Medical Physiology Online

Peer reviewed, open access journal. ISSN 1985-4811.

Question regarding “Choosing Sex”

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I refer to the article “Choosing Sex” by Professor Capel published recently in The Scientist [accessed 6 Oct 2009]

My question is what would happen if none of these signals (Wnt, SRY, FGF9) were present  in the first place. What would be the eventual fate of the bipotential gonad? Will both testes and ovaries develop or neither?

Ravivarma Panirselvam, 

Second Year Medical Student

AIMST University, 08100 Bedong, Kedah, Malaysia

E-mail: ravivarmarao at gmail dot com

Conflict of interests: none


Posted in the “Ask a Question” Section by E.S.Prakash, Editor, MPO.

Written by Elapulli S. Prakash

October 6, 2009 at 12:01 PM

Posted in 256080

Increasing kidney oxygenation as a potential therapeutic avenue for kidney disease

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Point of View

Increasing kidney oxygenation as a potential therapeutic avenue for kidney disease

Nikki R Adler, Department of Physiology, Monash University, PO BOx 13F, Melbourne, Victoria 3800, Melbourne, Australia. E-mail: nradl2 at student dot monash dot edu

Manuscript received 23 Jul 2009; first decision 5 Aug 2009; revised 3 Oct 2009; accepted and published 3 Oct 2009


It is important to investigate the mechanisms of chronic kidney disease as it is a public health problem worldwide. The unique architecture of the kidney vasculature underpins the kidney’s susceptibility to hypoxia. The countercurrent arrangement of arteries and veins in the renal cortex and of capillaries (ascending and descending) in the medulla contributes to decreased oxygen availability. Kidney disease is associated with loss of peritubular capillaries in the tubulointerstitium. Tissue hypoxia contributes to the progression and pathogenesis of chronic kidney disease. Hypoxia occurs in the tubulointerstitium prior to structural microvascular damage. Thus, hypoxia is a pathogenic factor in early stage renal disease. Approaches to increase intrarenal oxygenation form a potential therapeutic target. Presently, inhibition of the renin angiotensin system is used to treat chronic kidney disease. Angiotensin-II receptor antagonists and angiotensin-converting-enzyme inhibitors afford renoprotection in part by altering the balance between oxygen delivery and oxygen consumption, thereby treating chronic hypoxia in the tubulointerstitium. Erythropoietin (EPO) may confer renal cytoprotection and improve kidney oxygenation. However, its efficacy in the treatment of chronic renal disease in the human condition is yet to be established. Modulation of the hypoxia inducible factor (HIF) system, via prolyl hydroxylase inhibitors, is a potential therapeutic target for the treatment of chronic kidney disease. Additional research should be conducted to further elucidate the mechanisms of kidney oxygenation and the adaptive hypoxic response.

Conflict of interests: none

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Some rights reserved, N.R.Adler. This is an open access article distributed under the terms of the Creative Commons Attribution License

Written by Elapulli S. Prakash

October 3, 2009 at 3:05 PM

Posted in 256080

Letter regarding the article ‘Cold-activated brown adipose tissue in healthy men’ by Lichtenbelt et al.

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Using integrated 18F-fluorodeoxyglucose positron emission tomography and computed tomography, Lichtenbelt et al [1] have demonstrated cold induced brown adipose tissue activity in lean and overweight healthy men. The authors also find a significant negative correlation between body mass index and brown adipose tissue activity.

In this study, body mass index (BMI) was used to classify subjects as lean (BMI < 25 kg/m2) or overweight/obese (BMI ³ 25 kg/m2). However, the percentage of body fat in overweight/obese subjects varied from 16.9 – 41.8%, the lower limit of this being much lower than that in ‘lean’ subjects, indicating that at least some of the subjects who were classified as obese were not ‘excessively fat’. Indeed, for body fat percentage values between 10 and 20% (n = 10 in this study), the authors also found a steep inverse relationship between body fat percentage and brown adipose tissue activity (Figure 3B in Ref. 1). Although what is a healthy body fat percentage remains to be established from prospective studies [2] and obesity is not currently defined on the basis of body fat percentage or fat mass index (i.e., fat mass in kg divided by square of the height expressed in meters; Ref. 3), we are interested in knowing how the volume of brown adipose tissue and resting metabolic rate compared if subjects in this study were dichotomized on the basis of an arbitrary body fat percentage (say 20%) or fat mass index rather than BMI.

