|Year : 2016 | Volume
| Issue : 1 | Page : 25-27
Students' convoluted trouble with renal autoregulation: A teaching note for students and physiology educators
Hwee-Ming Cheng, See-Ziau Hoe
Department of Physiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
|Date of Submission||04-May-2016|
|Date of Acceptance||11-May-2016|
|Date of Web Publication||2-Jun-2016|
Department of Physiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur
Source of Support: None, Conflict of Interest: None
This teaching insight focused on the common misperceptions regarding renal autoregulation (RenAutoreg). The classical model of RenAutoreg is an intrinsic mechanism of a denervated kidney in an in vitro setup. The whole body homeostatic in vivo model of RenAutoreg in a few major texts accounts for the confusion in understanding the intrinsic nature of RenAutoreg first defined originally. RenAutoreg correctly distinguished will provide the basis for appreciating the other intrinsic renal mechanism called glomerulo-tubular balance and also the "second fiddle" role of RenAutoreg in the homeostasis of extracellular fluid/blood volume and arterial pressure.
Keywords: Educators, physiology, renal autoregulation, students
|How to cite this article:|
Cheng HM, Hoe SZ. Students' convoluted trouble with renal autoregulation: A teaching note for students and physiology educators. BLDE Univ J Health Sci 2016;1:25-7
|How to cite this URL:|
Cheng HM, Hoe SZ. Students' convoluted trouble with renal autoregulation: A teaching note for students and physiology educators. BLDE Univ J Health Sci [serial online] 2016 [cited 2019 May 21];1:25-7. Available from: http://www.bldeujournalhs.in/text.asp?2016/1/1/25/183281
Renal autoregulation (RenAutoreg) maintains intrinsically the renal blood flow (RBF) over a range of fluctuations in renal arterial or perfusion pressure. This inherent property of the nephron involves both the myogenic and the distal tubulo-glomerular feedback (t-g) mechanisms.
Our common experience with each batch of undergraduate students highlights for us several misperceptions of renal autoregulatory physiology. We share these teaching insights here to help both students and lecturers to discern through the relative complexities of this intrinsic renal phenomenon. This is described here in systematic point form to summarize the logic and rationale behind the correct understanding of RenAutoreg.
- The classical definition of RenAutoreg was derived from in vitro experimentations with a denervated kidney preparation. Hence, the term "intrinsic" means independent of extrinsic nerve or circulating hormone actions. I called this an "isolated kidney" model or i-Kid
- The i-Kid model is the one represented by the graph showing RenAutoreg in most physiology textbooks. The x-axis is the renal perfusion pressure, and the y-axis is the RBF. Over the 60-160 blood pressure mmHg range, a plateau phase demonstrates the intrinsic ability of the i-Kid to autoregulate its local blood flow
- This i-Kid model is thus independent of renal sympathetic action or any of the circulating vasoactive agents like angiotensin II (Ang II)
- The i-Kid model involves primarily the preglomerular afferent arteriole as the final target effector of RenAutoreg. The myogenic response is a special stretch/contraction reflex of the afferent arteriole. The t-g feedback mechanism involves the distal tubular macula densa cells that secrete a paracrine that acts ultimately on the preglomerular arteriole.
Some of the students' confusion in appreciating RenAutoreg is actually due to a different definition of RenAutoreg in Guyon's textbook of physiology.  Guyton's model of RenAutoreg is not the classical isolated, denervated i-Kid model. The picture of RenaAutoreg in Guyton's text is the role of the in vivo kidneys in the body. I will call this "Kid at Home" or KaH model.
Students who read Guyton or use powerpoint lecture notes based on Guyton will observe that the RenaAutoreg mechanism in the KaH model includes both the renal afferent and efferent arterioles. In particular, the postglomerular efferent arteriole participates by its response to the circulating vasoconstrictor Ang II. Ganong's review text characteristically, also make mention very briefly of the efferent arteriole/Ang II pathway in whole body RenAutoreg. 
Strictly defined, the KaH model is no longer an intrinsic renal phenomenon. It involves circulating hormones through activation of the renin-angiotensin pathway. An extrinsic renal sympathetic nerve that stimulates renin secretion is also a part of this RenAutoreg compensation for a decreased renal perfusion pressure.
We have made a survey of several physiology textbooks that defines and describes RenAutoreg [Table 1]. As noted, Guyton and Ganong are the only authors that have a different nonintrinsic view of RenAutoreg. This KaH model naturally will encompass a whole body homeostatic response (conversion of Ang I to Ang II in the lungs) and has the final actions on both the afferent and efferent arterioles.
|Table 1: Physiology textbooks that define and describe renal autoregulation|
Click here to view
The other physiology texts with the accompanying graph showing a plateau of constant, autoregulated RBF only include the preglomerular afferent arteriole in the RenAutoreg pathways.
