Cardiorespiratory effects of prolonged angiotensin II block in resting conscious dogs

2001 ◽  
Vol 79 (9) ◽  
pp. 825-830
Author(s):  
Donald B Jennings

Intravenous (iv) infusion of the angiotensin II (ANG II) receptor blocker saralasin in resting conscious dogs during physiological pertubations, such as hypotension and prolonged hypoxia, indicates the presence of an ANG II drive to increase respiration and decrease the arterial partial pressure of CO2 (PaCO2). In contrast, in eupneic resting dogs on a regular chow diet, iv infusion of saralasin for short periods (up to 30 min) provides no evidence of a tonic effect of circulating levels of ANG II on acid-base balance, respiration, metabolism, or circulation. However, ANG II influences physiological processes involving salt, water, and acid-base balances, which are potentially expressed beyond a 30 min time period, and could secondarily affect respiration. Therefore, we tested the hypothesis that blocking ANG II with iv saralasin would affect respiration and circulation over a 4-h period. Contrary to the hypothesis, iv infusion of saralasin in resting conscious eupneic dogs on a regular chow diet over a 4-h period had no effects on plasma strong ions, osmolality, acid-base balance, respiration, metabolism, or circulation when compared with similar control studies in the same animals. Thus, ANG II does not play a tonic modulatory role in respiratory control under "normal" physiological conditions.Key words: acid-base balance, arginine vasopressin, saralasin, strong ions, strong ion difference.

1992 ◽  
Vol 73 (4) ◽  
pp. 1549-1557 ◽  
Author(s):  
P. J. Ohtake ◽  
D. B. Jennings

Changes in arterial pressure commonly accompany respiratory adaptations. The purpose of this study was to determine, in awake dogs (n = 6), the degree to which small acute decreases in arterial pressure affect ventilation and acid-base balance. Mean arterial pressure (MAP) was reduced by 6 +/- 2, 10 +/- 3, and 16 +/- 2% by intravenous infusion of sodium nitroprusside for sequential 20-min periods. In another experiment, the ventilatory response to hypercapnia was determined during MAP reduction of 16 +/- 3%. Step reductions in MAP were accompanied by increases in minute ventilation (maximum increase 152 +/- 75%) and step reductions in arterial PCO2 (PaCO2; maximum reduction -4.8 +/- 0.8 Torr). Although eupneic PaCO2 threshold was lowered during MAP reduction, ventilatory sensitivity to CO2 remained unchanged. Despite the lowered PaCO2, arterial [H+] remained constant (acid-base balance was maintained) as a result of a concurrent decrease in strong ion difference. Plasma renin activity increased during MAP reduction (93 +/- 39%) and may have contributed to the increase in minute ventilation, inasmuch as angiotensin II can stimulate respiration by a central mechanism. Evidence is provided that nitroprusside is unlikely to be a primary factor in these hypotensive responses. We conclude that relatively modest decreases in MAP have a consistent stimulatory effect on respiratory control. Therefore it is important to take into account effects of small changes in MAP when interpreting mechanisms for respiratory responses in awake animals.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Motonobu Nakamura ◽  
Ayumi Shirai ◽  
Osamu Yamazaki ◽  
Nobuhiko Satoh ◽  
Masashi Suzuki ◽  
...  

Sodium-coupled bicarbonate absorption from renal proximal tubules (PTs) plays a pivotal role in the maintenance of systemic acid/base balance. Indeed, mutations in the Na+-HCO3-cotransporter NBCe1, which mediates a majority of bicarbonate exit from PTs, cause severe proximal renal tubular acidosis associated with ocular and other extrarenal abnormalities. Sodium transport in PTs also plays an important role in the regulation of blood pressure. For example, PT transport stimulation by insulin may be involved in the pathogenesis of hypertension associated with insulin resistance. Type 1 angiotensin (Ang) II receptors in PT are critical for blood pressure homeostasis. Paradoxically, the effects of Ang II on PT transport are known to be biphasic. Unlike in other species, however, Ang II is recently shown to dose-dependently stimulate human PT transport via nitric oxide/cGMP/ERK pathway, which may represent a novel therapeutic target in human hypertension. In this paper, we will review the physiological and pathophysiological roles of PT transport.