Secondly, since waist circumference, an estimate of abdominal adiposity, has been demonstrated to independently predict mortality, [4] we wonder if this was measured in this study and if so how it correlated with brown adipose tissue activity.

Conflict of interests: none

E.S.Prakash and K.R.Sethuraman,

Faculty of Medicine, AIMST University, 08100 Semeling, Kedah, Malaysia

E-mail: dresprakash at gmail dot com


E.S.Prakash is the Editor and Dr K.R.Sethuraman is a member of the Senior Advisory Board of Medical Physiology Online.

Editor for this Submission: This letter was reviewed and accepted for publication by Dr Roger Evans, Department of Physiology, Monash University, Melbourne, Australia. e-mail: roger dot evans at med dot monash dot edu dot au. Dr Evans is a member of the Senior Advisory Board for Medical Physiology Online.

Submitted 15 June 2009, revised 16 Jun 2009, accepted and published 17 Jun 2009.


[1] van Marken Lichtenbelt WD, Vanhommerig JW, Smulders NM, et al. Cold-activated brown adipose tissue in healthy men. New England Journal of Medicine 2009; 360:1500-8 [Abstract]

[2] Gallagher D, Heymsfield SB, Heo M, Jebb SA, Murgatroyd PR, and Sakamoto Y. Healthy percentage body fat ranges: an approach for developing guidelines based on body mass index. American Journal of Clinical Nutrition 2000; 72: 694–701. [Full text]

[3] Schutz Y, Kyle UUG and Pichard C. Fat-free mass index and fat mass index percentiles in Caucasians aged 18 – 98 y. International Journal of Obesity 2002; 26: 953–960. [Abstract]

[4] Pischon T, Boeing H, Hoffmann K, et al. General and abdominal adiposity and risk of death in Europe. New England Journal of Medicine 2008; 359: 2105-2120. [Full text]

Please cite this letter as E.S.Prakash and K.R.Sethuraman. Letter regarding the article ‘Cold-activated brown adipose tissue in healthy men’ by Lichtenbelt et al. Medical Physiology Online 2009; available from

Some rights reserved © E.S.Prakash and K.R.Sethuraman, 2009. This is an open access article distributed under the terms of the Creative Commons Attribution License

Written by Elapulli S. Prakash

June 17, 2009 at 11:19 AM

Cardiac inter-beat interval complexity is influenced by physical activity

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Benjamin J. Wilson1, Gus L. W. Hart2, and Allen C. Parcell3

1Department of Recreation Management and Youth Leadership, Brigham Young University, Provo, Utah; 2Department of Physics and Astronomy, Brigham Young University, Provo, Utah; 3Human Performance Research Center, Department of Exercise Sciences, Brigham Young University, Provo, Utah.

Correspondence to: Benjamin J. Wilson, 3838 S 1860 E, Salt Lake City, UT 84106, USA.

E-mail: benjaminjameswilson at gmail dot com

Submitted 25 Oct 2008; time to first decision 25 days; revision accepted and published 1 Jan 2009.


The complexity of physiological signals may be a more sensitive indicator of health than standard or average measurements. We examined cardiac inter-beat intervals of healthy subjects who are either physically active or sedentary to determine whether measures of complexity are more sensitive to subtle cardiac changes than standard measures. Subjects were pre-screened by self-report, and qualifying subjects were placed in either the active group (n = 10) or sedentary group (n = 10). Cardiac inter-beat intervals were recorded and subsequently analyzed using standard time and frequency domain heart rate variability measurements as well as multiscale entropy and the detrended fluctuation analysis, both measures of complexity. Of the measurements, the detrended fluctuation analysis was the only tool that significantly (P = 0.04) differentiated between the active and sedentary groups. This suggests that the complexity of physiologic signals is a more sensitive indicator of cardiac health than standard measures.