Recent comprehensive reviews of RenAutoreg also primarily focuses on the diverse candidates of the paracrines that are secreted by the macula densa (I abbreviate to McD for this generation of fast food chomping medics). ,, The paracrine vasoconstrictor and vasodilators from the McD alter the vascular resistance of the preglomerular afferent arteriole to effect the intrinsic RenAutoreg.
Whether the students use the i-Kid or the KaH model furthermore affects their conception of the homeostasis of blood volume and pressure regulation. To illustrate, when students are asked "What happens to RBF when the arterial blood pressure decreased to 80 mmHg?," a surprisingly high number of students will say that the RBF is maintained based on the RenAutoreg graph. Their incorrect answers highlight the essential point that the RenAutoreg characteristic profile is seen distinctly only in the isolated, denervated i-Kid model.
In the in vivo situation, a reduction to 80 mmHg will activate the baroreflex sympathetic effector response and this will constrict the renal arterioles and decrease RBF as a part of a temporal response to maintain blood volume/pressure. The renal sympathetic activity "masks" the intrinsic RenAutoreg.
Associated with the RenAutoreg is another intrinsic renal mechanisms called the glomerulo-tubular (g-t) balance. This g-t balance is also independent of extrinsic inputs from nerve or circulating hormones. The t-g and g-t mechanisms are quite similar sounding and are quite frequently mixed up by students. Arthur Vander made the helpful big picture point of the nephron that places the distal tubular macula densa t-g feedback and the g-t balance into a collaborative scheme of renal physiology. 
The t-g feedback functions (with the myogenic response) to maintain RBF and glomerular filtration rate (GFR), and hence the filtered load. However, the RenAutoreg is not perfect and any fluctuations of GFR and filtered load that still occur are then handled by the second intrinsic g-t balance that involves the proximal tubular epithelial cells.
We hope this teaching note is helpful for readers who teaches and interacts with your students in tutorials and in your office.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Guyton AC, Hall JE. Textbook of Medical Physiology. 11 th
ed. Philadelphia: Elsevier Saunders; 2006.
Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong′s Review of Medical Physiology. 24 th
ed. New York: McGraw-Hill Education; 2012.
Seeley RR, Stephens TD, Tate P. Anatomy & Physiology. 7 th
ed. New York: The McGraw-Hill Companies; 2006.
Johnson LR, editor. Essential Medical Physiology. 3 rd
ed. California: Elsevier Academic Press; 2003.
Sembulingam K, Sembulingam P. Essentials of Medical Physiology. 6 th
ed. New Delhi: Jaypee Brothers Medical Publishers; 2012.
Michael J, Sircar S. Fundamentals of Medical Physiology. New York: Thieme Medical Publishers; 2011.
Marieb EN, Hoehn K. Human Anatomy & Physiology. 9 th
ed. New York: Pearson Education; 2013.
Davies A, Blakeley A, Kidd C. Human Physiology. Edinburgh: Churchill Livingstone; 2001.
Fox SI. Human Physiology. 12 th
ed. New York: The McGraw-Hill Companies; 2011.
Rhoades R, Pflanzer R. Human Physiology. 4 th
ed. London: Thomson Brook/Cole; 2003.
Silverthorn DU. Human Physiology. An Integrated Approach. 6 th
ed. Boston: Pearson Education; 2014.
Sherwood L. Human Physiology. From Cells to Systems. 7 th
ed. Australia: Brooks/Cole, Cengage Learning; 2010.
Boron WF, Boulpaep EL. Medical Physiology. Updated. 2 nd
ed. Philadelphia: Elsevier Saunders; 2012.
Kibble JD, Halsey CR. Medical Physiology. The Big Picture. New York: The McGraw-Hill Companies; 2009.
Costanzo LS. Physiology. 4 th
ed. London: Saunders Elsevier; 2010.
Berne RM, Levy MN, Koeppen BM, Stanton BA. Physiology. 5 th
ed. St. Louis: Mosby, Elsevier Science; 2004.
Tortora GJ, Derrickson B. Principles of Anatomy & Physiology. 14 th
ed. New Jersey: John Wiley and Sons; 2014.
Stanfield CL, Germann WJ. Principles of Human Physiology. 3 rd
ed. San Francisco: Pearson Benjamin Cummings; 2008.
Eaton DC, Pooler JP. Vander′s Renal Physiology. 6 th
ed. New York: The McGraw-Hill Companies; 2004.
Just A. Mechanisms of renal blood flow autoregulation: Dynamics and contributions. Am J Physiol Regul Integr Comp Physiol 2007;292:R1-17.
Inscho EW. Lewis K. Dahl memorial lecture. Mysteries of renal autoregulation. Hypertension 2009;53:299-306.
Carlström M, Wilcox CS, Arendshorst WJ. Renal autoregulation in health and disease. Physiol Rev 2015;95:405-511.