Hypercalcemia In Dogs Research Articles

Prevalence of hypercalcemia in primary hypoadrenocorticism in dogs: Multicenter, retrospective study.

Hypoadrenocorticism is an important differential for hypercalcemia. The etiology of hypercalcemia in hypoadrenocorticism in dogs is unclear. To review the prevalence of hypercalcemia and use statistical models to identify clinical, demographic, and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism. One hundred ten dogs with primary hypoadrenocorticism; 107 with recorded total calcium (TCa), 43 recorded ionized calcium (iCa). Multicenter retrospective observational study at 4 UK referral hospitals. Univariable logistic regression analyses were performed to assess the association between independent variables of signalment, hypoadrenocorticism type (glucocorticoid only deficient hypoadrenocorticism [GHoC] vs glucocorticoid and mineralocorticoid deficient hypoadrenocorticism [GMHoC]), clinicopathological variables and hypercalcemia. Hypercalcemia was defined as elevated TCa, an elevated iCa, or both elevated TCa and iCa (Model 1) or as elevated iCa (Model 2). Overall prevalence of hypercalcemia was 34.5% (38/110). The odds of hypercalcemia (Model 1) were increased (P < .05) in dogs with GMHoC ([vs GHoC], OR [odds ratio] = 3.86, 95% confidence interval [CI] 1.105-13.463), higher serum creatinine (OR = 1.512, 95% CI 1.041-2.197), and higher serum albumin (OR = 4.187, 95% CI 1.744-10.048). The odds of ionized hypercalcemia (Model 2) were increased (P < .05) with reduced serum potassium concentration (OR = 0.401, 95% CI 0.184-0.876) and younger age (OR = 0.737, 95% CI 0.558-0.974). This study identified several key clinical and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism. These findings aid understanding of the pathophysiology and etiology of hypercalcemia in dogs with primary hypoadrenocorticism.

Hypercalcaemia in a dog with lymphoma without increases in parathyroid hormone, parathyroid hormone-related protein and vitamin D metabolites concentrations

Lymphoma is one of the most common causes of hypercalcaemia in dogs. Typically, the hypercalcaemic state is driven by ectopic production of parathyroid hormone-related protein by the malignant lymphoma cells....

Determination of a serum total calcium concentration threshold for accurate prediction of ionized hypercalcemia in dogs with and without hyperphosphatemia.

BackgroundTotal serum calcium (tCa) concentrations are poorly predictive of ionized calcium (iCa) status in dogs.HypothesisThere is an optimal threshold of tCa concentration that is highly predictive of ionized hypercalcemia and this threshold is higher in hyperphosphatemic dogs as compared to nonhyperphosphatemic dogs.AnimalsNonhyperphosphatemic (n = 1593) and hyperphosphatemic (n = 250) adult dogs.MethodsRetrospective medical record review of paired tCa and iCa concentration measurements in dogs presented to a university teaching hospital over a 5‐year period. Positive and negative predictive values, sensitivity, and specificity were calculated for tCa concentration thresholds of 11.0‐15.0 mg/dL (upper limit of laboratory reference interval = 11.5 mg/dL) in nonhyperphosphatemic and hyperphosphatemic groups.ResultsIn nonhyperphosphatemic dogs, an optimal tCa concentration threshold of 12.0 mg/dL resulted in a positive predictive value of 93% (95% confidence interval [CI], 84%‐98%) and sensitivity of 52% (95% CI, 43%‐61%) for ionized hypercalcemia. An optimal tCa concentration threshold was not identified for hyperphosphatemic dogs. The nonhyperphosphatemic dogs had a higher prevalence of ionized hypercalcemia than the hyperphosphatemic dogs (7 versus 3%, P = .04) and a lower prevalence of ionized hypocalcemia (23 versus 62%, respectively; P < .001).Conclusions and Clinical ImportanceHigh tCa concentrations are strongly predictive of ionized hypercalcemia in nonhyperphosphatemic adult dogs and should prompt further diagnostic testing to determine the underlying cause of hypercalcemia. In this population, dogs without increased tCa concentrations rarely had ionized hypercalcemia, but iCa concentrations still should be evaluated in patients with tCa concentrations within the reference interval if there is clinical suspicion for calcium abnormalities.