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Please cite this article as: Wilson BJ, Hart GLW, Parcell AC. Cardiac inter-beat interval complexity is influenced by physical activity. Medical Physiology Online, 1 Jan 2009, available from

Written by Elapulli S. Prakash

January 1, 2009 at 1:34 AM

Brief Review: Premature skeletal muscle fatigue in multiple sclerosis and its implications for exercise therapy

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Elizabeth Harper

Department of Health Studies, Program in Therapeutic Recreation,

New York University, NY, 10003, USA;

E-mail: eh403 at nyu dot edu

Submitted 19 March 2008; first decision 9 April 2008; revised 21 May 2008; revision accepted 19 Jun 2008; published 4 Jul 2008


This paper reviews work on skeletal muscle fatigue as it relates to multiple sclerosis. Accumulation of products of metabolism contribute significantly to the onset of fatigue in normal healthy muscles whereas the primary cause of muscle fatigue in multiple sclerosis is due to impairment of central nervous system activation of motor units followed by changes in muscle metabolism due to progressive disuse. As performing repetitive gross motor activity of the limbs becomes increasingly difficult, the MS individual becomes vulnerable to a host of secondary health concerns including weak respiratory muscles. Pranayam is a type of yogic exercise that focuses one’s attention on regulation of the breath. Many of the benefits of practicing pranayam are similar to the physiological and psychological benefits attributed to performing repetitive gross motor exercises of the limbs. Pranayam should be explored as a potential adjunctive therapeutic exercise modality in individuals with multiple sclerosis.

Content outline:

1. Introduction

1.1 Noninvasive muscle testing techniques

1.1A Electromyography

1.1B Magnetic resonance spectroscopy

2. Fatigue in healthy muscle

3. Fatigue in multiple sclerosis

3.1 Origin of fatigue in MS

3.2 Central motor drive in MS

3.3 Deconditioning in MS

3.4 Skeletal muscle fatigue vs. perceived fatigue

3.5 Exercise in the management of multiple sclerosis

3.6 Potential role of pranayam as adjunctive therapy

3.7 Summary and Research Directions

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Please cite this article as Harper E. Premature skeletal muscle fatigue in multiple sclerosis and its implications for exercise therapy. Medical Physiology Online, 4 Jul 2008, available from

Some rights reserved (C) 2008, E. Harper. This is an open access article distributed under the terms of the Creative Commons Attribution License

Written by Elapulli S. Prakash

July 4, 2008 at 10:00 AM

What is the link between psychologic stress, caffeine, sympathetic activity and ventricular ectopics?

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Karthik Viswanathan, Coronary Artery Disease Clinical Research Network Group, Leeds Institute for Genetic, Health & Therapeutics, Leeds, United Kingdom. E-mail: drkarthikv at gmail dot com

I see a lot of patients referred to us in the cardiology department with palpitations due to ventricular ectopics, and if there is no evidence of structural heart disease or coronary artery disease, we usually reassure and discharge these patients. Some of them have unifocal ventricular ectopics, some have multifocal ventricular ectopics, others have bigeminy or trigeminy. Few have pauses with compensatory tachycardia thereafter. Very often we get asked: Is there anything we can do to stop these symptoms? We usually say that reducing caffeine, alcohol, stress may help but I don’t really know if there is any physiological basis for this recommendation. Is there any evidence that physiological ventricular ectopics are driven by increased sympathetic activity or by increased levels of stress, caffeine in susceptible people?

Conflict of interests: none declared

Written by Elapulli S. Prakash

April 11, 2008 at 10:00 AM

When we measure extracellular fluid volume, is transcellular fluid volume also measured?

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When we measure extracellular fluid volume, is transcellular fluid volume also measured? How is the total volume of transcellular fluid determined?

Dineash Kumar, Year 1 Medical Student, School of Medicine, Asian Institute of Medicine, Science & Technology, 08100 Bedong, Kedah, Malaysia; e-mail: dineashkumar at yahoo dot com

Written by Elapulli S. Prakash

March 27, 2008 at 10:00 AM

Is 5% dextrose solution an effective osmole?

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Ravivarma Rao Panirselvam, Year 1 Medical Student, School of Medicine, Asian Institute of Medicine, Science & Technology, 08100 Bedong, Kedah, Malaysia; e-mail: unicorn063 at hotmail dot com

Written by Elapulli S. Prakash

March 27, 2008 at 10:00 AM

On the real cause of pyloric stenosis of infancy

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An interview with Ian Munro Rogers, School of Medicine, Asian Institute of Medicine, Science & Technology, 08100 Bedong, Kedah Darul Aman, Malaysia. 

