Neuronal nitric oxide synthase in macula densa cells modulates short-term tubuloglomerular feedback but not long-term renin release.
Distinguishes acute TGF from chronic renin roles of MD nNOS; leaves open therapeutic relevance in salt-sensitive hypertension.
In the juxtaglomerular apparatus of the kidney the distal tubule returns to its own glomerulus where specialised cells, the macula densa (MD) cells, are located so that they come in contact with the tubular fluid. It is well documented that MD cells sense the distal tubular flow-rate and that when the flow is too high they are activated, which leads to vasoconstriction of the afferent arteriolar, the tubuloglomerular feedback (TGF). Neuronal nitric oxide synthase (nNOS) is largely expressed in the MD cells. Acute inhibition of MD nNOS leads to an enhanced TGF response, indicating that nitric oxide (NO) is an important short-term modulator for volume regulation in the body. By contrast, the NO from the nNOS of the MD cells does not seem to play a role in the long-term adaptations of renin release in low- or high-salt diets.
No takes yet. Share an insight, caveat, or question.
Ollerstam et al. (2002) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: