, this review will present an overview of the evidence supporting the concept that selective changes in medullary perfusion can have a potent influence on sodium and water excretion with a long-term influence on arterial blood pressure regulation.


1986 ◽  
Vol 71 (4) ◽  
pp. 445-448 ◽  
Author(s):  
S. Sonkodi ◽  
B. Tichy ◽  
W. B. Brown ◽  
J. I. S. Robertson

1. The effects of polyethylene glycol (PEG) 200 administered by gavage on electrolyte and water excretion were investigated in the rat. 2. PEG 200 led, in intact rats, to dose-related increased drinking and to diuresis. 3. In the first 2 h after PEG 200 administration, water consumption in intact rats exceeded urine output. 4. PEG 200 enhanced the excretion of both sodium and potassium, but the sodium excretion was proportionately greater, resulting in an elevation of the urinary sodium/potassium ratio. 5. Bilateral nephrectomy was not accompanied by increased drinking in PEG 200-treated rats, although raised serum osmolality was seen. 6. Thus, given by gavage, PEG 200 is not an inert vehicle for drug administration.


1985 ◽  
Vol 63 (3) ◽  
pp. 220-223 ◽  
Author(s):  
Sue-Lin Wang ◽  
Joseph P. Gilmore

The effect of converting enzyme inhibitor (CEI) on the renal response to atrial natriuretic factor (ANF) was determined in the rat. In the absence of CEI, ANF produced rapid and significant increases in sodium, potassium, calcium, and urine excretions while blood pressure declined transiently. In the presence of CEI, ANF enhanced the excretion of sodium and potassium but not of calcium and urine. The activity of CEI was documented by observing that, in the presence of CEI, the elevation of blood pressure produced by angiotensin I was significantly attenuated. The potentiating effect of CEI on the natriuretic response to ANF supports the hypothesis that converting enzyme may be involved in the metabolism of ANF.


Sign in / Sign up

Export Citation Format

Share Document