Correspondence: irogers2000 at hotmail dot com
Interviewed by E.S.Prakash, Editor, Medical Physiology Online
Interviewed 4 Feb 2008; manuscript received 6 Feb 2008; accepted and published 11 Feb 2008.
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Abbreviations: PS – pyloric stenosis; ESP – E.S.Prakash; IMR – Ian Munro Rogers 

Background: Dr.I.M.Rogers has put forth the hypothesis that the inheritance of a higher than normal parietal cell mass and the ensuing hyperacidity is the primary cause of pyloric stenosis (PS) of infancy. See ref. [1] Rogers IM. The true cause of pyloric stenosis is hyperacidity. Acta Paediatrica 2006; 95: 132–136 available at In this interview, Dr. Rogers answers some questions that come in the wake of this hypothesis.

1. ESP: If the hypothesis that hyperacidity is the ultimate cause of PS of infancy is correct, then, patients with pronounced hyperacidity (example, patients with Zollinger-Ellison syndrome) should also develop this complication. Your comments on this.

IMR: Patients with Zollinger-Ellison syndrome usually have acid-induced peptic ulcers – normally duodenal ulcers which perforate and bleed. Some of them will have PS or rather duodenal stenosis. I think newborns with hyperacidity are a different kettle of fish in the sense that the pyloric canal is very narrow, and even a small further reduction due to acid-induced pyloric sphincter hypertrophy would be enough to precipitate functional stenosis. At this point, other factors which further increase acidity begin to operate and a self-perpetuating process begins, culminating in PS. In a sense, this condition occurs because the rate of pyloric narrowing due to acid exceeds the rate at which age related widening of the pyloric canal occurs. This may be the reason why this condition presents within 3-4 weeks (a narrow interval indeed) of birth. Further, hypergastrinaemia, a phenomenon known to occur at this time (as alluded to my in my review [1]), is also likely to facilitate hypertrophy of the sphincter.

2. ESP: You have mentioned in your review [1] that in babies with PS, the negative feedback relationship between fasting gastrin and acid secretion is not evident until the third week of life. Is this also true for normal babies? If so, what does this indicate?

IMR: Yes, it is true for normal babies. In papers from Dr. MacGuigan’s laboratory, Florida, USA [2, 3], normal babies were found to have hypergastrinaemia without postprandial elevation in gastrin up to 2 months of age. Between 3-4 months, fasting gastrin levels had fallen and postprandial gastrin responses became evident. The implication is that from birth to 2 months of age, gastrin is maximally stimulated and hence can not become higher when exposed to constitutional hyperacidity or after ingestion of a protein containing formula [2].

3. ESP: Are there any studies of plasma levels of secretin (the major humoral mediator regulating meal stimulated secretion of bicarbonate rich secretions from the gastrointestinal tract) in neonates with PS? The question comes as defects in neutralizing the effects of gastric acid might also predispose to the hyperacidity that you consider the prime pathogenetic mechanism in PS.

IMR: In 1975, we published a study [4] in which we evaluated the secretion of secretin in neonates. Curiously, the rise between day 1 and 4 was similar to that observed with gastrin. I know of no more investigations of secretin levels in neonates

4. ESP: Is hyperacidity a consistent feature of PS of infancy?

IMR: Strangely, there have been very few studies of gastric acid secretion in PS. In 1979, we first reported basal hyperacidity in babies with PS compared to normal babies [5]. Heine et al [6] reported higher histamine induced gastric acid secretion in babies with pyloric stenosis before and 1 week after pyloromyotomy.

5. ESP: Is there evidence that a high parietal cell mass is inherited?

IMR: Babies with PS do secrete more acid than normal babies, and this persists after pyloromyotomy [6]. Supporting evidence for primary acidity is the observation that babies who are vomiting and are alkalotic at this age invariably have PS. The condition is strongly familial; it is much more common in males compared to females (4: 1) as duodenal ulcers are in adults. Long term studies have documented problems with hyperacidity long after pyloromyotomy. Preterm normal male babies have been shown to secrete more acid than maturity matched female babies [7]. Thus, while there is no direct evidence of supernormal parietal cell mass, available evidence is indeed consistent with this theory.

6. ESP: Given your hypothesis, it is indeed surprising to me that the tumor does not disappear following gastroenterostomy; i.e., if hyperacidity were the primary cause of the growth of the pyloric sphincter, gastroenterostomy which allows drainage of acid should lead to a perceptible reduction in the size of the pyloric sphincter.

