According to Vander, there are 3 primary detectors that control renin secretion from JG cells:

(1) vascular baroreceptors, via renal sympathetic nerves acting on beta1-adrenergic recptors on JG cells.

(2) intrarenal baroreceptors, which are JG cells themselves. These cells work both as detectors (of renal arteriolar pressure) and effectors (releasing renin).

(3) macula densa cells. (Vander, p101 )

However, even though macula densa cells affect renin release following changes in the Na and Cl content in the lumen at the end of the thick ascending loop of Henle, the tubuloglomerular feedback mechanism is a locally medicated response that does not involve the renin-angiotensin-aldosterone system.

When Na and Cl content increases, the macula densa cells cause contraction of mesangial cells and afferent arteriolar smooth muscles via local chemical signals (ATP, ?adenosine). Thus increase in Na and Cl content in the tubular lumen leads to decreased RBF and GFR. (Vander, p112) Also apparently NO is not involved in _initiating_ tubuloglomerular feedback, but does play a "secondary" role in sustaining the response once it has been initiated. (Vander, p112).

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So in answer to your first question, the tubuloglomerular feedback is entirely local and doesn't seem to be mediated by renin-angiotensin II-aldosterone system, although changes in NaCl concentration in the lumen at the end of the ascending limb does also influence renin release. I am not sure if tubuloglomerular feedback mechanism affects the efferent arteriole though (without getting angiotensin involved).

Also, I don't think you can call it metabolic autoregulation. As I understand it, metabolic autoregulation is where the level of metabolic products (which would be directly related to the level of metabolic rate) changes the local blood flow. But with tubuloglomerular feedback, it is the changes in NaCl content, which changes the volume of the macula densa cells, which then leads to a few events, and eventually result in changes in GFR and RBF. It has nothing to do with the level of metabolic activities in mecula densa cells or even the kidney.

Glomerulotubular balance, according to Vander (page 115), is the phenomenon where "a change in GFR automatically induces a proportional change in the reabsorption of sodium by the proximal tubules, so that the fraction reabsorbed (but no the total amount) remains relatively constant." (assuming there are no other processes that changes GFR). Apparently this is entirely intrarenal and requires no external input.

 

 

 

 

 

 

Aldosterone release: stimulated by (1) ACTH (2) Angiotensin II (3) rise in [K+]

[WG21:p381]

 

 

 

 

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Regulation of renal blood flow

 

Mainly by intrinsic mechanisms [BL8:p258]

 

Over MABP of 75 to 170mmHg = autoregulation --> no change in renal blood flow

Pressure autoreguation by changing resistance in afferent arteriole

 

 

2 mechanisms

Myogenic mechanisms

Tubuloglomerular feedback

 

 

Stimulation of renal sympathetic nerves

Decrease RBF substantially, but only reduce GFR slightly

Constrict afferent and efferent arterioles, and proximal segment of the vasa recta.

 

 

Reduction of RBF exceed that of GFR because postglomerular constriction greater than preglomerular constriction

 

Arterial baroreceptor influence renal vasculature only sightly.

Activation of volume receptor elicits much larger reflex effects on renal circulation via aldosterone, ADH, angiotensin II [BL8:p191]

 

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