Dystrophic mineralization in uremic dogs: an update

ABSTRACT: Pathological mineralization is the abnormal deposition of minerals in body tissues, previously injured or not. In these lesions, in addition to calcium, other minerals can be found at lower concentrations. Classically, mineralization is divided into two types: dystrophic and metastatic. However, currently, there is no consensus among researchers on the type of mineralization that occurs in uremic dogs. The objective of this study was to elucidate the type of pathological mineralization that occurs in dogs with uremic syndrome through the correlation of biochemical examinations with gross and histopathological changes, given the existence of controversial information on this theme in the specialized literature. The Shapiro-Wilk, D’Agostino and Pearson tests were used to evaluate data normality distribution, and analysis of variance (ANOVA) was applied to compare the data between more than two groups. Additionally, the Dunnett’s multiple comparison test was used in the comparison between the Control Group (CG) and the Experimental Groups (G1, G2, and G3). Serum levels of urea, creatinine, total and ionized calcium, phosphorus, calcium-phosphorus product (CPP), parathyroid hormone (PTH), and albumin of 40 azotemic dogs with chronic kidney disease (CKD) were evaluated. Dogs were categorized by degree of azotemia (mild, moderate, and severe). Ionized hypocalcemia was observed in 97.5% (39/40) of the dogs, and no animals presented ionized hypercalcemia. Hyperphosphatemia was frequent (62.5%), especially in dogs with severe azotemia. PTH concentration increased with progression of azotemia, and high PTH levels were verified in 100% of the dogs with severe azotemia. CPP &gt;60mg2/dl2 was observed in 75% (30/40) of the dogs. Of the 29 dogs that died during the study period, 16 were necropsied. Soft tissue mineralization was observed in 93.7% (15/16) of these dogs at gross and histopathological evaluation (HE and Von Kossa), regardless of the degree of azotemia, in nine organs/tissues: kidneys (75%), lungs (50%), stomach (31.2%), heart (25%), larynx (25%), intercostal muscles (25%), aorta (6.2%), intestines (6.2%), and tongue (6.2%). In one animal, the serosa of all segments of the small intestine showed whitish, rough, irregular, multifocal plaques of varying sizes, confirmed by histopathology as dystrophic mineralization of the longitudinal outer muscular layer, which presented necrosis of coagulation and of the intestinal serosa. This intestinal lesion has not been described in dogs with uremic syndrome to date. In conclusion, the laboratory and histopathologic data previously described, especially regarding tissue and vascular mineralization, which occur in association with previous degenerative/necrotic lesions in the absence of hypercalcemia in dogs with CKD, assist with clarifying inconsistencies found in the existing literature. Therefore, conceptually, mineralization that occurs in uremic dogs should be considered dystrophic.

Severity of Ionized Hypercalcemia and Hypocalcemia Is Associated With Etiology in Dogs and Cats.

Background: Calcium disorders are common in small animals, but few studies have investigated the etiology of ionized hypercalcemia and hypocalcemia in large populations. This study aimed to determine the incidence of ionized calcium disorders in dogs and cats treated at a tertiary referral clinic and to describe the associated diseases.Methods: An electronic database of electrolyte analyses conducted at the Cornell University Hospital for Animals from 2007 to 2017 was searched. Dogs and cats with ionized hypercalcemia or hypocalcemia were identified based on institution reference intervals. Duplicate case entries were removed. Medical records were reviewed to identify the cause of the calcium abnormality. Chi-squared analysis with Bonferroni adjustment was performed to compare frequencies of disease processes between mild and moderate-severe disturbances.Results: The database included 15,277 dogs and 3,715 cats. Hypercalcemia was identified in 1,641 dogs and 119 cats. The incidence of canine and feline hypercalcemia was 10.7 and 3.2%, respectively. Hypocalcemia was identified in 1,467 dogs and 450 cats. The incidence of canine and feline hypocalcemia was 9.6% and 12.1%, respectively. The most common pathologic causes of hypercalcemia in dogs were malignancy-associated (12.9%), parathyroid-dependent (4.6%) and hypoadrenocorticism (1.7%). In cats, malignancy-associated hypercalcemia (22.7%), kidney injury (13.4%) and idiopathic hypercalcemia (12.6%) were most common. Dogs presenting with moderate-severe hypercalcemia vs. mild hypercalcemia were significantly more likely to have hyperparathyroidism, malignancy-associated hypercalcemia or hypervitaminosis D, whereas cats were significantly more likely to have malignancy-associated hypercalcemia or idiopathic hypercalcemia. The most common pathologic causes of hypocalcemia in dogs were critical illness (17.4%), kidney injury (10.4%) and toxicity (7.5%). In cats, kidney injury (21.6%), urethral obstruction (15.1%), and critical illness (14.7%) were most frequent. Dogs presenting with moderate-severe hypocalcemia were significantly more likely to have hypoparathyroidism, kidney injury, eclampsia or critical illness, whereas cats were significantly more likely to have kidney injury, soft tissue trauma or urethral obstruction.Conclusions: Mild calcium disturbances are most commonly associated with non-pathologic or transient conditions. Malignancy-associated hypercalcemia is the most common cause of ionized hypercalcemia in dogs and cats. Critical illness and kidney injury are frequent causes of ionized hypocalcemia in both species.