IMR: The extraordinary thing is that the pyloric tumour disappears within days of pyloromyotomy [8] and within weeks of successful medical treatment [9]. Regarding the failure of the tumor to regress following gastroenterostomy [1], it simply may be that unless the hypertrophied pyloric sphincter is divided, it can not relax or dilate with the passage of food. Further, a posterior gastroenterostomy may not drain the antrum well. A poorly drained alkaline antrum is a classical way of increasing gastrin levels – especially after vagotomy, and thus the continuing presence of trophic factors such as gastrin may in addition explain the persistence of the pyloric tumor following gastroenterostomy.  

7. ESP: Alternate causes for pyloric stenosis have been proposed; for example, a relative deficiency of neuronal nitric oxide synthase at the sphincter [10] may be primary to the condition – something like in achalasia. Your comments on this:

IMR: Deficiency of nitric oxide explains the pylorospasm. It does not explain the predominance of this condition in males; neither does it explain spontaneous self-cure after a certain age. The failure of this condition to recur after simply dividing the sphincter and the very good response to adequate medical therapy is also not explained. How does it explain the persistence and complications of high acidity after pyloromyotomy?

8. ESP: The observation that rats with an artificially narrowed pylorus secrete more acid and gastrin in response to a meal and the fact that gastrin producing antral cells become hyperplastic [11] in this model is interesting but in this instance hypergastrinaemia and hyperacidity are secondary to pyloric stenosis not the cause of it. What is your opinion?

IMR: First, the hypothesis that primary hyperacidity is the cause of PS is based on the premise that all babies are potentially at risk of acid induced pylorospasm at around 3-4 weeks; however, babies who develop PS are most vulnerable because the burden of constitutional hyperacidity proves too great. Secondly, in my review [1], I cited the study by Omura et al [11] to suggest that once PS is established, there are mechanisms that maintain hyperacidity. The authors [11] demonstrated hypergastrinaemia secondary to PS. Furthermore, there is evidence for a gastrin independent pyloro-oxyntic local neural reflex [12] that can induce acid secretion. Indeed, Talbot [13] has reported improvement in symptoms in patients with peptic ulcer induced gastric outlet obstruction treated with proton pump inhibitors.

9. ESP: Please tell us what you believe would be the most important research questions that need to be investigated in the management of infantile hypertrophic PS?

IMR: To evaluate the benefit of intravenous proton pump inhibitors after making a diagnosis of PS and while awaiting surgery. Indicators of improvement would be reduced acid and volume loss from the nasogastric aspirate and a reduction in metabolic alkalosis. A period of 2 days is not unusual between diagnosis and surgery; this should allow an adequate appraisal. Retrospective data on patients undergoing surgery for PS on whom 2 acid base studies (preoperatively and intraoperatively) are usual would allow a comparison to be made with the acid base changes as a result of treatment with proton pump inhibitors. In adults who have high acidity and who vomit; i.e., adult pyloric stenosis, preoperative administration of proton pump inhibitors is standard therapy to reduce loss of fluids as well as acid. Indeed, in some instances, the alleged pyloric stenosis is functionally improved or cured by this treatment alone – so the question is why babies in whom acid base and volume homeostasis is less secure should be denied this treatment. I believe that the baby diagnosed early enough to have PS but without access to safe surgery would be advantaged by the sole temporary use of proton pump inhibitors while awaiting the enhanced possibility of spontaneous cure. That is my opinion.

ESP: Thank you very much Dr. Rogers for sharing your thoughts with us.


Conflict of interests: none declared.