1994 ◽  
Vol 76 (3) ◽  
pp. 1211-1219 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones

The interaction between systems regulating acid-base balance (i.e., CO2, strong ions, week acids) was studied in six subjects for 10 min after 30 s of maximal isokinetic cycling during control conditions (CON) and after 3 days of chronic acetazolamide (ChACZ) administration (500 mg/8 h po) to inhibit carbonic anhydrase (CA). Gas exchange was measured; arterial and venous forearm blood was sampled for acid-base variables. Muscle power output was similar in ChACZ and CON, but peak O2 intake was lower in ChACZ; peak CO2 output was also lower in ChACZ (2,207 +/- 220 ml/min) than in CON (3,238 +/- 87 ml/min). Arterial PCO2 was lower at rest, and its fall after exercise was delayed in ChACZ. In ChACZ there was a higher arterial [Na+] and lower arterial [lactate-] ([La-]) accompanied by lower arterial [K+] and higher arterial [Cl-] during the first part of recovery, resulting in a higher arterial plasma strong ion difference (sigma [cations] - sigma [anions]). Venoarterial (v-a) differences across the forearm showed a similar uptake of Na+, K+, Cl-, and La- in ChACZ and CON. Arterial [H+] was higher and [HCO3-] was lower in ChACZ. Compared with CON, v-a [H+] was similar and v-a [HCO3-] was lower in ChACZ. Chronic CA inhibition impaired the efflux of CO2 from inactive muscle and its excretion by the lungs and also influenced the equilibration of strong ions.(ABSTRACT TRUNCATED AT 250 WORDS)


2003 ◽  
Vol 95 (6) ◽  
pp. 2333-2344 ◽  
Author(s):  
E. Wrenn Wooten

A general formalism for calculating parameters describing physiological acid-base balance in single compartments is extended to multicompartment systems and demonstrated for the multicompartment example of human whole blood. Expressions for total titratable base, strong ion difference, change in total titratable base, change in strong ion difference, and change in Van Slyke standard bicarbonate are derived, giving calculated values in agreement with experimental data. The equations for multicompartment systems are found to have the same mathematical interrelationships as those for single compartments, and the relationship of the present formalism to the traditional form of the Van Slyke equation is also demonstrated. The multicompartment model brings the strong ion difference theory to the same quantitative level as the base excess method.


2007 ◽  
Vol 197 (6) ◽  
pp. S182
Author(s):  
Yoni Cohen ◽  
Jessica Ascher Landsberg ◽  
Michael Kupferminc ◽  
Joseph B. Lessing ◽  
Adi Nimrod ◽  
...  

1982 ◽  
Vol 101 (1) ◽  
pp. 255-264 ◽  
Author(s):  
RAYMOND P. HENRY ◽  
JAMES N. CAMERON

When transferred from 865 to 250 m-osmol salinity, the blue crab C. sapidus maintains its blood Na+ and Cl− concentrations significantly above those in the medium. When branchial carbonic anhydrase is inhibited by acetazolamide, ion regulation fails and the animals do not survive the transfer. An alkalosis occurs in the blood at low salinity, indicated by an increase in HCO3− and pH at constant PCO2. The alkalosis is closely correlated with an increase in the Na+-Cl− difference, a convenient indicator of the overall strong ion difference. The contribution of changes in PCO2 to acid-base changes was negligible, but the change in the total weak acid (proteins) may be important. It is suggested that the change in blood acidbase status with salinity is related to an increase in the strong ion difference, which changes during the transition from osmoconformity to osmoregulation in the blue crab, and which is related to both carbonic anhydrase and ionactivated ATPases. Note:


1986 ◽  
Vol 126 (1) ◽  
pp. 271-296 ◽  
Author(s):  
CHRIS M. WOOD ◽  
R. G. BOUTILIER ◽  
D. J. RANDALL