Calcium metabolism in eight dogs with hypoadrenocorticism

Hypoadrenocorticism is a well-described endocrinopathy in dogs that results from deficient production and secretion of glucocorticoids and/or mineralocorticoids. Although hyperkalaemia, hyponatraemia and hypochloraemia are the most common electrolyte disturbances, hypercalcaemia also occurs in approximately 30 per cent of cases. The pathogenesis of hypercalcaemia in dogs with hypoadrenocorticism is unknown. This case series reports ionised calcium, parathyroid hormone, parathyroid hormone-related protein and vitamin D metabolite concentrations that were measured in eight dogs with concurrent hypercalcaemia and hypoadrenocorticism. Ionised calcium was increased in five of seven dogs with hypercalcaemia associated with hypoadrenocorticism. Parathyroid hormone, parathyroid hormone-related protein and 1,25 dihydroxyvitamin D concentrations were within their reference ranges in seven of eight dogs, six of seven cases and six of seven dogs, respectively. This case series highlights that hypercalcaemia associated with hypoadrenocorticism is rarely associated with increases in plasma parathyroid hormone, parathyroid hormone-related protein or serum 1,25 dihydroxyvitamin D concentrations.

Ionized Hypercalcemia in Dogs: A Retrospective Study of 109 Cases (1998–2003)

Serum hypercalcemia in dogs has been reported in association with a variety of diseases. Serum-ionized calcium (iCa) concentration is a more accurate measure of hypercalcemia than total serum calcium or corrected serum calcium concentrations. The severity of hypercalcemia has been utilized to suggest the most likely differential diagnosis for the hypercalcemia. Diseases causing ionized hypercalcemia may be different than those that cause increases in total or corrected serum calcium concentrations. The severity of ionized hypercalcemia in specific diseases cannot be used to determine the most likely differential diagnosis for ionized hypercalcemia. One-hundred and nine client-owned dogs with a definitive cause for their ionized hypercalcemia evaluated between 1998 and 2003 were included in this study. Retrospective, medical records review. Neoplasia, specifically lymphosarcoma, followed by renal failure, hyperparathyroidism, and hypoadrenocorticism were the most common causes of ionized hypercalcemia. Dogs with lymphoma and anal sac adenocarcinoma have higher serum iCa concentrations than those with renal failure, hypoadrenocorticism, and other types of neoplasia. The magnitude of serum-ionized hypercalcemia did not predict specific disease states. Serum-ionized hypercalcemia was most commonly associated with neoplasia, specifically lymphosarcoma. Although dogs with lymphosarcoma and anal sac adenocarcinoma had higher serum iCa concentrations than dogs with other diseases, the magnitude of the serum iCa concentration could not be used to predict the cause of hypercalcemia. Total serum calcium and corrected calcium concentrations did not accurately reflect the calcium status of the dogs in this study.