  1. Rogers IM. The true cause of pyloric stenosis is hyperacidity. Acta Paediatrica 2006; 95: 132–136. Free full text at
  2. Rodgers BM, Dix PM, Talbert JL, McGuigan JE. Fasting and postprandial serum gastrin in normal human neonates. Journal of Pediatric Surgery 1978; 13: 13–16; abstract at
  3. Moazam F, Kirby WJ, Rodgers BM, McGuigan JE. Physiology of serum gastrin production in neonates and infants. Annals of Surgery 1984; 199: 389–392. Free full text
  4. Rogers IM, Davidson DC, Lawrence J, Buchanan KD. Neonatal secretion of secretin. Archives of Disease in Childhood 1975; 50: 120–122. Abstract at
  5. Rogers IM, Drainer IK, Dougal AJ, Black J, Logan R. Serum cholecystokinin, basal acid secretion and infantile hypertrophic pyloric stenosis. Archives of Disease in Childhood 1979; 54: 773–775. Abstract at
  6. Heine W, Grager B, Litzenberger M, Drescher U. Results of Lambling gastric juice analysis in infants with spastic hypertrophic pyloric stenosis. Pädiatrie und Pädologie 1986; 21: 119–125 [Article in German] abstract at
  7. Yamataka A, Tsukada K, Laws YY, Murata M, Lane GJ, Osawa M,  Fujimoto T, Miyano T. Pyloromyotomy versus atropine sulphate for infantile hypertrophic pyloric stenosis. Journal of Pediatric Surgery 2000; 35: 338–341. Abstract at
  8. Yamamoto A, Kuno M, Sasaki T, Kobayashi Y. Ultrasonographic follow-up of the healing process of medically treated hypertrophy pyloric stenosis. Pediatric Radiology 1998; 28: 177–178. Abstract at
  9. Vanderwinden JM, Mailleux P, Schiffmann SN, Vanderhaeghen JJ, De Laet MH. Nitric oxide synthase activity in infantile hypertrophic pyloric stenosis. New England Journal of Medicine 1992; 327: 511–515. Abstract at
  10. Omura N, Kashiwagi H, Aoki T. Changes in gastric hormones associated with gastric outlet obstruction. An experimental study in rats. Scandinavian Journal of Gastroenterology 1993; 28: 59–62. Abstract at
  11. Proof of a pyloro-oxyntic reflex for stimulation of acid secretion. Gastroenterology 1974; 66: 526–532. Abstract at
  12. Talbot D. Treatment of adult pyloric stenosis: a pharmacological alternative? British Journal of Clinical Practice 1993; 47: 220–221. Abstract at

Copyright © IM Rogers, 2008. This is an open access article distributed under the terms of the Creative Commons Attribution License

Editor’s note (conflict of interest): I invited this manuscript from Dr. Rogers, reviewed and edited it. Both Dr. Rogers and I work in the School of Medicine, Asian Institute of Medicine, Science & Technology, Malaysia, but that wouldn’t affect my review and disposition of this manuscript. – E.S.Prakash, Editor, Medical Physiology Online.

Please cite this article as Rogers IM. On the real cause of pyloric stenosis of infancy. Medical Physiology Online, 11 Feb 2008, available from

Written by Elapulli S. Prakash

February 11, 2008 at 11:52 AM

Point of View: Denervation supersensitivity to noradrenaline in resistance vessels in denervated canine myocardium

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Angela J Drake-Holland1 and Mark I.M Noble2

1School of Pharmacy, Robert Gordon University, Aberdeen, AB10 1FR,  2Cardiovascular Medicine, Dept of Medicine and Therapeutics, University of Aberdeen Medical School, Foresterhill, Aberdeen, AB25 2ZN.

Correspondence to: Prof. AJ Drake-Holland, School of Pharmacy, Robert Gordon University, Aberdeen, AB10 1FR, E-mail: Prof M I M Noble can be reached at


[Received 25 January 2008; first decision 1 February 2008; revised, accepted and published 13 Feb 2008]


Cannon’s law states that a chronically denervated structure is supersensitive to the neurotransmitter it is normally regulated by. However, the present consensus is that myocardial arteriolar resistance vessels are not supersensitive to noradrenaline following chronic sympathetic denervation of the heart. We present an extended interpretation of results of a published study in which the volume of distribution of radiolabeled hydroxyephedrine and blood flow were measured in innervated and denervated regions of the same canine heart using positron emission tomography. For a given amount of noradrenaline, myocardial blood flow was lower in denervated than innervated myocardium, indicating denervation supersensitivity. This finding has implications for patients with cardiac autonomic neuropathy.

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Please cite this article as: Drake-Holland AJ and Noble MIM. Denervation supersensitivity to noradrenaline in resistance vessels in denervated canine myocardium. Medical Physiology Online, 13 Feb 2008, available from


Written by Elapulli S. Prakash

February 11, 2008 at 10:00 AM