Air-breathing Cardisoma carnifex, collected in Moorea, French Polynesia, were held in fresh water similar in chemical composition to that in their burrows. Under control conditions, which allowed branchial chamber flushing but not ventilation of the medium, crabs demonstrated net Na+ and Cl− uptake, and ammonia, urea and base excretion (= acidic equivalent uptake). Throughout 192 h of water deprivation, crabs dehydrated slowly at a rate of 0.55 g H2O kg−1 h−1, eventually reaching a near lethal 18% loss of total body water. Increases in haemolymph osmolytes were quite variable (0–29%); electrolyte excretion was negligible. MOO2 and MCOCO2 both decreased by approximately 55%, maintaining an unusually low gas exchange ratio (R = 0.53), and suggesting general metabolic depression. There was no evidence of internal hypoxia as haemolymph lactate remained at hydrated levels and PaOO2 actually increased. The dominant acid-base response was a progressive metabolic alkalosis accompanied by a partially compensating rise in PaCOCO2. Alkalosis was probably caused by blockage of the normal aquatic excretion of base produced by the metabolism of this herbivore. Other possible causes were eliminated: i.e. alkalaemia due to contraction of the ECFV; entrainment via strong ion shifts; CaCO3 mobilization; and ammonia accumulation in the haemolymph. In the absence of water, net ammonia production and excretion both appeared to cease, and alternate end products (urea, uric acid) did not generally accumulate. Within 2h of rehydration, crabs regained more than half the lost water, MOO2 and MCOCO2 increased above control levels, and ammonia excretion and haemolymph concentration both exhibited a prolonged (56 h) 4- to 6-fold rise. At the same time, metabolic alkalosis was reversed in association with elevated net base excretion into the water; the latter was correlated with an increase in the strong ion difference (SID) flux ([Na+ + K+ + Ca2+ + Mg2+ - Cl−]). Note:


2014 ◽  
Vol 44 (6) ◽  
pp. 1086-1092 ◽  
Author(s):  
Cláudio Luís Nina Gomes ◽  
José Dantas Ribeiro Filho ◽  
Rafael Resende Faleiros ◽  
Fernanda Timbó D'el Rey Dantas ◽  
Lincoln da Silva Amorim ◽  
...  

Large volumes of different electrolytes solutions are commonly used for ingesta hydration in horses with large colon impaction, but little is known about their consequences to blood acid-base balance. To evaluate the effects of PEG 3350 or enteral and parenteral electrolyte solutions on the blood gas analysis, anion gap and strong ion difference, five adult female horses were used in a 5x5 latin square design. The animals were divided in five groups and distributed to each of the following treatments: NaCl (0.9% sodium chloride solution); EES (enteral electrolyte solution), EES+LR (EES plus lactated Ringer's solution); PEG (balanced solution with PEG 3350) and PEG+LR (PEG plus lactated Ringer's solution). Treatments PEG or PEG + LR did not change or promoted minimal changes, while the EES caused a slight decrease in pH, but its association with lactated Ringer's solution induced increase in AG and SID values, as well as caused hypernatremia. In turn, the treatment NaCl generated metabolic acidosis. PEG 3350 did not alter the acid-base balance. Despite it's slight acidifying effect, the enteral electrolyte solution (EES) did not cause clinically relevant changes.


1983 ◽  
Vol 245 (4) ◽  
pp. F425-F432 ◽  
Author(s):  
H. R. Jacobson ◽  
D. W. Seldin

The study of derangements in salt, water, and acid-base homeostasis frequently reveals much about renal transport mechanisms and their regulation. The study of one such derangement, metabolic alkalosis, has played a special role in contributing to our knowledge of renal function. Elucidation of the kidney's role in the generation, maintenance, and correction of metabolic alkalosis has provided information about proximal tubule transport and its response to volume contraction, volume expansion, and K depletion. Also, distal nephron transport and its response to mineralocorticoids and dietary anion composition has been clarified by studies on metabolic alkalosis. Finally, we have learned about the importance of Na delivery to distal nephron sites and the avidity with which these distal nephron sites reabsorb sodium. Indeed, reviews on the subject of metabolic alkalosis have presented thorough and convincing physiologic arguments on how the kidney helps to generate and maintain this derangement in acid-base balance. However, more recent experimental work has led some to reconsider how the kidney functions in metabolic alkalosis. In an earlier paper in this journal [Am. J. Physiol. 244 (Renal Fluid Electrolyte Physiol. 13): F217-F221, 1983], Galla, Bonduris, and Luke present an argument for the correction of chloride-depletion alkalosis in the rat without volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)


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