Circadian Variation of the Ca2+–PTH Curve during Hypercalcaemia in Dogs

To test the hypothesis that the parathyroid hormone (PTH) response to hypercalcaemia is influenced by circadian rhythms, the Ca2+ -PTH curve was studied in six dogs after infusion of CaCl2 (0.66 mEq/kg/h) at daytime (09:00 h) and at night-time (21:00 h). Plasma Ca2+ and PTH values measured before or after CaCl2 infusion were not different at day and at night. However, in the recovery from hypercalcaemia, PTH concentrations were significantly lower (P < 0.05) at 21:00 h (23 +/- 7.5 pg/ml at Ca2+ = 1.30 mm) than at 09:00 h (38.8 +/- 6.9 pg/ml at Ca2+ = 1.30 mm). In addition, the Ca2+ -PTH curve showed hysteresis at daytime (for the same Ca2+ concentration, PTH values were higher during recovery than during induction of hypercalcaemia) but not at night-time (PTH values were lower during recovery than during induction of hypercalcaemia). In conclusion, a circadian variation in the PTH secretory pattern during recovery from hypercalcaemia has been identified in dogs.

Death of a dog caused by calcipotriene toxicity

Death of a dog caused by calcipotriene toxicity

Clodronate treatment of vitamin D‐induced hypercalcemia in dogs

AbstractObjective: To determine the effects of clodronate on vitamin D3‐induced hypercalcemia in dogs.Design: Prospective experimental study.Settings: University research laboratory.Animals: Fourteen healthy intact adult male and female mixed breed dogs.Interventions: Dogs received 7.5 mg of vitamin D3/kg of body weight once orally and were randomly assigned to 2 groups of 7 dogs each. Dogs in the saline control group were given intravenous infusions of 150 mL 0.9% NaCl solution 24 hours after vitamin D3 administration. Dogs in the clodronate group were given an infusion of 4 mg/kg of clodronate in 150 mL 0.9% NaCl solution 24 hours after vitamin D3 administration.Measurements and main results: Clinical signs of vitamin D3 toxicosis were evaluated 48 hours after ingestion of vitamin D3. Dogs that were given clodronate had significantly lower serum calcium (Ca), phosphorus (P), urea, and Ca × P values than dogs in the control group on days 4, 7, and 12 after administration. Additionally, alkaline phosphatase activity was significantly lower in the clodronate group compared with dogs in the control group on days 4 and 7.Conclusions: Parenteral administration of clodronate, a biphosphonate compound and osteoclastic activity inhibitor, may be a useful therapy when administered within the first 24 hours after ingestion of toxic doses of vitamin D3.

Bone Metabolic Effects of Single-Dose Zoledronate in Healthy Dogs

Zoledronate, an aminobisphosphonate with potent antiresorptive activity in bone, has the potential for treatment of malignant osteolysis and hypercalcemia in dogs. The purpose of this study was to evaluate the bone metabolic effects of a single dose of zoledronate in healthy dogs. Four skeletally mature, male, intact dogs received a 15-minute IV infusion of zoledronate at a dosage of 0.25 mg/kg. Urine N-telopeptide of type I collagen (NTx) excretion decreased significantly from baseline by 76, 63, 77, and 73% on days 7, 14, 21, and 28, respectively (P <. 0125). Serum bone-specific alkaline phosphatase (bALP) decreased significantly from baseline by 36 and 42% on days 21 and 28, respectively (P <. 0125). No changes were detected in indices of calcium homeostasis (ionized calcium, intact PTH, or urine calcium excretion). Single-dose IV zoledronate at 0.25 mg/kg appears to inhibit homeostatic osteolytic activity in healthy, skeletally mature dogs. Prospective studies should assess repeated-dose safety and activity in healthy and diseased animals of various age groups.

Pretreatment clinical and laboratory findings in dogs with primary hyperparathyroidism: 210 cases (1987–2004)

To evaluate pretreatment clinical and laboratory findings in dogs with naturally occurring primary hyperparathyroidism. Retrospective study. 210 dogs with primary hyperparathyroidism and 200 randomly selected, age-matched control dogs that did not have primary hyperparathyroidism. Medical records for dogs with primary hyperparathyroidism were reviewed for signalment; clinical features; and results of clinicopathologic testing, serum parathyroid hormone assays, and diagnostic imaging. Mean age of the dogs with primary hyperparathyroidism was 11.2 years (range, 6 to 17 years). The most common clinical signs were attributable to urolithiasis or urinary tract infection (ie, straining to urinate, increased frequency of urination, and hematuria). Most dogs (149 [71%]) did not have any observable abnormalities on physical examination. All dogs had hypercalcemia, and most (136 [65%]) had hypophosphatemia. Overall, 200 of the 210 (95%) dogs had BUN and serum creatinine concentrations within or less than the reference range, and serum parathyroid hormone concentration was within reference limits in 135 of 185 (73%) dogs in which it was measured. Urolithiasis was identified in 65 (31 %) dogs, and urinary tract infection was diagnosed in 61 (29%). Mean serum total calcium concentration for the control dogs-was significantly lower than mean concentration for the dogs with primary hyperparathyroidism, but mean BUN and serum creatinine concentrations for the control dogs were both significantly higher than concentrations for the dogs with primary hyperparathyroidism. Results suggest that urolithiasis and urinary tract infection may be associated with hypercalcemia in dogs-with primary hyperparathyroidism, but that development of renal insufficiency is uncommon.

Parathyroid hormone‐related peptide and hypercalcaemia in a dog with functional keratinizing ameloblastoma

This case report describes a 6-year-old dog with oral ameloblastoma and hypercalcaemia. Serum parathyroid hormone-related peptide (PTH-rp) levels were high. No other cause for hypercalcaemia was found. The hypercalcaemia resolved after hemimandibulectomy. We are not aware of the previous description of canine oral ameloblastoma and hypercalcaemia mediated by PTH-rp. This case report suggests that PTH-rp stimulation of the PTH receptor may result in hypercalcaemia in dogs with oral ameloblastoma or other odontogenic neoplasms.

Bone Metabolic Effects of Single-Dose Zoledronate in Healthy Dogs

Zoledronate, an aminobisphosphonate with potent antiresorptive activity in bone, has the potential for treatment of malignant osteolysis and hypercalcemia in dogs. The purpose of this study was to evaluate the bone metabolic effects of a single dose of zoledronate in healthy dogs. Four skeletally mature, male, intact dogs received a 15-minute i.v. infusion of zoledronate at a dosage of 0.25 mg/kg. Urine N-telopeptide of type I collagen (NTx) excretion decreased significantly from baseline by 76, 63, 77, and 73% on days 7, 14, 21, and 28, respectively (P < .0125). Serum bone-specific alkaline phosphatase (bALP) decreased significantly from baseline by 36 and 42% on days 21 and 28, respectively (P < .0125). No changes were detected in indices of calcium homeostasis (ionized calcium, intact PTH, or urine calcium excretion). Single-dose i.v. zoledronate at 0.25 mg/kg appears to inhibit homeostatic osteolytic activity in healthy, skeletally mature dogs. Prospective studies should assess repeated-dose safety and activity in healthy and diseased animals of various age groups.

Double-phase parathyroid scintigraphy in dogs using technetium-99M-sestamibi.

The purpose of this study was to evaluate the utility of double-phase parathyroid scintigraphy using 99mTc-sestamibi for detecting and localizing hyperfunctioning parathyroid glands in hypercalcemic dogs. Fifteen hypercalcemic dogs that underwent parathyroid scintigraphy were included in this study: 3 dogs with hypercalcemia of malignancy, and 12 dogs with hyperfunctioning parathyroid tissue (parathyroid adenoma or parathyroid hyperplasia). The presence of parathyroid adenoma or parathyroid hyperplasia was documented by histopathologic examination. In 3 dogs with hypercalcemia of malignancy, parathyroid scintigraphy was negative for hyperfunctioning parathyroid tissue and the scans were classified as true negative. Parathyroid scintigraphy correctly identified the presence and location of hyperfunctioning parathyroid tissue in only 1 of 6 dogs with a parathyroid adenoma. False positive and false negative results occurred in dogs with parathyroid adenomas. Parathyroid scintigraphy failed to detect hyperfunctioning parathyroid tissue in 5 of 6 dogs with parathyroid hyperplasia and were classified as false negative. False positive results were obtained in the remaining dog with parathyroid hyperplasia. Sensitivity of parathyroid scintigraphy for detecting and localizing hyperfunctioning parathyroid tissue was 11%, specificity was 50%, and overall accuracy was 27%. Positive and negative predictive value were 25% and 27%, respectively. Sensitivity for detection of parathyroid adenomas was 25%, and sensitivity for detection of hyperplastic glands was 0 %. Results of this study indicate that double-phase parathyroid scintigraphy does not appear to have acceptable accuracy in detecting hyperfunctioning parathyroid glands in dogs. Due to the poor sensitivity and specificity of the technique in dogs, parathyroid scintigraphy is not recommended for definitive identification of abnormal parathyroid glands as the cause of hypercalcemia in dogs.

Use of pamidronate to reverse vitamin D3-induced toxicosis in dogs

Abstract Objectives To determine whether pamidronate di-sodium can reduce vitamin D3-induced hypercalcemia in dogs and whether combination treatment with calcitonin is more effective than treatment with pamidronate alone. Animals 20 clinically normal male Beagles. Procedure All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were assigned randomly to 4 groups of 5 dogs each. Dogs were given 0.9% NaCl solution IV (group 1), calcitonin SC and 0.9% NaCl solution IV (group 2), pamidronate and 0.9% NaCl solution IV (group 3), or a combination of all 3 agents (group 4). Dogs were observed for 28 days, and serial blood and urine samples were collected for determination of serum biochemical, electrolyte, and 25(OH)D3 values, CBC, and urine mineral excretion. Samples of kidney, stomach, lung, aorta, liver, duodenum, and brain were evaluated by light microscopy and quantitative mineral analysis. Results Two dogs in group 1 were euthanatized 4 days after CCF administration because of severe clinical signs of disease. Dogs in group 3 lost less weight and had significantly lower serum phosphorus, total and ionized calcium, and urinary zinc concentrations, compared with dogs in group 1. On day 4, serum urea nitrogen concentration was significantly lower in dogs of groups 3 and 4, compared with dogs in group 1. Mild to moderate mineralization of kidneys and stomach were observed in the 2 group-1 dogs euthanatized on day 4. Conclusions Pamidronate administration effectively prevents CCF-induced hypercalcemia and mineralization of soft tissues. Clinical Relevance Pamidronate is a potentially useful antidote against CCF toxicosis in dogs. (Am J Vet Res 1999;60:1092-1097)

High-resolution parathyroid sonography.

The purpose of this study was to assess the diagnostic utility of parathyroid ultrasonography to differentiate causes of hypercalcemia in dogs. We analyzed qualitative and quantitative ultrasound imaging findings and clinical pathology data from 33 dogs that underwent parathyroid ultrasound examination as part of the diagnostic evaluation for hypercalcemia. Diagnoses of the diseases causing hypercalcemia included parathyroid carcinoma (n = 5), parathyroid adenoma (n = 15), parathyroid adenomatous hyperplasia (n = 6), chronic renal insufficiency (n = 3), and hypercalcemia of malignancy (n = 4). All parathyroid lesions were round or oval and hypoechoic compared with surrounding thyroid parenchyma. Adenomatous and adenocarcinomatous glands were 4 mm or larger in longest linear measurement on US examination and were statistically significantly larger than hyperplastic glands. (p < 0.001) Linear measurements of parathyroid glands acquired at the time of ultrasound examination correlated well with direct size determination after surgical excision. (r2 = 0.9, p < 0.0001) Parathyroid lesions > or = 4 mm are highly suspicious for parathyroid adenoma or carcinoma, while US lesions < 4 mm most likely represent primary adenomatous hyperplasia or secondary parathyroid hyperplasia. Parathyroid size estimation from ultrasound examination is an accurate predictor of true size.

Inhibition of the Vasodilator Effect of Hypercapnic Acidosis by Hypercalcemia in Dogs and Rats

The vasodilator effect of local hypercapnic acidosis, produced by intra-arterial infusion of an acid buffer solution consisting of a mixture of glycine and hydrochloric acid, in the perfused hind limb and in the perfused gastrocnemius muscle of anesthetized dogs was examined at normal plasma calcium concentration and during elevation of the plasma calcium concentration produced by intra-arterial infusion of calcium chloride. Hypercalcemia inhibited the vasodilator action of hypercapnic acidosis so that the effect was not apparent until venous blood pH decreased below 7. The dilator effect of local application of acidified Ringer's solution on arterioles of the cremaster muscle of the rat was also inhibited by elevation of the plasma calcium concentration induced by intravenous administration of calcium chloride. The available evidence suggests that this inhibition of the dilator effect of hypercapnic acidosis by calcium ions is related to competition between calcium and hydrogen ions for binding at one or more cellular sites such as the sarcolemma, the sarcoplasmic reticulum, or the contractile proteins of vascular smooth muscle.

Vasodilator effects of local hypercapnic acidosis in dog skeletal muscle.

ARTICLESVasodilator effects of local hypercapnic acidosis in dog skeletal muscleHA Kontos, MD Thames, A Lombana, CO Watlington, and F Jessee JrHA Kontos, MD Thames, A Lombana, CO Watlington, and F Jessee JrPublished Online:01 Jun 1971https://doi.org/10.1152/ajplegacy.1971.220.6.1569MoreSectionsPDF (811 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAcute hypoxia elicits lasting reductions in the sympathetic action potential transduction of arterial blood pressure in males5 January 2023 | The Journal of Physiology, Vol. 601, No. 3The exercise pressor reflex and chemoreflex interaction: cardiovascular implications for the exercising human27 April 2020 | The Journal of Physiology, Vol. 598, No. 12Local Analgesia18 July 2014α 1 -Adrenergic responsiveness in human skeletal muscle feed arteries: the impact of reducing extracellular pH15 August 2012 | Experimental Physiology, Vol. 98, No. 1Surgery of the Thoracic Wall18 July 2014Hypoxia augments muscle sympathetic neural response to leg cyclingKeisho Katayama, Koji Ishida, Erika Iwamoto, Motoyuki Iemitsu, Teruhiko Koike, and Mitsuru Saito1 August 2011 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 301, No. 2Sustained muscle sympathetic activity after hypercapnic but not hypocapnic hypoxia in normal humansRespiratory Physiology & Neurobiology, Vol. 141, No. 2A mathematical model of CO2 effect on cardiovascular regulationElisa Magosso and Mauro Ursino1 November 2001 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 281, No. 5Effects of Bicarbonate/Lactate Solution on Peritoneal Advanced Glycosylation End-Product Accumulation24 February 2020 | Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis, Vol. 20, No. 5_supplThe Effects of Ouabain and Potassium on Peritoneal Fluid and Solute Transport Characteristics24 February 2020 | Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis, Vol. 18, No. 4The Effect of Dialysate Acidity on Peritoneal Solute Transport in the Rat24 February 2020 | Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis, Vol. 15, No. 4Differential contractile effects of changes in carbon dioxide tension on rat mesenteric resistance arteries precontracted with noradrenalinePfl�gers Archiv European Journal of Physiology, Vol. 419, No. 1Sciatic nerve blood flow response to carbon dioxideBrain Research, Vol. 446, No. 1COUNTERCURRENT EXCHANGE OF EIIGHLY DIFFUSIBLE TRACERS IN SKELETAL MUSCLE: ITS ABSENCE IN THE LUNGClinical and Experimental Pharmacology and Physiology, Vol. 4, No. 2Effects of altered carbon dioxide tension on hemoglobin oxygenation in hamster cheek pouch microvesselsMicrovascular Research, Vol. 13, No. 2Inhibition of the Vasodilator Effect of Hypercapnic Acidosis by Hypercalcemia in Dogs and RatsCirculation Research, Vol. 35, No. 6Changes in Microvascular Diameter and Oxygen Tension Induced by Carbon DioxideCirculation Research, Vol. 32, No. 3 More from this issue > Volume 220Issue 6June 1971Pages 1569-1572 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.220.6.1569PubMed5087802History Published online 1 June 1971 Published in print 1 June 1971 Metrics

Recording of microvascular dimensions with an image-splitter television microscope.

Recording of microvascular dimensions with an image-splitter television microscope.